1301.NextSteps: Nursing homes deny admission to woman with Alzheimer's(October 01, 2006@www.post-gazette.com)
1302.Scientists Use Gene Signatures To Find Treatments For Cancer, Obesity And Alzheimer's Disease(02 Oct 2006@www.medilexicon.com)
1303.Alzheimer's a real mid-life crisis(Oct. 01, 2006@www.centredaily.com)
1304.Simple Eye Test Could Spot Alzheimer's Early On(02 October 2006@www.livescience.com)
1305.Curry may help body clear itself of Alzheimer's plaques(04/10/2006@www.scienceblog.com)
1306.Negative NHS labels 'demeaning'(October 4, 2006 www.guardian.co.uk)
1307.Regulatory Approval to Start PBT2 Phase IIa Clinical Trial in Alzheimer's Disease Patients(October 05, 2006 http://moneycentral.msn.com)
1308..Is it mild cognitive impairment? Many want to know(Reuters October 06, 2006)
1309.Diet May Influence Alzheimer's Risk Mediterranean Diet, Fish Oil Could Lower Risk, Two Studies Show(Oct. 9, 2006 WebMD1310.Old drug tried on Alzheimer's disease(10/11/2006 Ivanhoe Broadcast News)
1311.Study: Anti-psychotic drugs don't help most Alzheimer's patients(October 11, 2006 @CNN)
1312.Enzyme Could Play Role in Treating Alzheimer's(HealthDay News Oct 11th 2006)
1313.Boffins look to diagnose Alzheimer's earlier(13 Oct 2006@www.vnunet.com)
1314.Questionnaire May Help Discern Mild Cognitive Impairment From Early Alzheimer's Disease(October 11, 2006 Medscape)
1315.Drug candidate effective at reversing memory loss(16 October 2006 Neuren)
1316.Three Alzheimer's Drugs Are Found To Be Ineffective(10/16/2006@www.theeveningbulletin.com)
1317.Memory Pharmaceuticals Provides Update On Phase 2a Trial Of MEM 3454 In Alzheimer's Disease(17 Oct 2006 www.medilexicon.com)
1318.Several drugs show promise for alzheimer's(October 17, 2006 The Wall Street Journal)
1319.Yee Hong program to help treat dementia(Oct. 17, 2006@www.insidetoronto.ca)
1320.Martek's DHA Selected for NIH-Funded Alzheimer's Study (17 Oct 2006 Martek Biosciences Corporation)
1321.MICROSCOPIC BRAIN DAMAGE DETECTED IN EARLY ALZHEIMER'S DISEASE(October 18, 2006 www.scientistlive.com)
1322.Marijuana-Like Compound May Slow Alzheimer's(18.10.06, www.forbes.com)
1323.Durect says Voyager ends trial of Alzheimer's drug(Oct 19, 2006 Reuters)
1324.A New Alzheimer's Vaccine(October 19, 2006@www.technologyreview.com)
1325.New Alzheimer's Clinical Trials To Be Undertaken by NIA Nationwide Consortium(ADEAR center October 17, 2006)

1326.'Back NICE' government is urgedLast Updated: Friday, 20 October 2006, 00:17 GMT 01:17 UK BBC
1327.The Insidious Fog: A journey into Alzheimer's(October 21, 2006 www.canada.com)
1328.Dementia is Canada's challenge(October 21, 2006 www.canada.com)
1329.Alzheimer's disease linked to the common cold(23rd October 2006 www.dailymail.co.uk)
1330.Computer-based 'games' boost mental function in Alzheimer's patients: study(October 23, 2006 CBC News)
1331.Estrogen Plays Both Sides On Alzheimer's(22 Oct 2006 www.medicalnewstoday.com)
1332.Vegetables May Boost Brain Power in Older Adults(Oct. 23 HealthDay News)
1333.Naturally Occurring Enzyme Can Break Down Key Part of Alzheimer's Plaques(Washington University in St. Louis 23-Oct-2006)

1334.Anaesthetics link to Alzheimer's in elderly(http://news.scotsman.com 26/10/2006)
1335.Chronic drinking may damage brain, memory(Oct. 24 UPI)
1336.Alzheimer's jab trial resurrected(26 October 2006 BBC)
1337.Behavior Problems in Moderate to Severe Alzheimer's Disease Improved With Combined Memantine and Donepezil: Presented at ANA(DGDispatch October 10, 2006)

1338.Britain developing new treatments for Alzheimer's (www.chinaview.cn 2006-10-27)
1339.Activities of Daily Living Score Can Differentiate Mild Cognitive Impairment From Mild Alzheimer's Disease: Presented at ANA(DGDispatch October 10, 2006)
1340.UWM brain research supports drug development from jellyfish protein(27-Oct-2006 University of Wisconsin - Milwaukee)
1341.Hope Remains For Alzheimer's Sufferers(28 Oct 2006 www.medicalnewstoday.com)
1342.Into the fog: Alzheimer's numbers rising dramatically(October 28, 2006 www.canada.com/saskatoonstarphoenix)
1343.Test will diagnose Alzheimer's before onset of symptoms(Oct 2006@http://news.scotsman.com)@
1344.Naturally Occurring Enzyme Can Break Down Key Part Of Alzheimer's Plaques(30 Oct 2006@www.medilexicon.com)
1345.Battle against Alzheimer's also a battle against time (October 30 2006 www.paramuspost.com)
1346.Nanogen Awarded Additional Patents for Diabetes, Alzheimer's Disease Biomarkers(10/30/2006 www.freshnews.com)
1347.Alzheimer's - from curiosity to worldwide disease By Joern Bender (October 30, 2006 www.rawstory.com)
1348.New Dementia Screening Tool Is More Sensitive(Saint Louis University Medical Center 30-Oct-2006)
1348.1Dementia before Death in Ageing Societies? The Promise of Prevention and the Reality(October 31, 2006 http//medicine.plosjournals.org)
1349.Human Spirit Stays Alive on Canvas in Alzheimer's Art Show (01 November 2006 www.voanews.com)
1350.Wine: good. Salt: bad. Fries(November 02, 2006 @The Vancouver Sun)
1351.Massage May Help Dementia Patients With Agitation(02 Nov 2006 www.medicalnewstoday.com)
1352.Scientists discover how memory gene works(October 20, 2006 www.swissinfo.org)
1353.Moderate Drinking May Boost Memory and Protect Against Alzheimer's(www.seniorjournal.com November 2, 2006)
1354.Expert Panel Recommendations for the Treatment of Alzheimer's Disease and Related Dementias in Managed Care
(October 30, 2006 DGNews)

1355.The Big Question: It was discovered 100 years ago, but has treatment of Alzheimer's progressed? (03 November 2006@www.independent.co.uk)
1356.Alzheimer's cure in Ayurveda!(www.dailyindia.com Nov 4 )
1357.New Alzheimer's drug shows promise(SooToday.com November 04, 2006)
1358.Alzheimer's still somewhat a mystery( abcnews Nov. 3, 2006)
1359.Changing minds in Alzheimer's research(November 5, 2006 www.latimes.com)
1360.Can caffeine protect against Alzheimer's? (11/6/2006 www.usatoday.com)
1361.Study Suggests Underlying Cause of Dementia after Cancer Treatment(Wake Forest University Baptist Medical Center 06-Nov-2006)
1362.Samaritan Seeks FDA Nod For Human Testing Of Alzheimer's Drug(2006/11/06 financialwire.net)

1363.Neurochem Receives Recommendations from Data Safety Monitoring Boards to Continue Phase III Clinical Trials for Tramiprosate (Alzhemed)(November 06, 2006 PRNewswir)
1364.Diabetes and Alzheimer's: Insulin resistance increases risk(Mayo Clinic Nov 6, 2006)
1365.Medivation to Host Conference Call on November 15 to Provide Clinical Development Update for Lead Product Candidate Dimebon(TM) (08 Nov 2006 www.earthtimes.org)
1366.Phytopharm Preliminary Results for the Year Ended 31 August 2006(www.engelpub.com Nov. 8, 2006)
1367.Touch, massage may aid dementia patients(Nov 8, 2006 Reuters Health)
1368.No Link Between Mild Thyroid Disease and Cognitive Dysfunction, Mood Disorders(Medscape Medical News November 7, 2006)
1369.Alzheimer's disease evolving, but remains a mystery(November 10, 2006 www.harlandaily.com)
1370.Nursing homes take residents back to ethnic roots(Nov. 11, 2006 Associated Press)
1371.'Lifesaver' Helps Locate Lost Alzheimers Patients (www.topix.net November 12, 2006)
1372.How to prepare for the Alzheimer's wave(www.canada.com November 11, 2006)
1373.Easing the agony of Alzheimer's(November 9, 2006 www.boston.com)
1374.Supreme Court upholds $13M verdict against Beebe(11/14/06 www.capegazette.com)
1375.Assisted Living, Erratic Regulation(Nov.13, 2006 CBS)
1376.Complaints About Memory Are Associated With Alzheimer-Related Brain Damage(www.engelpub.com Nov. 14, 2006)
1377.Doctor to detail Scripps research(November 13, 2006 www.palmbeachdailynews.com)
1378.Elder Abuse Resources(Nov. 14, 2006 CBS)
1379.Omega-3 fatty acid may slash dementia risk - study(www.nutraingredients.com 15/11/2006)
1380.World's largest study into Alzheimer's launched(November 14, http://au.news.yahoo.com)

1381.Alzheimer's death toll soaring(Nov. 15 UPI)
1382.Analysis: Bracing for Alzheimer's avalanche(Nov. 15 UPI)
1383.On Alzheimer's 100-Year Anniversary, Scientists Warn Aging Boomers Will Multiply the Number of New Cases (http://journalism.berkeley.edu November 15, 2006)
1384.Science Journal: Alzheimer's research makes dramatic shift(November 17, 2006 www.post-gazette.com)
1385.Yeast model shows promise as Alzheimer's test(17-Nov-2006 University of Illinois at Chicago)
1386.Problems possible in Alzheimer treatment(Nov. 16 UPI)
1387.Occupational Therapy Helps Those With Dementia(11.16.06 www.forbes.com)
1388.Better Alzheimer's test developed (November 19, 2006 BBC Health News)
1389. Brain's Oxygen Supply Key to Alzheimer's Risk(HealthDay November 20, 2006)
1390.More insight into Alzheimer's disease with Stanford discovery of possible cause(2006-11-21 PressZoom)
1391.Hormone Replacement Therapy May Improve Visual Memory Of Postmenopausal Women(OBGYN News 22 Nov 2006)
1392.Playing catch-up in Alzheimer's labs(November 24, 2006 The Wall Street Journal)
1393.When love blossoms in the nursing home(Nov. 25, 2006 www.bradenton.com)
1394.Acumen, Merck amend Alzheimer's agreement(29th November 2006 www.pharmaceutical-business-review.com)
1395.Alzheimerfs Disease:a 21st century challenge - Part 2: Whofs at risk?(www.tenerifenews.com@29/11/2006)
1396.Ink paintings on sale to assist Alzheimer's patientsi29 Nov 2006 www.nst.com.my)
1397.Company to start human trials on Alzheimer's drug(Nov. 29, 2006@Las Vegas Review-Journal)
1398.Training for Missing Alzheimer's Persons Could Save Lives(WNEG NewsCHANNEL 32 November 28, 2006)

1399.Research Collaboration between the University of Pittsburgh and GE Healthcare Reaches Significant Milestone in Development of F-18 PiB for Brain Amyloid ImagingiNovember 29, 2006 BUSINESS WIRE)
1400.Senior Citizens Concerned About Memory but Reluctant to Tell Anyone(www.seniorjournal.com November 29, 2006)


1301.NextSteps: Nursing homes deny admission to woman with Alzheimer's
Sunday, October 01, 2006@http://www.post-gazette.com/

By Jan Warner and Jan Collins

Q: Since my mother, now 71, was diagnosed with Alzheimer's two years ago, she has declined steadily. At first, my father was able to take care of her with part-time help from me, but as time passed, she became too much for him to handle. And when he suffered a stroke and then a fatal heart attack, Mom's care became my total responsibility. I have her power of attorney and am an only child.

With my husband's agreement, I stopped work and moved her in with us; but I soon found that I could not meet her needs, especially when she became aggressive and, on occasion, physically abusive to me and our teenage son. We never knew what was going to set her off, and it got to the point that the stress was causing problems in my marriage and with my son who could not bring friends to our home. Even medication did not help.

So my husband and I decided to try to find a suitable place for her to stay, and have continued to strike out. This is why I am writing you.

Even though Mom receives nearly $3,500 each month from Social Security and my father's pension, and has a home valued at $125,000 and investments of $85,000, she has been denied admission to two nursing homes and three residential care facilities. I have learned that Medicare will pay nothing for her care. And even if she had no money, we are told that because she does not need "nursing care," Medicaid would not provide for her. It seems that people like her are slipping through the cracks. We as a family are having a very difficult time coping, and we know that she is miserable. With all we read about care for the elderly, why do we find ourselves in this situation, and what can we do?

A: Our health-care system is not prepared to deal with the estimated four or more million Americans with Alzheimer's disease and other forms of dementia, let alone those who have become aggressive. And with estimates of nearly four times that number by 2050, the future does not look bright unless there is a paradigm shift in the way care is provided.

While nursing homes were designed to care primarily for people with chronic, long-term medical problems of the body, not the mind, some estimate that two-thirds of the residents in these facilities suffer from some form of dementia, and a large percentage of them are very challenging to care for. The more challenging the care, the less likely an individual will be admitted. And if admitted, the more likely the facility will discharge the disruptive individual for a myriad of reasons, not the least of which is potential liability should another patient be attacked and hurt.

According to studies we have read, aggressive and violent behavior among Alzheimer's patients could be caused by a combination of paranoia, agitation and depression that sometimes come to the forefront as the disease cripples the mind and distorts one's view of events. For example, a person with Alzheimer's disease may believe he or she is being attacked, and acts out accordingly, if someone comes into his or her room. While aggressive Alzheimer's patients are not willfully causing harm to others, their conduct is a challenge that many facilities are not willing to take on.

While there don't seem to be statistical studies that outline the extent of this problem, as the number of seniors grows and as medical technology results in longer lives for those with this illness, the trend is expected to get worse.

Taking the NextStep: To be perfectly frank, we have not been able to find a solution for you. We ask that our readers provide us with any solutions that may be available, and we will be happy to print them in upcoming columns.

--------------------------------------------------------------------------------

(Jan Warner is a member of the National Academy of Elder Law Attorneys and has been practicing law for more than 30 years. Jan Collins is editor of the Business and Economic Review published by the University of South Carolina and a special correspondent for The Economist. You can learn more information about elder care law and write to the authors on www.nextsteps.net.)


1302.Scientists Use Gene Signatures To Find Treatments For Cancer, Obesity And Alzheimer's Disease
02 Oct 2006@http://www.medilexicon.com/

In one of the most ambitious spinoffs of the human genome project, researchers at Dana-Farber Cancer Institute, Children's Hospital Boston, the Broad Institute of Harvard and MIT, and other collaborating centers have unveiled a new, systematic approach to drug discovery that matches diseases with potential treatments using a universal language based on cells' distinctive gene activity profiles, or "signatures."

A set of three articles being published in the September 29 issue of Science and in the September 28 advance online edition of unveils the first steps toward what researchers have dubbed a "Human Connectivity Map."

"The Human Connectivity Map works much like a Google search to discover connections among drugs and diseases," explained Todd Golub, MD, who is an investigator at Dana-Farber, the head of the Cancer Program of the Broad Institute, an associate professor of pediatrics at Harvard Medical School, and a Howard Hughes Medical Institute Investigator. He is a senior author on two of the papers.

The paper in Science describes the concepts underlying the gene signature catalogue and gives an overview of its initial testing. "This should be particularly useful for pharmaceutical companies, so that academic scientists and companies alike can compare the signatures of diseases and compounds to signatures in the Connectivity Map database, and, from that, generate hypotheses," Golub said.

The strategy allows scientists to capture distinctive gene signatures of cancer and other disease cells and compare them with signatures of cells that have been treated with a large number of drugs, both old and new. The more closely the disease signature resembles the signature of a reference cell that has been treated by a particular drug, the greater the odds that the drug will be an effective treatment for that disease.

Conversely, the system can reveal the molecular mechanism of a treatment that is effective but whose method of action has been a mystery, and that knowledge can lead scientists to other, similarly-acting drug candidates.

The gene signatures are captured by devices called microarrays, or "gene chips," that take a snapshot of the tens of thousands of genes at the heart of every cell. The Connectivity Map system is based on the difference in gene activity patterns -- which genes are active, which are inactive -- in a disease cell compared with a normal cell, or a cell before it has been treated with a drug and after the drug has been administered. Usually there is a group of 100 or more genes whose activity differs between one state and the other: That set of genes makes up the signature.

The publications describe how the Connectivity Map, which in its initial edition contained links to 164 different drugs and other chemical compounds, was used to obtain information on treatments for obesity, Alzheimer's disease, and cancer, and to suggest new therapies for drug-resistant leukemia and advanced prostate cancer.

Scott Armstrong, MD, PhD, a pediatric oncologist at Dana-Farber and Children's Hospital Boston, is senior author on a paper in Cancer Cell that describes how the method successfully identified a drug that can overcome therapy-resistant cases of acute lymphoblastic leukemia (ALL) in children. So-called "glucocorticoid" drugs like prednisone are very effective in many cases of ALL, but in some patients the cancer cells are resistant to the drugs, which often can lead to fatal results.

"We took cells from ALL patients that were either resistant or sensitive to glucocorticoids and put them through the Connectivity Map database, and it predicted that one of the best drugs would be rapamycin," said Armstrong, who is also an assistant professor of pediatrics at Harvard Medical School. "Then we tested rapamycin to see if it made the ALL cells more sensitive to glucocorticoids, and in some cell lines it appears that it does," he said, adding that a clinical trial is being planned to try rapamycin in children who have had recurrences of initially successfully treated ALL.

Moreover, the comparison of gene signatures revealed that rapamycin's effectiveness was due in part to its action on a molecule that causes cancer cells to self-destruct.

The method also enabled researchers to match up a pair of natural products, known as celastrol and gedunin, with a mechanism by which some advanced prostate tumors continue to grow aggressively despite hormone-blocking treatments. A paper in Cancer Cell reports on this work, which made it possible for scientists to connect the action of the two natural products with known biological effects of other drugs. It turned out that celastrol and gedunin inhibit a molecule called HSPH90, which in turn blocks the overactive cell signaling of the androgen receptor in prostate cancer cells that drives their aggressive growth. Dana-Farber researcher Haley Hieronymus, PhD, who used the Connectivity Map to sift through thousands of drugs and compounds, is the paper's lead author.

The researchers said that in view of these promising results, they are proposing a large-scale effort -- along the lines of the Human Genome Project -- to map connections among genes and diseases to accelerate the development of new and improved therapies for a wide range of disorders. Like the data in the current papers, the information garnered in the course of such a project would be freely available to scientists everywhere.

###

Funding for the research was provided by the National Institutes of Health, the Howard Hughes Medical Institute, the Leukemia Lymphoma Society, and the Damon Runyan Cancer Research Foundation.

Dana-Farber Cancer Institute (http://www.dana-farber.org/) is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute.

Founded in 1869 as a 20-bed hospital for children, Children's Hospital Boston today is the nation's leading pediatric medical center, the largest provider of health care to Massachusetts children, and the primary pediatric teaching hospital of Harvard Medical School. In addition to 347 pediatric and adolescent inpatient beds and comprehensive outpatient programs, Children's houses the world's largest research enterprise based at a pediatric medical center, where its discoveries benefit both children and adults. More than 500 scientists, including eight members of the National Academy of Sciences, nine members of the Institute of Medicine and 11 members of the Howard Hughes Medical Institute comprise Children's research community. For more information about the hospital visit: http://www.childrenshospital.org/.

Contact: Bill Schaller
Dana-Farber Cancer Institute


Posted on Sun, Oct. 01, 2006@http://www.centredaily.com/mld/centredaily/
1303.Alzheimer's a real mid-life crisis
By Jackie Burrell
CONTRA COSTA TIMES

Suzie Smith's family first realized something was amiss when the 50-year-old Orinda shopkeeper couldn't remember what numbers were for.

Carol Kirsch's colleagues became concerned when the meticulous, 55-year-old Kaiser Permanente employee missed yet another meeting and got lost in her own office building.

And 38-year-old Tracy Mobley realized something was terribly wrong the day she spotted a strange animal on her porch.

"That's Daisy," her young son told her in a slightly anxious tone. "Our dog."

We tend to think of Alzheimer's disease as something that afflicts vacant-eyed 85-year-olds in nursing homes, not Stanford professors or vibrant moms who drive car pool. But nearly 500,000 Americans between the ages of 30 and 65 have this degenerative, memory-robbing form of dementia. And over the next 40 years, as the population and awareness of the disease grow, doctors expect the numbers for Alzheimer's as a whole -- both the Early Onset version and the more common Elderly Onset -- to skyrocket from 4.5 million to as many as 16 million.

Most Americans are at least vaguely aware of the disease. They may even be aware of their own unnerving odds -- one in 10 Americans over 65 and nearly half those over 85 have been diagnosed with it. But nearly one in 10 Alzheimer's patients are considerably younger. And although the disease is heartbreaking at any age, it poses additional, devastating challenges when it strikes decades early.

"For some, it's an absolute shock," said Judy Filippoff, who leads a support group for Early Onset patients in Lafayette. "Very often, they're the wage earner for the family. They may have young children at home. Imagine being the mom who can't be in the car pool anymore."

Because the emphasis is on elderly patients, there are few age-appropriate support systems in place for Early Onset victims, and the difficulty in getting a diagnosis -- who looks for dementia in a strong, healthy 40-year-old? -- can spell financial disaster.

They cannot work, or at least not the way they once did. Nearly a third have no health insurance. And there is a Catch-22: Although they have paid into the Social Security Disability Insurance fund for their entire working lives, they cannot get SSDI payments without a diagnosis, and they will not be eligible for SSI -- federal Supplemental Security Income -- until they are on SSDI. But getting that critical diagnosis takes one to six years, during which time there is a mortgage to be met and bills to pay.


The onset

On a recent August evening, the sound of rock 'n' roll and revelry wafted down a tiny Orinda street, while the breeze carried the spicy aroma of chili. For years, the Smith family has hosted the "Smith Ranch Cookoff" to raise support for the Alzheimer's Association's Memory Walk, which helps support research and caregiver training.

In some ways, it was the walk that saved the family, said daughter Ericka Smith, who now works for the association. When everything went to pieces in those early years after her mother's diagnosis, the Memory Walk gave Ericka, her sister, Shannon, and their father, Rick, a way to tell extended family and friends what had happened to their beloved Suzie. It also brought them into a community that understands.

Although there is a genetic link for most Early Onset Alzheimer's cases, it did not exist on the Smith family tree. And when it struck nine years ago, when Suzie was 50, the family was stunned.

Rick had just retired. The girls had just graduated from college. Suzie was running a little boutique in Orinda Theater Square, and she began forgetting little things and, eventually, troubling things.

Whenever she tallied the register receipts at the Squirrel's Nest, for example, Suzie wrote the figures down neatly on an envelope and tucked the register slips inside. But gradually, the jotted numbers became misshapen. They began to veer at odd angles and run off the edge. Then Suzie stopped writing numbers altogether.

"It's an insidious onset," said Ann Davidson, an Alzheimer's family consultant whose husband, Julian, a Stanford physiology professor, died of complications from Early Onset Alzheimer's in 2001. "It is not a heart attack, not a stroke. There is not one thing that happens. It just creeps up on you in ways that you don't even notice. Then when you get the diagnosis, you look back and go, 'Oh my goodness, of course.'"

Suzie Smith got lost in downtown Walnut Creek. Stoplights ceased to have meaning. Confused, she devised circuitous routes to avoid the traffic signals between her Orinda home and the supermarket a half-mile away.

The family took away Suzie's car keys -- a move that continued to infuriate her long after she had lost the ability to find the garage.

Meanwhile, Erika and Shannon hit the Internet, searching for answers. Then, shaken, they urged their father to call the doctor to discuss Alzheimer's disease.

"It was," Ericka said, "totally heartbreaking."

The Smiths entered the doctor's office with the word on their lips and were referred, almost immediately, to a neurologist for a three-day battery of diagnostic cognitive tests.

The 'A'-word

But even families with a known genetic predisposition to the disease can have trouble getting it diagnosed.

Four generations of Bryans, a Texan family, have faced Early Onset Alzheimer's.

But Silas Bryan III's neurologist had never seen a case so young, said his wife, Carol, and the doctor kept hinting that it was psychosomatic.

Carol did her own research online, switched neurologists and did everything she could "to help the doctor help me."

There has been progress in recent years, both in drug treatments, which have slowed the disease in some patients, and in diagnosis. New types of brain scans -- including the PETscan, which measures not only the brain's appearance but also levels of activity in its different parts -- can help diagnose the disease with 85 to 90 percent certainty, said Dr. Michael McCloud, a geriatrician at UC Davis Medical Center.

Before, the diagnosis was uncertain without a brain autopsy. By then, the issue was academic, at least to the patient.

Yet getting an accurate diagnosis is one of the biggest issues facing Early Onset patients. And most doctors are not looking for Alzheimer's in their 40-year-old patients.

"They're diagnosed with anxiety and depression, some kind of mental health disorder," Filippoff said. "They go through a complete trauma before they even get a diagnosis of Alzheimer's, which is bad enough."

It's ironic, McCloud said, because the very first diagnosed case of Alzheimer's was a 51-year-old woman with Early Onset. Her 1906 autopsy showed the telltale brain lesions, severely shrunken cerebral cortex and hippocampus, where memories are imprinted on the brain.

But until recently, most research focused on Elderly Onset. Early Onset patients could not even participate in clinical trials because the age cutoff was 65.

That is changing. Alzheimer's experts testified before Congress in June to ask for federal support for Early Onset research, training programs to help doctors diagnose the disease in younger people, caregiver support (until now, federal support for caregivers was limited to those 65 and older), and expansion of age-appropriate services for patients and their families.

Because of the difficulty in diagnosis and lack of tracking, no one is sure exactly how many Early Onset cases there are -- up to 600,000 is the best guess. Estimates put life expectancy at three to 20 years from the time of diagnosis, which assumes the case is ever diagnosed.

And it took years for Tracy Mobley to get that diagnosis.

No more carpool

Mobley, who lives in Buffalo, Mo., was in her mid-30s when she started forgetting things: decisions, bills, directions.

"I even began getting lost at my job," the former intensive care nurse said. "I'd be sent to another department and once I got there, I had to call and ask what I was supposed to do."

But concern turned to panic the day she failed to recognize her own dog, Daisy.

Her doctor thought it was stress and exhaustion, a natural consequence of working full time in the ICU, moonlighting at her in-law's grocery store, and juggling home and parenting responsibilities. But cutting back hours did not help. Anti-depressants did not help, and neither did the hysterectomy her doctor prescribed for his patient, then 36, when he thought the problem might be hormonal.

"Things were getting worse," she said. "I went to see I don't know how many psychologists, one psychiatrist. I thought they'd tell me I was crazy."

She was finally diagnosed at age 38.

"At the time, we didn't really know much about the disease," she said. "The biggest thing was, 'How long do I have? How old is (my son) going to be? Will I see him get through junior high? Will I be here when he starts driving?'"

And how does one explain Alzheimer's to a child?

Mobley and her son, Austin, now 12, have written two books about Alzheimer's, including a just-released picture book that tries to put the disease into children's terms because, she said, every stricken family grapples with these questions.

Every family searches for analogies to frame the answer. Mobley's husband, Allen, uses strawberry milkshakes. Sweetly familiar, but every now and then, a piece of strawberry gets lodged in the drinking straw, and there is nothing.

Others compare it to a short circuit in a computer, or to a puzzle when the piece you're trying to place in one corner belongs on the opposite side.

In the disease's early stages, the puzzle piece eventually finds its way home, with patience. But as the disease progresses, language falters and words begin to evaporate. It's no longer a "toothbrush," it's "that thing for my mouth." Gradually, even that disappears.

There's no secret about what lies ahead. Patients forget their surroundings, their families, themselves and, gradually, even how to swallow.

Mobley's neurologist was so horrified, he could not even bring himself to voice the diagnosis. He wrote "Early Onset Alzheimer's" on a piece of paper and handed it to her.

Julian Davidson's doctor did not tell him at all. He told Julian's wife, Ann, and notified the Department of Motor Vehicles, as required by law. But for months, Julian did not know. Ann said she did not have the heart to tell him. Julian found out he had Alzheimer's from the DMV examiner who confiscated his driver's license.

But everything hinges on that diagnosis and the care that follows -- and, meanwhile, there are chores to be done and children to raise.

"It's different in your 80s. You're not trying to do 800 things," Ericka Smith said. "Everyone plans their future, kids out of the house, travel and, all of a sudden, that plan is completely obliterated. There's an extreme sense of loss."

Helping hands

There's also an extreme need for caregiving, which becomes a team effort as the disease enters its second stage, when the cognitive decline deepens and anger management issues arise. Patients need help with familiar tasks. They wander and get lost in their own neighborhoods. Soon, they cannot be left alone for any period of time.

Silas Bryan does not drive anymore, but in his last days behind the wheel, Silas and his young daughter Rayna, now 12, ran errands together, short hops to the library or to grab a burger. She would remind him to turn on the blinker, her mother said, or to come to a complete stop. These days, they hang out together, taking care of the family's horses and goats, while Carol works.

But Silas is changing and, as much as they have talked it out and comforted each other, his last outburst frightened them all.

"It's sinking in," Carol said. "Daddy's sick. But for as long as medicine works, if the medicine works, we'll just keep an eye on him, remind him to take his medicine. (Rayna) knows there are changes down the road. When, we don't know, but she knows that."

Carol looks to Mobley and other members of their "Dementia Rescue" online support group. But, she said, she would really like to find an Early Onset family support group close to her home, near Dallas, both for herself and for Rayna.

There are thousands of Alzheimer's support groups nationwide, but it is difficult to relate to the concerns of grief-stricken 80-year-old spouses when you're 12 or even 45.

Ericka Smith started her own Early Onset family group in Berkeley with help from the Northern California Alzheimer's Association. And Filippoff, who has been counseling Alzheimer's patients for 25 years, started her Early Onset group in Lafayette 10 years ago.

"They really wanted a group for younger people," she said. "They're really attempting to pull themselves up by the bootstraps and delay progression. They're incredibly savvy -- change my diet to the healthiest diet I can have, exercise, take whatever medicines are available to delay, take control of this disease."

Even amid the serious discussions of finances, medicine and coping, there is laughter. Members compare notes, joke about their latest gaffe and sing the occasional "Happy Birthday."

"We laugh a lot in our group, and that's a good thing," said Carol Kirsch, who was 55 when she was first diagnosed. "We laugh about ourselves and the mistakes we make, and when we're not laughing, we're really supporting each other."

It was Kirsch's colleagues at Kaiser who first noticed something was wrong.

"We'd have meetings and I'd forget to go to them," the Oakland resident said. "I'd been a very valuable contributor to my department, and the people who knew me best could really see a difference. I'm still very close with some of those people and grateful to them."

It has been three years since the diagnosis. Kirsch no longer works, but she stays busy. She and her husband sing with the Berkeley Broadway Singers, and she keeps a journal so her future grandchildren will someday know her.

"It feels somewhat stable right now, but of course I have no idea how long this will last," she said. "I know at some point it will get worse, but I'm very lucky to have a fabulous husband who is really my support."

But teens have no support, other than their families, and that realization is finally starting to dawn on an international level. A recent Japanese documentary about Early Onset -- known as "Recognition Deterioration" there -- focused on the impact not just on families but on children.

And in January, at the urging of a Staten Island teenager, the American Alzheimer's Foundation launched a teen division to help build awareness and boost support for children affected by a family member's condition.

The panel's teen message boards provide peer support, and the 10-member teen advisory panel includes Courtney Henley, a New York teen who helps care for her father, Michael, who was diagnosed at age 36 with Early Onset.

The AFA Teen discussion boards are intended as a "safe haven," said AFA executive vice president Carol Steinberg, for teens to interact with other teens in similar circumstances.

"There is still tremendous stigma and fear surrounding this disease," she said, "and teenagers in particular are often very embarrassed by their situations and afraid to share information about it with their friends."

And there is an added concern for families with Early Onset Alzheimer's. The Bryans have not had genetic testing done, but the thought lingers in Carol's mind as she talks quietly about her only child. So much progress has been made in diagnosing the disease and finding the genetic markers in the past several decades. Perhaps, she said softly, there will be a cure before Rayna turns 40.

The end

"I can't live today with the load of tomorrow and the next day and the next," said Thad Raushi, a former New York college counselor who wrote about his experiences with Early Onset Alzheimer's in the book "A View from Within." "In fact, not one of us knows our next tomorrow, even whether there will be one for us."

In truth, you could be hit by a truck tomorrow, waste away from any number of cancers or keel over with a heart attack. Live long enough, though, and Alzheimer's becomes, if not a 50-50, then a 47-53 chance -- and people are living much, much longer. That's the reason behind the soaring numbers.

The families arriving on Treasure Island next weekend for the fund-raising Memory Walk are well aware of the big picture, as well as the personal struggle. They speak of "the cure" in hushed tones, but that pharmaceutical miracle is a long way -- and hundreds of millions of dollars -- off.

According to a 2004 CNN report, between $600 and $700 million is spent on Alzheimer's research each year, compared with $1.9 billion for HIV and AIDS. So families walk, hoping to add another million to the coffers.

Unfortunately, Alzheimer's has no pink ribbons or yellow bracelets, said Ericka Smith. There are no cheery survivors with inspirational tales of how they beat the disease, just stories of families doing the best they can.

Yes, you had this grand life, filled with happy expectations, Ann Davidson said, and that future is gone now. But you can still have a life -- altered, but joyful.

"You have to constantly live in the present," she said. "Accept the person they are now and stop grieving for the person they used to be and the life you lost. All caregivers do that, but you can drown in despair if you do that, and then you miss what joyful moments you have."


--------------------------------------------------------------------------------
Reach Jackie Burrell at 925-977-8568 or jburrell@cctimes.com.


Recent Comments

Vote out the Bible beater Republicans and their faux holier than...
I am a married male age 71 and I am exibiting the cognitive...
?Read More
Post Your Comment

Name:
Alzheimer's disease is the most common form of dementia. Often seen in elderly patients, it can also affect people in their 30s, 40s and 50s. It takes a brain autopsy to produce a definitive diagnosis, but a doctor can diagnose "probable Alzheimer's" by using brain scans and cognitive tests. Early Onset Alzheimer's is frequently misdiagnosed because patients otherwise appear so healthy and young that doctors do not look for the disease, or they misinterpret the symptoms as depression or stress. New drug treatments have shown great promise in slowing the progression of the disease, but early diagnosis is critical in getting appropriate care. If you or someone you know is experiencing the symptoms below, contact your doctor or call the Alzheimer's Association help line, 1-800-272-3900.

ALZHEIMER'S SYMPTOMS

? MEMORY LOSS. Everyone misplaces keys or forgets things now and then, but memory loss is significantly more frequent and severe in individuals with Alzheimer's disease. They forget things more frequently and cannot recall the information later. They do not just misplace car keys, they stash them in the freezer or sugar bowl, or they forget what keys are for.

? DIFFICULTY PERFORMING FAMILIAR TASKS. They cannot remember how to operate the toaster, participate in a favorite hobby or do tasks they have done a million times.

? LANGUAGE PROBLEMS. They forget simple words or substitute odd phrases, such as "that thing for my mouth" instead of "toothbrush."

? DISORIENTATION. They forget where they are, how they got there and how to get home.

? DECREASED JUDGMENT. They may give away large sums of money, make poor choices or dress inappropriately, like wearing layers of woolly clothes on a hot day.

? PROBLEMS WITH ABSTRACT THINKING. This goes beyond balancing a checkbook. People with Alzheimer's may forget what numbers are or how they should be used.

? DRAMATIC MOOD OR PERSONALITY CHANGES. They become emotional, fearful or enraged for no discernible reason. Or they become very passive, sitting in front of the TV for hours, sleeping too much or refusing to do usual activities.

--Source: Alzheimer's Association and the American Health Assistance Foundation

STAGES OF ALZHEIMER'S DISEASE

The life expectancy for patients with Alzheimer's disease ranges from three to 20 years. Patients' cognitive abilities fade as their nerve cells degenerate, beginning with the portion of the brain that controls learning and memory functions, and eventually spreading to include not only thinking and behavior, but also muscle movement. There is no cure, but new drug therapies have shown some success in slowing the progression of the disease.

EARLY STAGE: Mild cognitive decline noticeable to family and friends. May include trouble finding words or recalling names. Performance issues at work, slowly growing to include forgetfulness of recent events, impaired ability to complete challenging math problems (such as counting backward from 100 by 7s) and increasing difficulty with complex tasks, such as paying bills, marketing or planning dinner parties.

MID-STAGE: Major gaps in memory and cognitive abilities become apparent. Some assistance is required with daily tasks. Patients get confused about where they are and what day and season it is. They have trouble with simple arithmetic problems (counting backwards from 20 by 2s), and cannot remember important personal data such as their own address and birth date, but they still know the names of family members. They may need help selecting clothing but can dress, eat and handle personal hygiene by themselves. As this stage progresses, patients experience a change in personality, worsening of memory and deterioration of sense of their surroundings. They tend to wander and get lost. By the end of this stage, they require extensive assistance with personal hygiene and other daily tasks.

SEVERE STAGE: In the final stage of the disease, patients no longer can speak coherently. They no longer recognize even family members as familiar, and they have no concept of where they are. They have difficulty walking without support, then sitting, then holding their heads up, and finally, all muscle control.

-- Source: Alzheimer's Association

MEMORY WALK

The Treasure Island Memory Walk on Saturday is the Alzheimer's Association's biggest Bay Area event. The walk, which raises funds for Alzheimer's research and caregiver support programs, and includes 3.0- and 1.5-mile courses. The event also includes live music, a Family Pavilion, "Memory Lane" (a concourse of information booths), and food and drink vendors. All areas open at 7:30 a.m., the walk begins at 9:30 a.m., and free shuttle service will be available from BART's Embarcadero station from 7 a.m. to 12:30 p.m. For details, donation information or to register your team, visit www.alznorcal.org and click on the Memory Walk link.

RESOURCES

THE ALZHEIMER'S ASSOCIATION. The Northern California/Nevada chapter runs a 24-hour help line, more than 60 support groups, "savvy caregiver" training, family workshops and an online help line. Its Web site also offers links to a vast array of local and national resources. Find the Northern California chapter at www.alznorcal.org or call the help line at 1-800-272-3900. The chapter is based in Mountain View, but support groups meet across the Bay Area, including at the association's East Bay branch office at 251 Lafayette Circle, Suite 250, Lafayette, which can be reached at 925-284-7942. The national Alzheimer's Association Web site is www.alz.org.

THE FAMILY CAREGIVER ALLIANCE. A Bay Area-based resource for families and patients struggling with brain disorders, including Alzheimer's, other forms of dementia, stroke and brain injuries. The alliance's Web site is www.caregiver.org.

THE ALZHEIMER'S FOUNDATION OF AMERICA. This national foundation helps caregivers find local training and support. The hot line, 866-232-8484, is open weekdays from 6 a.m. to 2 p.m., and information also can be found at www.alzfdn.org. The foundation launched a teen panel earlier this year to help raise awareness and provide support for teens whose families are facing this disease. For information on AFA teens, visit www.afateens.org.

GUIDE TO LIVING WITH EARLY ONSET ALZHEIMER'S DISEASE from the Cleveland Clinic Health System. The guide includes medical information, practical tips for coping with the disease, interacting with family and friends, and dealing with career issues and medical and legal decisions. The guide can be found at www.cchs.net/health/health-info/docs/2400/2498.asp?index=9592%20.

UCSF MEMORY AND AGING CENTER. This San Francisco facility treats Alzheimer's, educates caregivers and families, and conducts research in the hopes of finding a cure. Learn more about UCSF's services at www.memory.ucsf.edu or by calling 415-476-6880.

UC DAVIS ALZHEIMER'S DISEASE CENTER. A diagnostic clinic, research and resource center based in Martinez. For more information, visit http://alzheimer.ucdavis.edu/ or call 925-372-2485.

BOOKS BY ALZHEIMER'S PATIENTS AND CAREGIVERS. These first-person accounts are available through the Alzheimer's Association and at bookstores. Among them:

? "Alzheimer's, A Love Story: One Year in My Husband's Journey," Palo Alto speech pathologist Ann Davidson's account of life after her husband, Stanford physiology professor Julian Davidson, was diagnosed with Early Onset Alzheimer's;

? "Show Me the Way to Go Home," a memoir by retired electrical engineer Larry Rose, who was diagnosed at age 54;

? "Young Hope" by Tracy Mobley and "I Remember When," a children's book about Alzheimer's disease co-written by Mobley and her son, 12-year-old Austin. The latter comes out this fall and will be available at WanderingSageBooks.com.


1304.Simple Eye Test Could Spot Alzheimer's Early On

By Charles Q. Choi
Special to LiveScience
posted: 02 October 2006@http://www.livescience.com/
12:02 pm ET

Scanning the eyes with lasers could help detect signs of Alzheimer's even before symptoms of the disease appear in the brain.

These laser tests could improve patients' chances of starting Alzheimer's treatments earlier, before the onset of irreparable damage to the brain.

"We need to catch the disease before symptoms emerge to give us the greatest chance to alter its course and ultimately cure it," researcher Lee Goldstein, an interdisciplinary neuroscientist at Harvard Medical School, told LiveScience.

In 2003, Goldstein and his colleagues discovered that the exact same malformed amyloid beta proteins that are hallmarks of Alzheimer's disease are also found in the eye's lens and its surrounding fluid. Last year, they revealed a pair of noninvasive tests that scan the eye for these telltale molecules to potentially detect the disease in its earliest stages.

Both tests very briefly shine a low-power near-infrared laser into the eye. The light is safe, not visible to the patient, and does not cause any discomfort.

One test scans for clumps of the aberrant protein in part of the lens where they collect to form cataracts. The other test is used in conjunction with special eye drops that bind only to the molecules and fluoresce in response to the laser. While the eye-drop test provides more detailed molecular information about the proteins, the other test yields more biophysical data, such as the number and size of the particles.

In his latest experiments, Goldstein and his colleagues found in mice that they could pick up signs of the malformed proteins in the eye even before they began accumulating in the brain. The researchers have also recently completed initial human clinical trials of their tests for safety.

The tests are slated to enter phase III multicenter human clinical trials over the next year. In the end, the tests might cost less than $300 per patient. Goldstein hopes they can become a routine part of an annual physical exam starting in middle age. He is cofounder of Neuroptix, which is developing these tests for clinical use, although Goldstein is not receiving any sponsorship from the company.

Goldstein noted these tests could also potentially speed up the development of new Alzheimer's drugs by giving investigators rapid feedback on whether the medicine they are testing is doing its job of removing the harmful proteins from the body.

"We're having great difficulty testing the many drugs against Alzheimer's we have in the pipeline right now. Testing is the real bottleneck when it comes to developing these drugs," Goldstein said.

In addition, the researchers are exploring whether or not their tests can also help detect the aberrant proteins detected with mad cow disease and related ailments.

Goldstein will present his team's latest findings on Oct. 9 at the annual meeting of the Optical Society of America in Rochester, N.Y.

Art Boosts Alzheimer's Patients' Spirits
Red Wine May Help Prevent Alzheimer's
Alzheimer's Find: Molecular Janitors Quit Cleaning Up
New Tool to Provide Insight on Alzheimerfs, Parkinsonfs
Mental Exercise Nearly Halves Risk of Dementia


1305.Curry may help body clear itself of Alzheimer's plaques
04/10/2006@http://www.scienceblog.com/cms/
UCLA/VA researchers found that curcumin -- a chemical found in curry and turmeric -- may help the immune system clear the brain of amyloid beta, which form the plaques found in Alzheimer's disease.

Published in the Oct. 9 issue of the Journal of Alzheimer's Disease, the early laboratory findings may lead to a new approach in treating Alzheimer's disease by enhancing the natural function of the immune system using curcumin, known for its anti-inflammatory and anti-oxidant properties.

Using blood samples from six Alzheimer's disease patients and three healthy control patients, the researchers isolated cells called macrophages, which are the immune system's PacMen that travel through the brain and body, gobbling up waste products, including amyloid beta.

The team treated the macrophages with a drug derived from curcumin for 24 hours in a cell culture and then introduced amyloid beta. Treated macrophages from three out of six Alzheimer's disease patients showed improved uptake or ingestion of the waste product compared to the patients' macrophages not treated with curcumin. Macrophages from the healthy controls, which were already effectively clearing amyloid beta, showed no change when curcumin was added.

"Curcumin improved ingestion of amyloid beta by immune cells in 50 percent of patients with Alzheimer's disease. These initial findings demonstrate that curcumin may help boost the immune system of specific Alzheimer's disease patients," said Dr. Milan Fiala, study author and a researcher with the David Geffen School of Medicine at UCLA and the VA Greater Los Angeles Health Care System. "We are hopeful that these positive results in a test tube may translate to clinical use, but more studies need to be done before curcumin can be recommended." The patients ranged in age from 65 to 84. Fiala noted that the patients whose immune cells responded were younger and had higher scores on a Mini-Mental State Examination suggesting that curcumin may help those with less advanced dementia. Some of the patients may have already had additional curcumin in their systems due to participation in another UCLA study, which may have impacted findings.

"Our next step will be to identify the factors that helped these immune cells respond," said Laura Zhang, a study author and a UCLA/VA research assistant in Fiala's lab.

Fiala noted that the method researchers used to test the immune cell response of macrophages may provide a novel way of evaluating the effectiveness of drugs in clearing amyloid beta from the brain and may help to individualize Alzheimer's disease treatment.

According to Fiala, macrophages are the soldiers of the innate immune system -- the part of the immune system which is present at birth. Curcumin may support the body's natural immune fighting function in directly helping macrophages clean away amyloid-beta. The treatment of macrophages with curcumin is radically different from some of the vaccine approaches currently being studied.

from UCLA


1306.Negative NHS labels 'demeaning'
Press Association
Wednesday October 4, 2006 1:28 AM@http://www.guardian.co.uk/

Using negative language in the NHS to describe patients is demeaning and shifts the blame, the national director for patients and the public has said.

Harry Cayton, who works for the Department of Health, said using words like "dement" to describe somebody with Alzheimer's disease, or simply referring to people as "hip" and "joint" was alienating and dehumanising.

Writing in the Journal of the Royal Society of Medicine, he said the term "frequent flyer" - used in management and the media - referred to frail, mainly older people who came in and out of hospital on a regular basis.

He said: "The term 'frequent flyer' in this context is demeaning, trivialising and of course plain wrong.

"It implies that somehow these people want regular trips to hospital, that they are collecting points, that they enjoy the health and life-threatening roundabout of continual admission, treatment and discharge."

Other phrases, such as bed-blockers, shifted the blame from the NHS to the patient, and further examples of labels included referring to those who do not turn up for appointments as "DNAs".

He continued: "Labelling people in this way is the most common way in which the NHS dehumanises those it is supposed to care for.

"As well as notorious terms such as "crinklies" and "crumblies" sometimes used in geriatric wards, people are also reduced to no more than their condition: 'We have two hips and a knee in today' in the surgical ward or the diminution of a human being with Alzheimer's disease to no more than a 'Dement'."

He said most of the language was used to describe elderly people, possibly reflecting an ageist culture.

Mr Cayton said he understood that health workers needed to create distance due to the stresses of the job. But there were other ways of achieving that distance rather than using the language of blame and disrespect, he said.

? Copyright Press Association Ltd 2006, All Rights Reserved


October 05, 2006 08:30:00 AM ET@http://moneycentral.msn.com/home.asp
1307.Regulatory Approval to Start PBT2 Phase IIa Clinical Trial in Alzheimer's Disease Patients

MELBOURNE, Australia, Oct. 5 /PRNewswire-FirstCall/ -- Prana Biotechnology Limited (Nasdaq: PRAN; ASX: PBT), today announced that it has received regulatory approval from Sweden's Medical Products Agency (MPA) to start a Phase IIa clinical trial of its proprietary lead compound, PBT2, in patients with early Alzheimer's disease. The trial will be conducted in seven centres in Sweden.

The study, which will commence next month, will evaluate the safety and tolerability of PBT2. In addition, it will examine the drug's mechanism of action and indicators of potential efficacy in treating Alzheimer's disease. Results are expected to be announced in the fourth quarter of 2007.

"The earlier clinical finding with PBT1 (Prana's proof-of-concept compound), together with our recently announced data that there is a rapid and potent onset of benefits in transgenic mice treated with PBT2, leads us to believe that we may see biochemical, and possibly cognitive, benefit in the relatively short time frame of our Phase IIa trial of mildly affected patients. The best hope is that in the course of its development PBT2 could be shown to be disease modifying, offering real hope to Alzheimer's disease patients. Currently there are no approved disease modifying treatments available to patients," stated Professor Colin Masters of the University of Melbourne and the Mental Health Research Institute, and a director of Prana.

The Phase IIa study is a randomised, double blind, placebo-controlled design, in which 80 Alzheimer's disease patients will receive three months of either one of two oral dose levels of PBT2, or placebo. In addition to examining safety and tolerability, the study will investigate the ability of PBT2 to affect multiple cerebrospinal fluid (CSF) and blood biomarkers of Alzheimer's disease during the treatment period. Outcomes will include measures of CSF A-beta and tau levels, as well as neurocognitive and behavioural changes.

This trial forms part of Prana's strategy to assess the behaviour of PBT2 across a broad dose range, in a manner that is also consistent with the new European Medicines Agency (EMEA) regulations that permit accelerated conditional marketing approval for treatments of seriously debilitating diseases such as Alzheimer's disease. These regulations enable marketing for such agents in parallel with pivotal, final stage clinical trials. Mr Geoffrey Kempler, Executive Chairman and CEO commented, "If we qualify under these regulations we could significantly accelerate PBT2's pathway to market in Europe.

"We are very pleased with PBT2's development to date. Besides having successfully completed Phase I, we have also demonstrated, in nonclinical studies, that PBT2 can prevent the formation of the toxic oligomers of the A-beta protein, dissolve existing oligomers, and attenuate the production of free radicals. More recently we have announced that, in transgenic animal models, (i) PBT2 can improve memory performance within 5 days of oral dosing, (ii) PBT2 rapidly reduces the levels of soluble A-beta in the brain, and (iii) PBT2 restores normal function of a-beta impaired synapses. This gives us great confidence in our commitment to the strategic development plan for PBT2 as a treatment for the underlying causes of Alzheimer's disease," concluded Mr. Kempler.

About Prana Biotechnology Limited

Prana Biotechnology was established to commercialise research into Alzheimer's disease and other major age-related degenerative disorders. The company was incorporated in 1997 and listed on the Australian Stock Exchange in March 2000 and listed on NASDAQ in September 2002. Researchers at prominent international institutions including the University of Melbourne, The Mental Health Research Institute and Massachusetts General Hospital, a teaching hospital of Harvard Medical School, discovered Prana's technology.

For further information, please visit our web site at http://www.pranabio.com.

This press release may contain "forward looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995 regarding the Company's business strategy and future plans of operation. Forward-looking statements involve known and unknown risks and uncertainties; both general and specific to the matters discussed in this press release. These and other important factors, including those mentioned in various Securities and Exchange Commission filings made by the Company, may cause the Company's actual results and performance to differ materially from the future results and performance expressed in or implied by such forward-looking statements. The forward-looking statements contained in this press release speak only as of the date hereof and the Company expressly disclaims any obligation to provide public updates, revisions or amendments to any forward-looking statements made herein to reflect changes in the Company's expectations or future events.

Contacts: Investor and media relations
Ivette Almeida
The Global Consulting Group
Tel. 646-284-9455? 2006 PRNewswire


1308..Is it mild cognitive impairment? Many want to know
(Reuters October 06, 2006)

On the present evidence, despite the enthusiasm of the (medical) profession, and probably the public, screening for mild cognitive impairment is not justified. By Megan Rauscher

NEW YORK (Reuters Health) - There appears to be considerable interest among healthy older adults in screening and treatment for mild cognitive impairment, a condition now generally considered to be a precursor to Alzheimer's disease.

Among 149 healthy adults aged 35 and older, 98 percent said they would be willing to be tested for mild cognitive impairment if a family member suggested they had memory problems. African Americans were more willing than whites to be screened at the suggestion of a family member (75 percent vs. 57 percent).

Ninety-nine percent would be willing to take a drug if it would halve their risk of progressing from mild cognitive impairment to Alzheimer's disease, while 92 percent would take a medication to delay onset of AD by 1 year.

Dr. William Dale from the University of Chicago and colleagues report their survey results in the Journal of the American Geriatrics Society.

"We were somewhat surprised interest was this high," Dale noted in an E-mail to Reuters Health. "For the responses to some questions, it was nearly unanimous that people wanted screening for a disease they knew little about."

Although mild cognitive impairment is a risk factor for Alzheimer's, the condition can also be relatively stable.

Such high interest in screening and treatment for mild cognitive impairment is "potentially troubling," Dale said, "because current screening tests do not meet basic scientific standards for justifying their use in standard medical practice."

Furthermore, "none of the available therapies for mild cognitive impairment...have been shown to substantively impact the clinical course of the disease and there may be negative psychological, social, and ethical considerations from being given the label of mild cognitive impairment, which has been linked to Alzheimer disease."

The author of a commentary states: "On the present evidence, despite the enthusiasm of the (medical) profession, and probably the public, screening for mild cognitive impairment is not justified."

Echoing Dale's view, Dr. A. Mark Clarfield of Soroka Hospital, Beer-Sheva, Israel warns that being given the label mild cognitive impairment "may offer to otherwise normal older people a new diagnostic concern about which they did not have previously to worry about."

SOURCE: Journal of the American Geriatrics Society, September 2006.


1309.Diet May Influence Alzheimer's Risk Mediterranean Diet, Fish Oil Could Lower Risk, Two Studies Show(Oct. 9, 2006 WebMD)

What you eat today just may help determine your risk for Alzheimer's disease late in life.

Two new studies offer preliminary evidence that dietary choices could help prevent age-related mental decline or slow its progression.

In one, people who followed the so-called Mediterranean diet, which includes plenty of fruits and vegetables but little red meat, had a lower risk of developing Alzheimer's than people who did not follow the diet. In the other, taking omega-3 fatty acid supplements seemed to slow disease progression in people with very early Alzheimer's disease.

Population-based studies and trials in animals have long suggested that Alzheimer's risk may be influenced by diet. But there have been few direct studies in humans examining whether diet and other lifestyle factors play a role in the disease.

"We have identified genes that may be responsible for 2 percent to 3 percent of Alzheimer's cases, but in the vast majority of cases we don't know what causes this disease," Nikolaos Scarmeas, MD, of Columbia University, tells WebMD.

"Certainly, there may be genetic predispositions that we haven't discovered yet. But there is plenty of room for environmental influences, like diet, to play a role."

Lowering Risk With Olive Oil

Scarmeas and colleagues first reported a link between the Mediterranean diet and Alzheimer's risk in a study involving 2,258 New Yorkers published in June in the Annals of Neurology.

In an effort to confirm the findings, the Columbia University researchers repeated the trial in roughly 2,000 people who either had the disease or were at risk for developing it. The average age of the participants was 76, and roughly one in 10 had a diagnosis of Alzheimer's disease.

The researchers reviewed the diets of all study participants over the course of a year to determine how closely the subjects adhered to the principles of the Mediterranean diet.

Long suspected of lowering the risk of heart disease and diabetes, the Mediterranean diet consists of large amounts of fruits, vegetables, beans, grains, and nuts. Red meats are eaten only rarely and poultry, eggs, and dairy products are eaten in moderation. Olive oil and fatty fish are the main sources of fat in the diet.

Just as with their previous study, Scarmeas and colleagues found that people who most closely followed the Mediterranean model had the lowest Alzheimer's risk.

People who most closely adhered to the diet had an Alzheimer's risk that was 40 percent to 65 percent lower than people who were least likely to follow the diet, Scarmeas tells WebMD.

The study was published today in an advance online issue of the journal Archives of Neurology.

Fatty Fish and Alzheimer's

In a separate study, published in the October issue of Archives of Neurology, researchers from Sweden's Karolinska Institute and Uppsala University Hospital investigated the potential benefits of treating Alzheimer's patients with omega-3 supplements.

The overall results were disappointing, with no difference seen in the rate of mental decline between 204 patients with mild to moderate Alzheimer's disease who did and did not take the supplements for six months.

But a positive benefit was seen among the 32 patients in the study with very mild mental decline identified at the beginning of the study. These patients experienced less rate of decline in mental function than similarly functioning patients who took placebo capsules that did not contain omega-3 fatty acid.

Patients who took the placebo capsules during the first six months of the trial were switched to the omega-3 supplements for another six months. During this second phase of the trial, patients with mild disease seemed to experience a slowing of disease progression.

Tommy Cederholm, MD, PhD, of Uppsala University Hospital characterizes the effect as "clinically relevant, but not dramatic," in an interview with WebMD.

"This could ba chance finding," he says. "We need larger studies to answer this question."

Several larger studies are under way, prompted by promising animal research and research showing a lower incidence of Alzheimer's disease in populations that regularly eat omega-3-rich fish.

In the meantime, Cederholm says it is far too early to recommend fish oil supplements for people with Alzheimer's or those at risk for developing the disease. But he adds that eating fatty fish such as salmon, trout, and tuna regularly may help lower Alzheimer's risk and the risk of other chronic diseases.

SOURCES: Levi-Freund, Y. Archives of Neurology, October 2006; vol 63: pp 1402-1408. Scarmeas, N. Archives of Neurology, Oct. 9, 2006; advanced online edition. Tommy Cederholm, MD, PhD, department of public health and caring sciences, clinical Nutrition and metabolism, Uppsala University Hospital, Uppsala, Sweden. Nikolaos Scarmeas, MD, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University Medical Center, New York.

By Salynn Boyles
Reviewed by Louise Chang
Copyright 2006, WebMD Inc. All rights reserved.


1310.Old drug tried on Alzheimer's disease

10/11/2006 2:46 PM
By: Ivanhoe Broadcast News

Alzheimer's disease is a progressive brain disorder with no known cause or cure.

According to the American Health Assistance Foundation, more than 4.5 million Americans are thought to have Alzheimer's disease. By 2050, that number could increase to 13.2 million. Worldwide, statistics suggest there are currently 18 million people with Alzheimer's disease. By 2025, that number is expected to nearly double to 34 million people.

Symptoms include memory loss, confusion, impaired judgment, personality changes, disorientation, and loss of language skills. Aggression is one of the most common behaviors people with Alzheimer's disease.

Half of the people with Alzheimer's develop aggression at some point in the disease, Dr. Saleem Ismail, of the University of Rochester, said.

Researchers are testing an old drug to delay the onset of aggression in people with Alzheimer's disease. The drug, valproate, is already FDA-approved for epilepsy, migraine headaches and bipolar disorder. The study, led by researchers at the University of Rochester, is looking at whether the drug delays the onset the agitation common with Alzheimer's disease. Previous studies have shown valproate does provide a beneficial effect for agitation in some, though not all, patients.

Researchers are excited by more than valproate's effects on agitation. They say the drug may actually help protect the brain.

"[Valproate] can actually modify what is happening at the cellular level. We are hoping that it actually protects the cell from being stressed out or being damaged. If those cells could be preserved longer, that would translate into meaningful outcomes," Ismail said.

The study is the first of its kind to study a drug that could block one of the hallmarks of AD -- "tangles." Tangles are abnormal brain tissue structures formed by abnormal processing of a protein called tau. In healthy people, tau is critical for intracellular functioning and structure. In patients with Alzheimer's disease, stringy clusters of tau and phosphate molecules form. This leads to an impairment of the cells' ability to transport material within the cell.

When the cell does not function the way it should it cannot communicate efficiently with other cells. Eventually, this process leads to cell death.

"This is just one aspect of what we think is valproate's potential to work. More recently, there has been evidence that it works [another way]," Ismail said.

The drug also probably works on the clearance and production of amyloid. Amyloid plaques are found outside the neurons and neurofibrillary plaques are found inside the neurons. Neurons are the nerve cells within the brain. These plaques are found in large amounts in people with Alzheimer's disease.

Ismail is hopeful that valproate will offer new hope.

"It's very exciting. Scientifically, it is novel. The theory behind it is very impressive, and the good thing about it is that the evidence is growing," Ismail said.


1311.Study: Anti-psychotic drugs don't help most Alzheimer's patients
POSTED: 2249 GMT (0649 HKT), October 11, 2006 @CNN
Adjust font size:
TRENTON, New Jersey (AP) -- Widely prescribed anti-psychotic drugs do not help most Alzheimer's patients with delusions and aggression and are not worth the risk of sudden death and other side effects, the first major study on sufferers outside nursing homes concludes.

The finding could increase the burden on families struggling to care for relatives with the mind-robbing disease at home.

"These medications are not the answer," said Dr. Thomas Insel, director of the National Institute of Mental Health, which paid for the study. He said better medications are at least several years away.

Three-fourths of the 4.5 million Americans with Alzheimer's disease develop aggression, hallucinations or delusions, which can lead them to lash out at caregivers or harm themselves. This behavior is the most common reason families put people with Alzheimer's in nursing homes.

The study tested Zyprexa, Risperdal and Seroquel -- newer drugs developed for schizophrenia that doctors are free to prescribe for any use. However, the drugs carry a strong warning that they increase the risk of death for elderly people with dementia-related psychotic symptoms, mainly because of heart problems and pneumonia, and that they are not approved for such patients.

Yet roughly one-quarter of nursing home patients are on these drugs, and at least that many patients at home have used them, mainly because there are no great alternatives and there was some evidence they might help a little, experts say.

The study tested the drugs on 421 patients at 42 medical centers who needed considerable care but were living in their own home, a relative's or an assisted-living facility. The findings were reported in Thursday's New England Journal of Medicine.

Each patient got one of the drugs or a dummy pill, without knowing what they received. The doctor could raise the dose if needed. Patients were followed for nine months, longer than in most prior tests.

About four in five patients stopped taking their pills early -- on average, within five to eight weeks -- because the medications were ineffective or had side effects that included grogginess, worsening confusion, weight gain, and Parkinson's-like symptoms such as rigidity and trouble walking.

Five deaths were reported among the patients on the medication, versus two among those in the placebo group. But researchers said the difference could be a matter of chance. The causes of death were not disclosed.

Symptoms did improve in about 30 percent of patients taking the drugs, as well as in 21 percent of those getting dummy pills, partly because symptoms can naturally wax and wane.

Some patients who stopped taking one pill were switched to another treatment for the study's second phase, results of which are to be reported next spring.

While the U.S. government paid for the study, the medications were supplied by the manufacturers: AstraZeneca Pharmaceuticals LP, maker of Seroquel; Eli Lilly and Co., maker of Zyprexa; and Johnson & Johnson, maker of Risperdal. Most of the researchers have received grants or consulting or lecture fees from the industry.

Dr. Jason Karlawish of the University of Pennsylvania's Alzheimer's Disease Center wrote in an editorial that the drugs did help a small group of patients who had little or no side effects. He said Zyprexa and Risperdal were both better than Seroquel or the placebo in treating the behavioral problems.

Lead researcher Dr. Lon Schneider, director of the Alzheimer's Disease Center of California and a University of Southern California professor, said doctors should try the drugs if necessary, but watch patients closely and switch to something else after a few weeks if there is no improvement or side effects are too severe.

"Patients are put on these kinds of medications and not particularly monitored and treated for indefinite periods of time," Schneider said. "That just maximizes risk."

Schneider said nursing home residents need the drugs more because their behavior problems are generally worse than patients still at home, but their health is more fragile, raising the danger of side effects.

Dr. Claudia Kawas, an adviser to the Alzheimer's Association and a neurology professor at University of California-Irvine, noted that with the U.S. population aging, the number of Alzheimer's patients is expected to quadruple by mid-century to about 18 million.

Copyright 2006 The Associated Press. All rights reserved.This material may not be published, broadcast, rewritten, or redistributed.


1312.Enzyme Could Play Role in Treating Alzheimer's
(HealthDay News)
by By Steven Reinberg
HealthDay Reporter
Updated: Oct 11th 2006

WEDNESDAY, Oct. 11 (HealthDay News) -- Manipulating an enzyme that dilutes amyloid-beta could lead to new drugs that reduce the abnormal levels of this protein in the brains of people with Alzheimer's disease, a new study suggests.

Insulin-degrading enzyme (IDE) is unusual because it can bind diverse substances together. Now researchers have determined the structure of IDE in four substances, including amyloid-beta, which is the plaque-forming protein structure found in the brains of Alzheimer's patients.

The findings are published in the Oct. 11 online edition of Nature.

"We have identified the three-dimensional structure of IDE," said lead researcher Wei-Jen Tang, an associate professor at the University of Chicago's Ben May Institute for Cancer Research.

This finding may lead to a way of preventing Alzheimer's disease and slowing its progression, Tang said. However, the research at this point is in its early states, he cautioned, meaning the prospect for drugs to treat Alzheimer's is a long way off.

In its study, Tang's team shows that IDE undergoes changes when it binds to proteins like insulin and amyloid-beta, forming an enclosed chamber shaped like a triangular prism.

"We have also found a way to make IDE degrade at a higher rate," Tang said. Mutations in IDE can cause the chamber to open, increasing the rate that IDE and amyloid-beta will break down by up to 40-fold, he said.

"This highlights the possibility that we can manipulate the enzyme [IDE] or even use the enzyme itself as a potential therapeutic agent," Tang said.

Knowing what IDE looks like and how it works may make it possible to develop drugs that act like IDE mutations. This, in turn, might help clear the accumulation of amyloid-beta found in the brains of Alzheimer's patients, Tang said.

One expert thinks these findings might help in discovering a drug to break down amyloid-beta in the brain.

"One potential therapy for Alzheimer's involves finding a drug that will help the brain to degrade poisonous clumps of a material called amyloid," said Dr. Sam Gandy, chairman of the medical and scientific advisory council at the Alzheimer's Association, and director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.

IDE is an enzyme that can play such a role, Gandy said. "The new paper shows that IDE has some unusual properties that one would never have guessed. The new information could be useful in designing a medicine to stimulate IDE breakdown of amyloid. The unsuspected aspects of the way IDE acts may tell us how to achieve our goal while minimizing side effects," he said.

Another expert agrees that targeting IDE may be a potentially effective Alzheimer's therapy.

"Since IDE also regulates levels of important hormones, this approach has potential to cause side-effect problems. But there may be a therapeutic window where IDE could be increased just enough to tip the balance toward amyloid-beta clearance and slow down development of Alzheimer's without causing problems," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System, and associate director of the Alzheimer's Disease Research Center at the University of California, Los Angeles, David Geffen School of Medicine.


1313.Boffins look to diagnose Alzheimer's earlier
Sub-atomic process examines folded protein molecules

Andrew Charlesworth, vnunet.com 13 Oct 2006@http://www.vnunet.com/

Using one of the latest advances in sub-atomic technology, scientists at Lancaster University have developed a technique which could potentially allow the early diagnosis of diseases such as Alzheimer's and Parkinson's.

By the time such diseases are diagnosed conventionally, significant brain damage has already occurred. But more advanced drug treatments are likely to be increasingly effective if the disease can be diagnosed earlier.

The breakthrough technique also allows scientists to monitor the effectiveness of drugs and other inhibitors on the aggregation of key proteins that accumulate in the brain in Alzheimer's and related disorders.

The process involves monitoring protein aggregation in vitro and is non-invasive. It can generate results rapidly, potentially speeding up the drug discovery process. The research was partly funded by the Alzheimer's Society.

Central to the success of the breakthrough was protein measuring equipment from UK company Farfield Scientific. This uses a laser-based technology known as dual polarisation interferometry to detect and study the structure and aggregation of disease-related proteins.

Using Fairfield's equipment, the researchers at Lancaster University can precisely measure in vitro the protein interactions that lead to aggregation in real time.

"The technique can be used to gain a better understanding of many diseases at a molecular level," said Professor David Allsop of Lancaster University.

"This is done by measuring protein structures as they interact with each other, with other proteins or with candidate drug molecules."

The technique can detect these interactions at a very early stage, when aggregation of proteins is thought to be most toxic to brain cells and which leads to the rapid progress of the disease.

The Farfield equipment is capable of recording changes smaller than 0.1 angstroms (one hundredth of a nanometre or 0.00000001mm) which is considerably smaller than the protein molecules.

Proteins are very large complex molecules that can fold into a variety of different shapes. This 3D shape is extremely important and can radically affect the protein's properties.

Misfolded proteins are also the source of prion-based diseases, the suspected infective agent for diseases such as BSE in cows and Creutzfeldt-Jakob disease in humans.

How these 'rogue' proteins behave at a molecular level is a key to understanding the mechanisms of these diseases.

This dual polarisation interferometry technique behind the breakthrough uses the principle of optical interference, where two light sources are made to interact (or interfere) with each other to produce a 'fringe' pattern demonstrating the wave-like nature of light.

The Farfield system employs two waveguides with a laser light source. A waveguide is an optical structure that guides light.

The changes in the behaviour of light passing through the device enable parameters such as the size, density and mass of molecules attached to the sample surface to be determined extremely accurately


Medscape
1314.Questionnaire May Help Discern Mild Cognitive Impairment From Early Alzheimer's Disease
Paula Moyer, MA
Medscape Medical News

October 11, 2006 (Chicago) Patients with mild cognitive impairment who need help with key activities of daily living may be more likely to progress to Alzheimer's disease, according to investigators who presented their findings here at American Neurological Association (ANA) 131st Annual Meeting.

"Our findings show that analyses of individual assessments of activities of daily living, such as the Functional Activities Questionnaire [FAQ], may be useful for diagnosing mild cognitive impairment," said principal investigator Edmond Teng, MD, PhD, at his presentation. Dr. Teng is a fellow at the Alzheimer Disease Center at the David Geffen School of Medicine at the University of California, Los Angeles.

The assessment tool used in the study, the FAQ, is administered to the patient's caregiver and assesses the patient's ability to participate in 10 categories of instrumental activities of daily living (IADLs). Although the FAQ scores in some domains overlapped between those with mild cognitive impairment and those with Alzheimer's disease, the ability or inability to travel independently out of one's own neighborhood most effectively discriminated between the 2 conditions (P = .001), he said.

The 10 domains addressed by the FAQ include:
1. Writing checks and maintaining other financial records.
2. Assembling tax or business records.
3. Shopping alone.
4. Playing a game of skill.
5. Making coffee or tea.
6. Preparing a balanced meal.
7. Keeping track of current events.
8. Attending to and understanding a television program, book, or magazine.
9. Remembering appointments, family occasions, and medications.
10. Traveling out of the neighborhood.

The caregiver gave the patient a score of zero to 3 on each activity, with zero equaling normal independent participation in the activity; 1 indicating the patient's ability to do the activity alone but with difficulty; 2 indicating that the patient requires assistance; and 3 indicating that the patient depends on others to conduct the activity.

The investigators conducted the study because other research had shown that people with mild cognitive impairment continue to have essentially intact functional abilities. However, other research has shown that such patients have declines in IADLs. Therefore, they wanted to know whether they could use the FAQ to distinguish subjects with mild cognitive impairment and those with mild Alzheimer's disease.

They analyzed the FAQ responses for 65 normal control subjects, 42 with mild cognitive impairment, and 22 with mild Alzheimer's disease. They further categorized those with mild cognitive impairment as those with memory deficits in a single domain, in multiple domains, or not having memory deficits; and subdivided mild Alzheimer's disease into possible and probable disease.

The total FAQ scores in patients with mild cognitive impairment were similar across subtypes but significantly different from the controls and the mild Alzheimer's disease groups (P < .001 for each). As Dr. Teng indicated, the ability to manage transportation and travel outside of one's neighborhood most effectively discriminated between mild cognitive impairment and Alzheimer's disease. A cutoff of greater than 1 on this item yielded classification rates of 86% between all mild cognitive impairment and all Alzheimer's disease subjects; further, on this score, there was a classification rate of 87% between those with mild cognitive impairment who had memory deficits across multiple domains and subjects with probable Alzheimer's disease.

"Any neuropsychological instrument that was truly reliably predictive of the subpopulation of patients with mild cognitive impairment destined to convert to Alzheimer's disease within a defined period of time would be an enormous advance, not only in providing for planning . . . but for testing the newest generation of Alzheimer's medicines," Sam Gandy, MD, PhD, told Medscape in an interview. Dr. Gandy, who was not involved in the study, is the director of the Farber Institute for Neurosciences at Thomas Jefferson University, in Philadelphia, Pennsylvania, and the chair of the National Medical and Scientific Advisory Council of the Alzheimer's Association.

"These drugs are largely aimed at the buildup of amyloid. . . . We believe that amyloid buildup is a very, very early event in Alzheimer's, and the earlier in the process we can assess these new drugs in clinical trials, the better," he added. "Otherwise, we might get 'false-negative' results of medicines if we tested them too late in the disease when, in fact, these very medicines might be fabulously effective if only administered early enough. The extreme example of 'early enough,' of course, is primary, preclinical prevention, which is where we eventually want to be: we want to know who is at risk before any impairment is present, and 'head amyloid off at the pass.' "

Another expert agreed that the FAQ is useful in this setting. "Impairments in complex IADLs are often the earliest functional impairment seen in individuals with mild cognitive impairment," wrote Leon Thal, MD, chair of neurosciences at the University of California, San Diego, in an e-mail. "The FAQ is a useful instrument for measuring IADLs."

ANA 131st Annual Meeting: Abstract S-20. Presented October 8, 2006.

Medscape Medical News 2006. (C) 2006 Medscape


1315.Drug candidate effective at reversing memory loss
Monday, 16 October 2006, 2:19 pm
Press Release: Neuren
Neurenfs third lead drug candidate, NNZ-2591, proves effective at reversing memory loss
Key points:

- Neurenfs oral drug candidate NNZ-2591 has successfully reversed experimental memory loss, a common outcome associated with dementia and with many Parkinsonfs disease patients

- This improvement was seen in both ordinary (non-aged) animals with induced memory loss and older (aged) animals, the latter indicated the reversal of aged related memory loss as well

- Previous preclinical data for oral NNZ-2591 has shown improvement in the motor effects associated with Parkinsonfs

- NNZ-2591 now has preclinical evidence that it reverses both the motor effect and the memory loss effect associated with Parkinsonfs disease

- There is currently only one drug approved for Parkinson disease dementia but none approved that treats both the motor and the dementia effects

- Neuren intends to accelerate development of NNZ-2591 as a clinical candidate for treatment of Parkinsonfs disease dementia


Neuren Pharmaceuticals Ltd (ASX: NEU) today announced that its third lead candidate from its diketopiperazine (DKP) family, NNZ-2591, has reported positive preclinical effects of improved learning and memory after oral dosing. Memory was improved to pre-injury levels (100%), a statistically significant effect (p<0.03).

The results suggest that NNZ-2591 has the capacity to improve learning and memory processes after short-term treatment. The new data extends the potential application of NNZ-2591 as a treatment for dementias such as those associated with over 50% of Parkinsonfs disease patients. This is a much less competitive market when compared to the many drug therapies that are available for the treatment of the loss of motor skills associated with the Parkinsonfs disease.

Improvements were observed as early as two days after initial treatment and were observed throughout the four day study. NNZ-2591 was administered as an oral dose to the animals in each test, further supporting the development of this drug as an oral treatment for chronic disorders.

ADVERTISEMENT
In addition results for NNZ-2591 in aged animals showed an improvement in aged related memory loss, often associated with the early stages of Alzheimerfs disease and dementia. In the aged model, besides the improvement in recognition and memory, histology (analysis of brain cells) also showed an improvement in the connections between neurons (synaptic improvement). This indicates the potentially wide applicability of NNZ-2591 across a range of conditions.

Previous studies have shown that NNZ-2591 is effective at improving the motor skills impairment seen in an experimental model of Parkinsonfs disease and also showed that the drug produced a long-term benefit in this model of the disease, rather than just temporary symptomatic relief.

A drug capable of reducing the loss of motor skills and dementia symptoms directly meets the important needs of late-stage Parkinsonfs disease patients.

Neuren intends to accelerate development of NNZ-2591 as a clinical candidate for treatment of Parkinsonfs disease dementia. Further studies will assess the breadth of effect of NNZ-2591 on learning and memory processes to fully evaluate its potential for the treatment of other dementias, including Alzheimerfs disease.

Mr David Clarke, CEO of Neuren said: gThese are very promising preclinical results for NNZ-2591. A treatment for Alzheimerfs and Parkinsonfs disease that improves memory would be very exciting. Importantly there is only one current drug on the market for Parkinsonfs dementia, and none that can address both the motor effects and the dementia effects. We will now put NZ-2591 through our clinical development path.h

Appendix

The study was conducted in 55 rats using a learning and memory test called the Morris Water Maze. This test involves placing each animal in a pool of opaque (tinted) water in which a small platform is hidden just beneath the surface. The rats must swim to the platform in order to reach esafe groundf. With subsequent tests, rats find the platform quicker as they learn where it is, and recall this information. Scopolamine causes the animals to take much longer to learn and recall where the platform is, as it induces a cognitive impairment. They therefore take longer to reach the platform.

Orally administered NNZ-2591 was given after the injected scopolamine had been given. 12 rats were controls, 16 received NNZ-2591 but not scopolamine, 12 received scopolamine plus vehicle (water) and 15 received scopolamine plus NNZ-2591 dissolved in water. Scopolamine significantly impaired memory (time to platform approximately 208% of control on day 4) and while NNZ-2591 had no effect in rats that were not treated with scopolamine, NNZ-2591 significantly reversed the cognitive impairment induced by scopolamine (time to platform 98% of control) and animals that received both scopolamine and NNZ-2591 found the platform in very similar times to those that were not treated (controls with normal memory performance).

Time taken to find platform (seconds) on the 4th day after treatment (mean plus standard error of mean)

Number Mean time to platform (seconds) SEM

Saline/water (control) 12 8.8 1.1
Saline/NZ2591 16 11.0 1.2
Scopolamine/water 12 18.2 2.3
Scoplomaine/NZ2591 15 8.6 2.0

(SEM= standard error of the mean)

The scopolamine only group is different to all other groups by analysis of variance (p<0.03).

Other measures such as the time taken to enter the quadrant in which the platform is hidden showed similar conclusions

About Parkinsonfs and Alzheimerfs diseases

Parkinsonfs disease is a progressive, degenerative neurological condition that affects the control of body movements. Market estimates of treatment costs are in the range of US$2.4 billion. In addition over 50% of Parkinsonfs patients go on to develop some form of dementia. It is estimated that approximately 1-2 people per 1,000 have Parkinsonfs, with the incidence increasing to one in 100 over the age of 60. In Australia there are approximately 40,000 people with Parkinsonfs, with one in seven people with Parkinsonfs being diagnosed before the age of 50 years.

Parkinsonfs disease dementia is characterised by cognitive slowing, attention deficit, and executive, visuospatial, and memory impairments. Dementia associated with Parkinson's disease is accompanied by a reduced quality of life for both patients and caregivers and by rapid functional and motor decline.

Overall the most common form of dementia among older people is Alzheimer's disease (AD), which involves the parts of the brain that control thought, memory, and language.

The disease usually begins after age 60, and the risk of developing AD goes up with age. While younger people may also get AD, it is much less common. About 5 percent of men and women aged 65 to 74 have AD, and nearly half of those aged 85 and older may have the disease. It is important to note, however, that AD is not a normal part of aging.

There are presently 4-5 million AD patients in the US alone with an estimated 15 million worldwide. The market for AD therapy is expected to exceed US$3 billion by 2009.

Statistics

- More than 162,000 Australians have a diagnosis of dementia, with perhaps as many again in the early stages of dementia

- Australians over the age of 65 have a one in 15 chance of developing AD

- Among people aged 80 to 84 the rate is one in nine

- Among those aged over 85 it is one in four

- The disease affects mostly people in their 70s and 80s, but can appear in people who are in their 40s or younger


How is Parkinsonfs and Alzheimerfs disease currently treated?

No current treatment can stop Parkinsonfs disease or Alzheimerfs disease. However, for some people in the early and middle stages of the disease, drugs may help prevent some symptoms from becoming worse for a limited time. Rivastigmine is a drug for the treatment of mild-to-moderate Alzheimerfs disease and is the only drug currently approved for treatment of Parkinsonfs disease dementia.

About Neuren Pharmaceuticals:

Neuren Pharmaceuticals (ASX: NEU) is a biopharmaceutical company developing novel therapeutics in the fields of brain injury and diseases and metabolic disorders. The Neuren portfolio consists of six product families, targeting markets with large unmet needs and limited competition. Neuren has three lead candidates, Glypromate? and NNZ-2566, presently in clinical trials to treat a range of acute neurological conditions, and NNZ-2591 in preclinical development for Parkinsonfs and other chronic conditions. Neuren has commercial and development partnerships, including with the US Army Walter Reed Army Institute of Research, Metabolic Pharmaceuticals, UCLA Medical Center and the National Trauma Research Institute in Melbourne.

For more information, please visit Neurenfs website at www.neurenpharma.com

ENDS


1316.Three Alzheimer's Drugs Are Found To Be Ineffective
By: Herb Denenberg, Special To The Evening Bulletin
10/16/2006@http://www.theeveningbulletin.com/site/news.asp?brd=2737
Email to a friendPost a CommentPrinter-friendly
We've done many columns on the risks and dangers of new drugs, and here is another variation on that theme - off-label use of drugs. That refers to drugs approved for one reason, but used for another reason unapproved by the FDA. The off-label drugs may even be riskier than the new drugs, which at least have been approved by the FDA.
Off-label use is commonplace, but it is not based on scientific study and has not gone through the FDA-approval process involving clinical trials. But under the law, doctors can prescribe any drug for an unapproved use. That rule is based on the concept that the FDA does not regulate the practice of medicine, and can't tell doctors what to prescribe. In fact, at times, it seems no one regulates the practice of medicine.
The doctor may go to an off-label use based on his theories about the drug, based on his experience with the drug and also based on recommendations from those touting the drug, or on anything else.
Now, there's new proof that, whatever intuition or other powers doctors draw on when making off-label prescriptions, they sometimes miss the mark.
A common off-label use for three drugs in the class called atypical antipsychotics is to treat agitation and aggression of Alzheimer's patients. The new study finds that the drugs are no more effective than placebos, but in addition, they can cause serious and even fatal adverse effects. In other words, the three drugs are worse than nothing.
Here are the names of those three drugs: Zyprexa, Risperdal and Seroquel. Those drugs, for on-label and off-label uses, ring up about $2 billion in sales a year. This new study passed no judgment on these drugs when used for approved purposes.
According to one published report, the drugs are prescribed on this off-label basis because families are so desperate to try to help an Alzheimer's victim, because the drugs seem to help once in a while, because company-sponsored doctors are out pushing the off-label uses and perhaps because doctors often prescribe ineffective and/or unsafe drugs.
I found this great revelation from this study published in the New England Journal of Medicine so interesting because, for years, doctors have been indicating these drugs are of little value and, their benefits, if any, are so negligible as not to be worth the risk of adverse effects, which include increased risk of death (compared to a placebo), sedation and confusion causing increased risk of falls and, in the case of Zyprexa and Risperdal, tremors and other Parkinson-like symptoms.
Another interesting aspect of the study involves the sponsor. The sponsor that financed the study is the National Institute of Mental Health. If this agency did not finance the study, the virtually useless and sometimes dangerous use of these drugs would probably have continued for many years, if not decades. You can be sure the drug industry is not likely to finance any after-approval-of-the-drug study to see if one of its products works or doesn't work. Perhaps an outcome, like the one in question, would be too likely for its tastes.
Still another interesting aspect of the study relates to the prescribing information, which states that patients with Alzheimer's-related psychosis "are at increased risk of death compared to placebo." This suggests that doctors either don't read prescribing information or don't consider death such a big deal when dealing with Alzheimer's patients.
In a published report in The New York Times, Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in the Bronx, observed that the drugs produce improvement that is modest at best, but that environment and behavior are more important in managing the combative behaviors of the patients (which the drugs are used to control). But the health delivery system is so obsessed with drugs that managing environment, behavior and other variables is not high on the priority list, even if such action would produce better outcomes. Prescribing and testing take the place of many things, including managing environment and behavior and talking to patients. It's much easier to write a prescription, especially when the prescribing pen is pushed by the marketing and legalized bribery of the drug industry, than to explore other more promising approaches.
Another expert, Dr. Jason Karlawish of the University of Pennsylvania, says the three drugs may be of use for "a subgroup of patients who can tolerate them, and in facilities that have the expertise to manage side effects." It would be reassuring to think that all facilities would have expertise to manage the side effects of drugs they give their patients, but apparently that is not the case.
Still another point of interest is that the study in question is the third in a series that finds this class of drugs, the atypical antipsychotics, is not as safe as are usually portrayed. When it comes to drugs, what else is new?
Finally, some observers say this study proves we need more research on how to handle the behavioral problems of Alzheimer's. My guess is this conclusion could have been reached by anyone of modest intelligence without the benefit of this study.

Advertisement

Herb Denenberg, a former Pennsylvania insurance commissioner and professor at the Wharton School, is a longtime Philadelphia journalist and consumer advocate. He is also a member of the National Academy of Arts and Sciences. His column appears daily in The Evening Bulletin. You can reach him at advocate@theeveningbulletin.com.


1317.Memory Pharmaceuticals Provides Update On Phase 2a Trial Of MEM 3454 In Alzheimer's Disease
17 Oct 2006@http://www.medilexicon.com/

Memory Pharmaceuticals Corp. (Nasdaq: MEMY) today announced an update on the investigational new drug application (IND) filed in September 2006 with the U.S. Food and Drug Administration (FDA) for MEM 3454. The FDA has advised the Company that in order to fully review the toxicology reports that were submitted with the IND, the agency requires further explanations of revisions that were made to those reports since they were submitted with the Company's first IND for this trial in May, and as a result the proposed Phase 2a clinical trial for MEM 3454 in Alzheimer's disease has been placed on clinical hold. The FDA has also deferred assessment of the adequacy of the Investigator's Brochure for the trial pending submission of the additional information.

Memory Pharmaceuticals also reported that the FDA confirmed that the clinical hold was not related to any manufacturing issues with MEM 3454 and that the potential impurities issue, previously raised by the FDA in connection with the Company's first IND for the proposed Phase 2a clinical trial of MEM 3454, had been adequately resolved.

The Company believes that no additional studies or data will be required to address the FDA's questions and that, as a result, it should be able to provide to the FDA, by early November, the information necessary to facilitate the FDA's review.

"Commencing the Phase 2a trial of MEM 3454 in Alzheimer's disease is a top priority, and we are committed to resolving this issue as quickly as possible and, ideally, in a timeframe that would enable us to still initiate the Phase 2a clinical trial for this drug candidate near the end of the year," stated Jim Sulat, President and Chief Executive Officer of Memory Pharmaceuticals. "We continue to believe that MEM 3454 has the potential to offer a new approach for the treatment of debilitating central nervous system disorders based on the safety and pharmacokinetic results of the Phase 1 trial of MEM 3454, coupled with the positive cognitive data generated in that trial."

Separately, the Company announced today the closing of the first tranche of its recently announced private placement of common stock, raising gross proceeds of approximately $26.7 million. Under the terms of the transaction, Memory Pharmaceuticals issued approximately 23.2 million shares of common stock and warrants for the purchase of approximately 7.1 million additional shares of common stock at an exercise price of $1.33 per share. The closing of the second tranche, which is expected to raise an additional $5.5 million through the sale of approximately 5.0 million newly issued shares, is subject to stockholder approval and the Company intends to call a special stockholders meeting to approve the second tranche as soon as practicable.

Conference Call and Webcast Information

Memory Pharmaceuticals will hold a conference call today, Monday, October 16, 2006, at 5:00 p.m. EDT to provide an update on the Phase 2a clinical trial of MEM 3454. The conference call will also be broadcast live from the "Investors" section of the Company's website. Memory Pharmaceuticals' senior management will host the conference call. Investors and other interested parties may access the call as follows:

-- Date:
Monday, October 16, 2006

-- Time:
5:00 p.m. EDT

-- Webcast:
http://www.memorypharma.com under the "Investors" section

An audio replay of the conference call will be available from 7:00 p.m. EDT on Monday, October 16, 2006, until Monday, October 23, 2006. To access the replay, please dial 888-286-8010 (U.S.) or 617-801-6888 (international) and enter passcode number 67986370. An audio replay of the conference call will also be available under the "Investors" section of the Company's website during the same period.

About MEM 3454

MEM 3454 is a partial agonist of the nicotinic alpha-7 receptor. The nicotinic alpha-7 receptor is a highly specialized receptor found in the CNS. Compounds acting on this receptor could be beneficial in the treatment of Alzheimer's disease and schizophrenia, as well as other psychiatric and neurological disorders. MEM 3454 is the Company's lead drug candidate from its nicotinic alpha-7 agonist program. Memory Pharmaceuticals is developing MEM 3454 as potential therapy for Alzheimer's disease and considering developing the compound as a treatment for schizophrenia.

About the Company

Memory Pharmaceuticals Corp., a biopharmaceutical company, is focused on developing innovative drugs for the treatment of debilitating CNS disorders such as Alzheimer's disease, schizophrenia, depression and bipolar disorder. For additional information, please visit our website at http://www.memorypharma.com.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks and uncertainties. All statements, other than statements of historical facts, regarding management's expectations, beliefs, goals, plans or Memory Pharmaceuticals' prospects, future financial position, future revenues and projected costs should be considered forward-looking. Readers are cautioned that actual results may differ materially from projections or estimates due to a variety of important factors, including the risks and uncertainties associated with: obtaining additional financing to support Memory Pharmaceuticals' R&D and clinical activities and operations; conducting preclinical and clinical trials of Memory Pharmaceuticals' drug candidates that demonstrate these candidates' safety and effectiveness; obtaining regulatory approvals to conduct clinical trials and to commercialize Memory Pharmaceuticals' drug candidates; Memory Pharmaceuticals' ability to enter into and maintain collaborations with third parties for its drug development programs; Memory Pharmaceuticals' dependence on its collaborations and its license relationship with Bayer; achieving milestones under Memory Pharmaceuticals' collaborations; Memory Pharmaceuticals' dependence on third- party preclinical or clinical research organizations, manufacturers and consultants; and protecting the intellectual property developed by or licensed to Memory Pharmaceuticals. These and other risks are described in greater detail in Memory Pharmaceuticals' filings with the Securities and Exchange Commission. Memory Pharmaceuticals may not actually achieve the goals or plans described in its forward-looking statements, and investors should not place undue reliance on these statements. Memory Pharmaceuticals disclaims any intent or obligation to update any forward-looking statements as a result of developments occurring after the date of this press release.

Memory Pharmaceuticals Corp
http://www.memorypharma.com


1318.Several drugs show promise for alzheimer's
Tuesday, October 17, 2006

By Elena Cherney, The Wall Street Journal

Scientists are exploring several promising avenues in drug research that could strengthen the battery of weapons used to slow the scourge of Alzheimer's disease.

A handful of drugs -- some originally approved for other diseases -- are showing some success in clinical trials at slowing the cognitive decline that is the hallmark of Alzheimer's. A few, including a prostate-cancer drug, a diabetes drug and a medicine derived from an old class of anti-inflammatory drugs, are in late-stage trials. Their makers say they expect to seek regulatory approval for the treatment of Alzheimer's within a few years. Other compounds, including cholesterol-lowering statins and antibodies that bolster the immune response against the disease, are also showing promise.

If approved for Alzheimer's, the drugs could be a huge breakthrough because they seek to modify the brain processes that cause Alzheimer's, even though those processes aren't fully understood. In contrast, none of the currently approved medicines attack the underlying mechanisms of the disease, offering only limited relief from some symptoms. The four drugs currently approved for Alzheimer's -- Aricept, Exelon, Razadyne and Namenda -- are a huge business. Alone, sales of Aricept, co-marketed in the U.S. by Pfizer Inc. and Eisai Inc., totaled $1.06 billion in the year ended March 31. But typically, patients gain only modest cognitive improvement for less than 18 months. Then, they start to deteriorate again.

Many leading researchers say they believe at least some of the drugs being studied are likely to win approval for Alzheimer's. "I can't promise," says Sam Gandy, director of the Farber Institute for Neurosciences at Thomas Jefferson University. But "there could be compounds in as few as three years."

In the meantime, a growing number of doctors are experimenting with new ways to use existing Alzheimer's drugs. In particular, doctors are giving medications such as Aricept earlier in the course of the illness -- often before patients are even sick enough to be diagnosed with Alzheimer's. Recent studies of patients with so-called mild cognitive impairment, which involves loss of mental function and sometimes progresses to include dementia and full-blown Alzheimer's, have turned up some evidence that the deterioration into Alzheimer's could be delayed by starting treatment.

The need for better treatments has never been more pressing, as the first members of the Baby Boom generation reach their 60s, the age at which the risk of developing Alzheimer's starts to climb. An estimated 4.5 million Americans have the disease, more than double the 1980 number, according to the Alzheimer's Association.

Here is a look at some of the emerging trends in Alzheimer's research:

Existing Alzheimer's Drugs

Wayne Lindley, an 83-year-old North Carolina retiree, started to notice a few years ago that he was having trouble remembering how to perform certain computer functions for his part-time record-keeping job. When Mr. Lindley and his wife, Sarah, consulted an Alzheimer's specialist last year, Mrs. Lindley says, "his opinion was, you don't have Alzheimer's but I'm going to put you on Aricept."

Mr. Lindley is among those people showing early signs of Alzheimer's who are taking approved Alzheimer's drugs before a firm diagnosis. Despite recent evidence that early treatment with Alzheimer's drugs can stave off cognitive decline, Mr. Lindley says he hasn't noticed any improvement: "The other day, I looked at all the pills and wondered, do I still need all these things?" he says. Still, he says he will continue participating in a neuroimaging study at Duke University in which his doctor enrolled him, and he hopes that tests he is undergoing will give his family more information about his prognosis. "I don't want to be in the dark about anything," he says.

Researchers caution that patients with mild cognitive impairment should think carefully before starting on Alzheimer's medication before there is a diagnosis. The drugs can have side effects ranging from mild nausea to stomach bleeding. Some neurologists consider mild cognitive impairment to be early-stage Alzheimer's if it is progressive and not caused by a different health problem, but the condition doesn't necessarily progress to Alzheimer's.

Nevertheless, "over the last year or so, we've seen a dramatic increase in the number of people who don't yet meet the criteria for Alzheimer's and are coming in on medication already," says Gregory Jicha, an assistant professor of neurology at the Alzheimer's Disease Center at the University of Kentucky.

Drugs for Other Conditions

Most researchers say a protein called beta-amyloid is at the root of Alzheimer's. The protein appears to build up into plaques in the brain and progressively kill neurons, or nerve cells, in a process known as the "amyloid cascade." Many of the drugs being studied aim to interrupt this cascade.

Some of the most promising results to date involve Flurizan, which is derived from an anti-inflammatory and is being tested by Myriad Technologies. The drug targets an enzyme, called gamma secretase, that is believed to play a role in the build-up of amyloid. The company is scheduled to finish its final U.S. study in the spring of 2008, and hopes to apply to the Food and Drug Administration that summer, says Executive Vice President Bill Hockett.

Some researchers think that the best approach may turn out to be a cocktail of different compounds. Different drugs may also work better for different patients, depending on gender and genetics. For example, leuprolide, the prostate-cancer drug that is being tested in Alzheimer's patients by Voyager Pharmaceuticals Inc. of Raleigh, N.C., has appeared more effective in women than in men. Leuprolide, approved as Lupron for prostate cancer, targets luteinizing hormone, a pituitary hormone believed to promote the production of beta-amyloid.

In a study of 50 women presented this summer in Madrid, women with mild to moderate Alzheimer's disease who took the drug for 48 weeks saw a dramatic slowing of their deterioration, compared with women who didn't get the drug. "The men's study was not as compelling," says Brian Reynolds, Voyager's director of medical information. That could be in part because while luteinizing hormone increases dramatically in women after menopause, its increase is more gradual in men. A Phase III trial will wrap up next fall, Mr. Reynolds says, and the company hopes to have data by early 2008 to prepare an application to the FDA.

Patient responses to a form of the GlaxoSmithKline diabetes drug Avandia suggest that genetics may play a part in determining treatment. In an earlier trial of the drug involving 511 people, patients with a gene that made them more susceptible to Alzheimer's didn't benefit, while those lacking the gene showed improvement. The diabetes drug is believed to play a role in how brain cells metabolize glucose, a process that GlaxoSmithKline researcher Allen Roses believes will eventually prove to be the culprit in Alzheimer's. Dr. Roses says he is "optimistic" that Phase III trials now getting under way will pave the way for approval of the drug for Alzheimer's. Those trials will enroll about 2,800 patients in the U.S. and 32 other countries, according to a Glaxo spokesman.

Cholesterol-lowering statin drugs are also showing some promise. Through the National Institute on Aging, the NIH has funded a recently completed study to test whether the statin Zocor, from Merck & Co., can stall Alzheimer's in patients with normal cholesterol levels. "The idea is that lipid lowering seems to also lower the amount of amyloid in the brain," says Mary Sano, director of the Alzheimer's Disease Research Center at Mount Sinai Hospital in New York. In addition, Pfizer is recruiting patients for a study of Lipitor in Alzheimer's patients.

A note of caution: While these drugs are already on the market for other conditions, doctors and researchers say it would be unwise to prescribe or use any medicines "off-label" for Alzheimer's. The patients who are taking them now are in the controlled environment of a clinical trial with heavy oversight, researchers note, and problems could still crop up, even during the last rounds of testing.

New Drugs

Researchers also tout Alzhemed, a drug being developed by a Canadian company, Neurochem Inc., in a Montreal suburb. In an earlier study, patients with mild Alzheimer's remained stable for 20 months. Some patients who participated in an extended study have been getting the medication for three years and "have stayed the same," says spokeswoman Lise Hebert.

Some researchers are looking at ways to stimulate the immune system to fight the disease. Researchers at Eli Lilly & Co. are in the early stages of trials of an antibody that binds to beta-amyloid and prevents it from building up. That study is still recruiting patients. Lilly investigators are further along in trials of a drug that moderates the activity of an enzyme that appears to promote the production of amyloid, says company researcher Eric Siemers. Also, Wyeth, Madison, N.J., is working with Elan Pharmaceuticals Inc. to develop an injectable protein that would prevent the build-up of beta amyloid.


1319.Yee Hong program to help treat dementia
Scarborough facility a pioneer in treatment for Chinese seniors

MIKE ADLER
Oct. 17, 2006@http://www.insidetoronto.ca/to/scarborough/

A family doctor in Scarborough thinks the elderly Chinese patient in his office has Alzheimer's disease, but he's wrong.
Meanwhile, Chinese seniors in the community who really are in early stages of dementia are afraid to get tested.

Scarborough's Yee Hong Centre for Geriatric Care is trying to change all that with the memory program it announced last Friday, the first such program in Canada designed for Chinese seniors and their caregivers.

The 2001 census suggests about 6,200 Chinese seniors in Greater Toronto have dementia and that number is expected to increase dramatically as the city's population grows and ages.

Family doctors may not be able to accurately test such seniors for dementia because they don't have tests that are culturally sensitive or in Chinese, said Eric Hong, Yee Hong's director of corporate development.

One standard dementia test asks the patient to spell the English word "world" backwards, he noted.

"If I don't know English or if I'm barely speaking English, that test isn't going to be too accurate is it?"

Dr. Gabriel Chan, a geriatrician who will be testing Chinese seniors part time for signs of dementia at Yee Hong's Scarborough McNicoll Medical Centre, said memory loss can also be due to depression, shock, reaction to medication or other causes.

Doctors find it hard to accurately assess a patient's mental status if they must rely on a translator, Chan said.

He added that if, for example, a depressed senior is wrongly diagnosed as suffering from Alzheimer's, the depression will go untreated and that patient may also suffer side effects from dementia medication.

The Chinese term for dementia means "catatonic" or "crazy," so the condition comes with a cultural stigma for seniors, said Chan, adding people must be told they shouldn't be ashamed of memory loss.

"If I have a problem, I should surface."

If the program is successful, dementia in Chinese seniors will be correctly diagnosed at earlier stages, where treatment can help patients a great deal, Chan said.

"We cannot reverse (the effects of dementia), we can only delay and prevent."

Yee Hong, an organization that pioneered culturally specific care to make its residents feel more comfortable, already has an adult day program for people diagnosed as being in early stages of Alzheimer's or other dementia and has long-term-care beds for those in later stages.

Yee Hong said it hopes some day to extend its Chinese-specific care to seniors of other cultural groups. Meanwhile, it will operate the Chinese memory program part time and ask the province and its Local Health Integration Networks for further support.

The Scarborough-based organization celebrated receiving $30,000 to launch the program from dementia medication manufacturer Novartis, saying the support comes with no strings attached.

"We will never tie the hands of our clinicians as to what resources they can use," Hong said.

The industry is spending a lot to produce better dementia drugs and progress is being made, with two new classes of medication becoming available in the next five years, said Don Swainson, Novartis Canada's vice-president of neuroscience.

"I think there's a lot of hope on the horizon."


1320.Martek's DHA Selected for NIH-Funded Alzheimer's Study
Posted on : Tue, 17 Oct 2006 19:36:00 GMT | Author : Martek Biosciences Corporation
News Category : PressRelease

Sponsored by the National Institute on Aging (NIA), one of the 27 Institutes and Centers of NIH, the study will determine whether DHA supplementation slows the progression of cognitive and functional decline in patients with mild to moderate Alzheimer's disease. This study is being funded by a NIA/NIH grant to the Alzheimer's Disease Cooperative Study (ADCS), a cooperative agreement between the NIA and the University of California San Diego that was founded to advance research in the development of drugs that might be useful for treating Alzheimer's, particularly those therapies that might be overlooked by industry. Approximately $10.5 million of the ADCS grant is earmarked to fund the DHA study.


"DHA has great promise as a treatment strategy for Alzheimer's disease, with favorable effects on the same biochemical 'targets' which are being pursued with experimental drugs," said Joseph Quinn, M.D., lead investigator of the study. "One big advantage of DHA is that its biology is well known, so that the DHA approach should be less risky than many other experimental drugs under study."

The study, "Effects of DHA in Slowing the Progression of Alzheimer's Disease," is a multi-center, double-blind, placebo-controlled study of 400 subjects with mild to moderate Alzheimer's disease. The patients will be treated for 18 months, during which patients will be given either two grams per day of DHA orally, or placebo. The patients will be able to take their other Alzheimer's medications while in the study.

Director of ADCS, Dr. Leon Thal, notes that, "This is an important study designed to slow disease progression in Alzheimer's disease. We are delighted to be able to work with Martek."

As part of the study, the lead investigator will file an investigational new drug application (IND) with the U.S. Food & Drug Administration (FDA) for DHA for the treatment of patients with mild to moderate Alzheimer's disease. The study will take approximately three years to complete.

"We are looking forward to seeing the results of this study, and hope that it will benefit those impacted by Alzheimer's disease," said Steve Dubin, CEO of Martek. "Research continues to indicate that DHA is important to health throughout life, and we are pleased that NIH-supported clinicians have confidence in our DHA omega-3, and are choosing it for use in this important clinical study."

DHA omega-3 is a long-chain polyunsaturated omega-3 fatty acid found throughout the body. It is a major structural fat in the brain and accounts for up to 97 percent of the omega-3 fats in the brain. Numerous studies confirm that all age groups, from infants to adults, benefit from an adequate supply of DHA omega-3. Additionally, low levels of DHA have been associated with an increased risk of Alzheimer's disease.

Martek's DHA omega-3 products are marketed to consumers and included as an ingredient in foods under the brand life'sDHA(TM). Life'sDHA(TM) is a DHA omega-3 from a sustainable and vegetarian source. Isolated from microalgae under tightly controlled manufacturing conditions, life'sDHA(TM) is free of oceanic contaminants that may be present in certain fish or fish oil sources of omega-3's. Microalgae are the only vegetarian source of DHA omega-3.

Sections of this release contain forward-looking statements concerning, among other things, expectations regarding the use of Martek products in an NIH-funded study of the use of DHA for Alzheimer's. These statements are based upon numerous assumptions which Martek cannot control and involve risks and uncertainties that could cause actual results to differ. These statements should be understood in light of the risk factors set forth in the Company's filings with the Securities and Exchange Commission, including, but not limited to, the Company's Form 10-Q for the fiscal quarter ended July 31, 2006 and other filed reports on Form 10-K, Form 10-K/A, Form 10-Q and Form 8-K.

Martek Biosciences Corporation


1321.MICROSCOPIC BRAIN DAMAGE DETECTED IN EARLY ALZHEIMER'S DISEASE
October 18, 2006@http://www.scientistlive.com/index.thtml


Researchers have developed a new computer-aided analysis technique to identify early cellular damage in Alzheimer's disease, allowing intervention to slow down disease progression.

"With increasing longevity among the population, the incidence of AD is expected to rise rapidly, creating a great burden not only for patients and their families, but also for society," said Min-Ying Su, Ph.D., author and associate professor in the Department of Radiological Sciences & the Tu and Yuen Center for Functional Onco-Imaging at the University of California at Irvine. "Our methods may enable earlier diagnosis of AD, allowing earlier intervention to slow down disease progression," she added.

As AD progresses, cell membranes in the brain may be damaged, allowing water molecules to move throughout the brain more freely. This phenomenon can disrupt neural processes and cause neuron cells to die, leading to brain atrophy.

This process of cellular damage causes an increase in the "apparent diffusion coefficient," or ADC, which is a measurement used to study the distribution of water in the brain.

Thirteen elderly patients with mild cognitive impairment (MCI) were enrolled in Dr. Su's study. Patients with MCI are at high risk for developing AD. These 13 patients and 13 elderly control subjects underwent magnetic resonance imaging (MRI) of the brain and performed recall tasks.

On MRI images, ADC values were measured in grey- and white-matter regions by using the computer-aided analysis program. Findings were compared between patients and healthy controls.

The computerised mapping technique allowed researchers to evaluate ADC values in large regions of the brain. In patients with MCI, researchers identified regions of brain atrophy and increased water content in white-matter areas.

Additionally, high ADC values were found in the hippocampus, temporal lobe grey matter and the corpus callosum, which connects the two cerebral hemispheres. The ADC values in the hippocampus were significantly correlated with worse memory performance scores.

"The results have supported our objective to develop a computer-based analysis technique that can analyze different regions in the entire brain, to provide a comprehensive evaluation of cellular changes," Dr. Su said.

Until now, ADC values from grey matter in various lobes of the brain have not been reported, due to the difficulty of obtaining measurements in these regions. This new technology may allow researchers to learn more about how AD develops in the brain and to cultivate better treatment strategies for patients based on their individual cognitive needs.

"Patients with MCI who are very likely to progress to AD may start early treatment interventions, while patients who may remain stable with MCI can be spared from treatment and the associated side effects," added Dr. Su. "The diagnostic accuracy in identifying AD needs to be greatly improved."

The study is featured in the October issue of the monthly scientific journal Radiology.


1322.Marijuana-Like Compound May Slow Alzheimer's
10.18.06, 12:00 AM ET@http://www.forbes.com/

WEDNESDAY, Oct. 18 (HealthDay News) -- A new U.S. study finds that marijuana may help slow the progression of Alzheimer's disease, while a second report suggests the "club drug" Ecstasy could yield insights into Parkinson's disease.

Both findings were presented Wednesday at the annual meeting of the Society for Neuroscience, in Atlanta.

In the first presentation, researchers from Ohio State University in Columbus found that marijuana may contain compounds that can slow memory loss associated with Alzheimer's disease.

In their study involving rats, a team led by psychology professor Gary Wenk searched for ways to reduce Alzheimer's-linked brain inflammation.

Wenk was already familiar with data that found that long-term marijuana users had lower rates of Alzheimer's disease than the general population. His team sought to find a compound that might reduce disease-linked brain inflammation but avoid the drug's psychoactive effects.

"We are using a component of marijuana that stimulates the same centers in the brain that marijuana does," Wenk said. The synthetic compound, which is very similar in composition to marijuana, is called WIN-55212-2 (WIN).

Experiments conducted on young and old rats revealed that WIN is "a very effective anti-inflammatory, it reduces brain inflammation," Wenk said.

What makes this discovery special is that this compound can cross the blood-brain barrier, Wenk explained. The results of a special rat "maze test" suggested that WIN "also reversed the memory impairment in the older rats," he said.

Brain inflammation is characteristic of many diseases other than Alzheimer's, including multiple sclerosis, ALS, AIDS, Huntington's and Parkinson's, Wenk noted. "We are beginning to notice that brain inflammation is always in the background as people get older," he said. "Inflammation doesn't cause the disease, it contributes to the pathology," he said.

WIN is not appropriate for use in humans because it still contains substances that may trigger a "high." However, Wenk hopes that some form of this compound might be used to benefit people with neurological diseases.

"We have the added advantage that millions of doses [of marijuana] have been taken by millions of people over the past centuries," he said. "We already know a lot about its actions in the body and its toxicity, or lack of toxicity. The only problem we have is that it's illegal."

Wenk is not suggesting that Alzheimer's patients start using marijuana. "Patients would have to be so careful not to get too much," he said. "That would only worsen the symptoms of their dementia."

The challenge is to find a dose that has an anti-inflammatory effect but does not make patients high, Wenk said. "It's hopeful," he said, "but it's not a therapy until we find a way to make it work in humans."

One expert believes it may be possible to derive therapeutic benefits from marijuana without inducing other effects that could be harmful to Alzheimer's patients.

"These are still early days for thinking about drugs derived from cannabis," said Dr. Samuel Gandy, director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.

"Still, we know the structure of tetrahydrocannabinol (THC) [the active ingredient in cannabis] in detail, and it is not inconceivable that helpful THC-based drugs could be created chemically that benefit brain function but lack the 'high' that currently stigmatizes the compound," Gandy added.

In the second report, researchers from the University of Cincinnati found that, in rats, MDMA (methylenedioxymethamphetamine) -- more commonly known as the illegal drug Ecstasy -- increases the survival of dopamine-releasing cells in the brain during fetal development.

"The club drug Ecstasy can cause dopamine neurons to grow and prevent them from dying off," explained lead researcher Jack Lipton, a professor of psychiatry.

Dopamine cells are critical to the regulation of voluntary movement. This discovery might lead to better therapies for neurological diseases such as Parkinson's, the researchers said.

Ecstasy, as is, is not beneficial for Parkinson's patients, Lipton cautioned. But a part of MDMA may be.

The trick now is to find the components of MDMA that have this effect on dopamine cells and develop ways to use it to help Parkinson's patients, Lipton said. It could also be used as an adjunct to stem cell transplantation, something that's now being studied in Parkinson's patients.

"It could help transplants take better and have more cells survive," Lipton said.


1323.Durect says Voyager ends trial of Alzheimer's drug
Thu Oct 19, 2006 6:46am ET

NEW YORK, Oct 19 (Reuters) - Durect Corp. (DRRX.O: Quote, Profile, Research) on Thursday said that Voyager Pharmaceutical is ending its late-stage trials of an Alzheimer's disease treatment that uses Durect's sustained-release technology.

Durect, which specializes in drug-delivery technology, said Voyager had ended the Phase III trials of its drug, called Memryte, "in order to get an earlier look at potential efficacy" from over 600 patients.

Durect did not provide any additional information about the trial stoppage in its release and company officials could not be immediately be reached for comment.


Thursday, October 19, 2006@http://www.technologyreview.com/index.aspx

1324.A New Alzheimer's Vaccine
New approaches to immunizing patients against the harmful protein buildup characteristic of Alzheimer's disease offer hope for safer treatments.

By Emily Singer

Vaccination against Alzheimer's disease is one of the most promising treatment strategies. But safety concerns arising after initial human trials have slowed clinical development of such vaccines. Now new research that aims to bring the benefits of vaccines without the harmful side effects are raising hopes once again for this largely untreatable disease.

"There is tremendous interest in this approach," says Neil Buckholtz, chief of the dementias of aging branch at the National Institute on Aging (NIA), in Bethesda, MD. "People believe this could be a promising therapeutic, but they are proceeding slowly because of safety concerns."

Alzheimer's vaccines work by preventing or clearing the buildup of a protein, known as beta-amyloid, which clogs the brains of Alzheimer's patients. A patient can be injected with either an active or passive vaccine. Active vaccines contain the protein itself, triggering the body's immune response to produce protein-specific antibodies that tag the protein for clearance. Passive vaccines, on the other hand, contain antibodies to the protein and therefore may not require an active immune response.

Animal tests of both approaches have been promising: animals given the vaccines showed less buildup of the toxic protein and better performance on cognitive tests. But an early clinical trial of an active vaccine, sponsored by the Ireland-based Elan Corporation, was stopped in 2002 after four patients developed encephalitis, an inflammation of the brain. Later, autopsies of these patients' brains showed that despite the inflammation, the vaccine did clear the toxic protein from the brain.

"The challenge now is, are there other ways to use the immunotherapy approach to get the benefits without the adverse effects?" says Richard J. Hodes, director of the NIA.

The NIA is sponsoring a new trial, announced earlier this week at the Society for Neurosciences conference, in Atlanta, of a different type of antibody therapy: intravenous immunoglobulin (IVIg), a blood product used to treat immune disorders. IVIg contains a mix of different antibodies, including one against amyloid. Because the product has already been used to treat thousands of people with immune disease, scientists say it is unlikely to cause the inflammatory problems seen in the first Elan trial. "We have a good understanding of the side effects and how to avoid them," says Hodes.

Elan is also testing a passive vaccine, currently in clinical trials.

Scientists still aren't sure exactly what part of the complex immune response is necessary to successfully clear amyloid protein or what part triggers excessive inflammation, as seen in the first Elan trial. But second-generation vaccines that create more-targeted responses might soon answer that question.

William Bowers and Howard Federoff of the University of Rochester Medical Center, in New York, are working on a gene-therapy vaccine delivered via a stripped-down herpes-simplex virus. Their vaccine carries both the code for the toxic protein and the code for genes involved in different aspects of the immune response. "We can shape the response and evoke different kinds of antibodies and different immune responses," says Bowers, who presented his findings at the neuroscience meeting. In addition, the researchers can use different genetic "promoters"--genetic sequences that control where and when a gene is expressed--to target the vaccine to specific cell types. By testing different varieties of the vaccines, they hope to tease apart each component's effects.

"This is an example of how to deal with a promising pre-clinical therapy that didn't work in the clinic," says Marcelle Morrison-Bogorad, associate director of NIA's neuroscience and neuropsychology of aging program. "Don't give up--just go back to the bench."


FOR IMMEDIATE RELEASE@ADEARcenter
Tuesday, October 17, 2006, 3:30 p.m. ET

1325.New Alzheimer's Clinical Trials To Be Undertaken by NIA Nationwide Consortium

The Alzheimer's Disease Cooperative Study (ADCS), a federally-established consortium conducting clinical trials on Alzheimer's disease (AD), will receive $52 million over six years to conduct several new trials, the National Institutes of Health (NIH) announced today. The award is a cooperative agreement between the NIH's National Institute on Aging (NIA) and the University of California, San Diego (UCSD), which coordinates the consortium of nearly 70 sites in the United States and Canada.

The purpose of the award is to test drugs for their effectiveness in slowing down the progression or treating the symptoms of AD, as well as to investigate new methods for conducting dementia research. Specifically, researchers will focus on possible therapies aimed at affecting the beta amyloid peptide and the tau protein, both involved in the development of AD.

"We have learned a great deal from basic and observational research about how Alzheimer's and other neurodegenerative diseases develop," says Richard J. Hodes, M.D., Director of the NIA. "The consortium's work will translate this knowledge in clinical trials of interventions that target the mechanisms underlying Alzheimer's disease."

Among the new studies to be undertaken are:

Docosahexaenoic Acid (DHA) - This trial will examine whether treatment with DHA, an omega-3 fatty acid found in fish, will slow decline in AD. Observational studies associate high fish consumption with reduced risk of AD in people, and studies in mouse models of AD show that dietary DHA reduces brain levels of beta amyloid, oxidative damage associated with beta amyloid, and neurotoxicity.
Intravenous Immunoglobulin (IVIg) -- There is increased interest in passive immunization strategies against AD. IVIg contains naturally-occurring antibodies against beta amyloid, and preliminary studies have shown that IVIg may improve cognition. In addition, research has demonstrated that IVIg increased levels of anti-beta amyloid antibodies in plasma and promoted clearance of beta amyloid from cerebrospinal fluid. The new ADCS trial will more definitively demonstrate whether IVIg is useful clinically for treating AD.
Lithium -- The biological activity of lithium, which has been shown in animal models to block abnormal changes in tau, has created interest in lithium as a novel treatment for AD. ADCS investigators will undertake a pilot biomarker study to see whether the drug can lower tau and beta amyloid levels in cerebrospinal fluid and be safely tolerated in older AD patients.
Home-Based Assessment -- Older individuals, particularly the very elderly, may have physical, social and health limitations that make it difficult for them to take part in research trials. This study, conducted in people aged 75 and older, will examine the use of mail-in questionnaires, automated telephone technology and computerized data collection to assess cognitive, functional, and other factors in the home environment to see how home-based assessments might be used in primary prevention trials. Such an approach could significantly reduce the cost and increase the feasibility of participation in these long-term, costly clinical trials.
These projects join ongoing ADCS trials testing whether statins and high-dose folate/B6/B12 supplements can slow the clinical signs of AD, as well as a study of valproate to determine whether this drug can either slow decline or help delay the agitation and psychosis that often emerge in AD patients.

Leon Thal, M.D., chair of the Department of Neurosciences at the UCSD School of Medicine and principal investigator of the ADCS, notes that the selection of compounds for testing was enhanced by seeking ideas from the biotechnology sector as well as from individual investigators and the consortium's members. "We have been able to bring together a larger universe of people studying therapies for Alzheimer's, and I think this group of studies reflects new thinking in how to approach the disease," he says.

This ADCS consortium was first established in 1991 as an infrastructure of leading researchers to carry out clinical trials for promising new therapies for AD. Investigators have tested such compounds as vitamin E, the anti-Parkinson's disease drug selegiline, estrogen, anti-inflammatories and donepezil for their potential in slowing down or preventing cognitive impairment and/or dementia. Recently, positive but limited effects have been shown in slowing the development of dementia with donepezil.

To date, approximately 4,600 people have participated in the ADCS studies. Neil Buckholtz, Ph.D., who leads the federal government's partnership with the consortium as chief of the Dementias of Aging Branch of the NIA, recognized the efforts of the study participants and their families. "Participating in research takes time and dedication, and the efforts of the participants and their families stand out," Buckholtz notes. "We are deeply grateful for their help in finding new and better ways to treat and prevent Alzheimer's disease." As the new round of trials gets underway, stepped up public participation will be essential for their success, Buckholtz says, and he urges the public to learn more about how to take part in such research. (See information, below)

Alzheimer's disease affects an estimated 4.5 million people in the U.S. It increases dramatically with age, affecting approximately 40-50 percent of people age 85 and older. The numbers of people with AD are expected to rise dramatically with the aging of the population over the next few decades.

The NIA, one of 27 institutes and centers at the NIH, is part of the U.S. Department of Health and Human Services. It leads the federal effort to support and conduct basic, clinical, and social and behavioral studies on aging generally and AD specifically. NIA supports the Alzheimer's Disease Education and Referral (ADEAR) Center, which provides information on clinical studies and other research to the public, health professionals, and the media. ADEAR can be contacted toll-free at 1-800-438-4380 or by viewing www.nia.nih.gov/alzheimers.

As the studies mentioned above move forward, more information will be available at the ADEAR website about participation. NIA invites the public to sign up for e-mail alerts, which will let subscribers know when trials begin recruitment and generally when new information about AD is available.

A list of the 35 primary ADCS sites appears below.

Last Updated: Friday, 20 October 2006, 00:17 GMT 01:17 UK BBC

1326.'Back NICE' government is urged

The government needs to show vocal support for the National Institute for Health and Clinical Excellence (NICE), a leading medical journal says.
A Lancet editorial said the NHS drugs watchdog should be backed for being the best way to ensure fairness across the country's health system.

The call follows Alzheimer's groups accusing NICE of "blatant cost cutting" over a decision on drugs.

The government said the body should operate without political interference.

NICE was set up seven years ago to advise ministers in England and Wales on what treatments should be available on the NHS.

'Not a rationing body'

Last week it rejected five appeals against its guidance to restrict the use of four drugs for Alzheimer's disease, prompting condemnation from support groups.

The government's response at the time was to say that it would be "entirely inappropriate" to overrule NICE's decision.

The Lancet says NICE's recommendations are necessary to make the best use of limited NHS funds and the government's patient choice agenda ignores the need for rational spending.

The Department of Health said: "It [NICE] is not a rationing body.

"The institute was established to give advice to the NHS where there was uncertainty over the clinical and cost effectiveness of specific drugs and other treatments.

"NICE's remit is to produce robust, workable and evidence based guidance, free from political interference and we support the Institute in this role."

But the Lancet said: "If the government really wants to extend choice within the NHS, as it has pledged, it should launch a debate about the health-financing framework necessary to support this philosophy.

"But its first obligation should be to show vocal support for NICE as the best mechanism to ensure equity in the UK's current health system."


1327.The Insidious Fog: A journey into Alzheimer's

Mike Shahin, Citizen Special
Published: Saturday, October 21, 2006 http://www.canada.com/
With the strains of a Wag-ner opera floating through his London flat and a looking glass at his side, William Utermohlen picked up his paintbrush and began to record his descent into Alzheimer's.

It was 1995, and Mr. Utermohlen, 61, had just been diagnosed with the disease he knew had been stalking him for years. The artist decided that he needed to figure out what was wrong with him, to understand the illness that was robbing him of his memories and his abilities.

So he began to create self-portraits.

By looking into his own eyes, reflected in the mirror, Mr. Utermohlen peered into the depths of the disease. "He was frightened," said his wife, Patricia Utermohlen. "But he wanted to help others. He wanted to show how he was changing."

What he saw -- and what came through on the canvas over five years -- was a man who was trapped, a man "not sure about the spaces he was occupying" when it came to memory, Mrs. Utermohlen said.

A misplaced ear. A face trapped behind bars. Angry eyes. Confusion. The smudge marks of erasure, of memories lost.

Mr. Utermohlen's first works were glimpsed by one of his medical caregivers. That man encouraged him to continue painting and drawing; the artist responded by creating more than a dozen pieces, which stand today as one of the most powerful artistic commentaries on the ravages of Alzheimer's.

Although he had painted before the disease, it was Mr. Utermohlen's Alzheimer's oeuvre that brought him wide recognition. He was featured by his doctors in a Lancet journal article on the impact of dementia on visual artists. His series of self-portraits has been exhibited in Paris, London and Philadelphia, his place of birth. The portraits will be shown at the New York Academy of Medicine for a week beginning tomorrow; Mrs. Utermohlen, 79, an art historian, will travel there from England to take part in a panel discussion on Alzheimer's.

Mr. Utermohlen, meanwhile, is oblivious to the fuss being made in medical and artistic communities over his work.

Over the years, the disease has limited him, reduced him, and, finally, smothered his artistic force. He forgot to show up to teach his classes. He couldn't sign his name. Dancing, one of his great pleasures, became impossible. He wandered, and got lost. He put his shoes on the wrong feet.

His last work, in 2001, consisted of a circle representing a face. He didn't know where to put the eyes or nose, his wife said -- so he stopped.

Mr. Utermohlen, now 72, has been in a hospital long-term care ward for a year, too weak to move on his own and too lost to recognize his partner of more than 35 years.

But his art, with all its power and meaning, promises to speak to people about Alzheimer's for years to come.

"You have to approach something like this positively and throw yourself into it," he told a reporter five years ago.

"It's not fighting back -- you can't fight it. But I wanted to try to understand what was happening to me in the only way I can."

mshahin@thecitizen.canwest.com

? The Ottawa Citizen 2006


1328.Dementia is Canada's challenge

Andrew Duffy, CanWest News Service
Published: Saturday, October 21, 2006
http://www.canada.com/calgaryherald/index.html
On most days you'll find Gerry McKee treading across the wide, polished floors of Ottawa's Bayshore Shopping Mall in the peaceful hour before the stores open.

His wife, Joan, is always beside him for what has become their morning ritual: a few laps around the mall with other members of the Bayshore walking club.

Married for 52 years, the McKees are closer than ever now. It's a state of affairs that reflects both the strength of their relationship and the scourge that is Alzheimer's disease.

McKee, 73, has for five years lived with the brain disease that slowly corrodes an individual's mental, physical and social condition. In that time, he has grown progressively more dependent on his wife.

"My wife is a very strong person," McKee says, smiling. "She runs things now. I have nothing to do with anything."

The disease affects everyone differently; McKee has experienced a slow onset. Still, his wife now manages their household, keeping close tabs on his medication and his whereabouts.

"I've learned to write things down, which is how I keep my memory," says McKee. "I can't contain it in my head the way I used to."

McKee's journey into what British writer John Bayley called an "insidious fog" is one that more than a million Canadians will follow in the coming decades.

About 420,000 Canadians older than 65 suffer from Alzheimer's or a related dementia. With the baby boomers poised to cascade into their retirement years, those numbers are projected to swell dramatically. By 2031, one of every four Canadians will be older than 65. The country will have to manage the health problems of 9.3 million seniors. Chief among those challenges will be Alzheimer's, a slow-moving, progressive disease that attacks memory then harms other brain functions.

"There's a huge wave coming behind us and we need to get ready," said Scott Dudgeon, director of the Alzheimer Society of Canada.

Dementia is the world's leading cause of disability among the elderly. Surveys show it is the principal reason for nursing home admissions. In Canada, plans to mitigate the suffering and expense wrought by Alzheimer's remain in their infancy.

The National Advisory Council on Aging issued a report in October 2004 warning "the challenges posed by dementia to individuals, communities and Canada's health and social care systems will be enormous." It urgently called for a national strategy.

"The current challenges related to Alzheimer's disease are serious," the council concluded, "but the real ones are ahead of us."

Among the key challenges to come are:

- Housing: About half of all people with Alzheimer's disease live in nursing homes or other long-term care facilities ill-suited to the needs of Alzheimer's patients;

- Affordability: A bed in long-term care costs between $18,100 and $24,700 a year;

- Caring for caregivers: Surveys show 75 per cent of those who look after Alzheimer's patients at home are women. Many suffer their own health problems due to the physical demands and emotional stress;

- Health-care staff: A study estimates Canada has fewer than 200 doctors who specialize in geriatric medicine, a third of what's required;

- Aggressive dementia patients: A Toronto inquest last year heard that 11 long-term care residents in Ontario were killed between 1999 and 2004 by fellow residents. Assaults in nursing homes rose precipitously in the same period;

- Research: Scientists have yet to discover precisely what triggers the disease, or how to halt its slow and steady progress. Ottawa has, over the last five years, doubled its annual spending on Alzheimer's research to $18.7 million.

? The Calgary Herald 2006


1329.Alzheimer's disease linked to the common cold
Last updated at 21:19pm on 23rd October 2006
http://www.dailymail.co.uk
Viruses linked to the common cold could be causing memory loss and Alzheimer's disease in millions of people, new research suggests.

Experts suspect that common viruses which infect around one billion people worldwide each year may be invading the central nervous system and damaging the brain. In later life this could lead to symptoms of memory loss and declining mental ability.

See also:
? Flu jab for pregnant women as research reveals risk of leukaemia to unborn child
?How to lower your risk of Alzheimer's disease

The viruses involved belong to a large family called picornaviruses. They include rhinoviruses, which are associated with the common cold, and enteroviruses, which cause stomach upsets. Picornaviruses are also responsible for serious conditions such as encephalitis, meningitis, inflammation of the heart, hepatitis A and polio.

Evidence of harm to the brain has emerged from a study of mice infected with a polio-like picornavirus.

The animals had difficulty learning to navigate a maze designed to test various components of spatial memory. Scientists found that the degree of impairment was directly related to the number of cells dying in the hippocampus brain region, which plays an important role in memory and learning.

Study leader Dr Charles Howe, from the Mayo Clinic in Rochester, Minnesota, said: "Our study suggests that virus-induced memory loss could accumulate over the lifetime of an individual and eventually lead to clinical cognitive memory deficits."

Many people suffer two or three rhinovirus or enterovirus infections each year. It was already known that in rare cases picornoviruses can get into the brains of children and cause long-lasting injury.

Polio is the best known example. After entering the central nervous system, the virus can damage the spinal cord and parts of the brain responsible for motor function, leading to paralysis.

However the Mayo scientists thinks picornoviruses might be having much more common brain effects that are being missed.

Clinical studies suggested that picornavirus infections might trigger damaging inflammation in the brain. Brain inflammation is associated with learning and memory loss, and is a key element of Alzheimer's disease.


1330.Computer-based 'games' boost mental function in Alzheimer's patients: study
Last Updated: Monday, October 23, 2006 | 3:44 PM ET
CBC News

Internet-based computer activities may improve cognition in patients with Alzheimer's disease, according to research published in this month's issue of the Journal of Neurology, Neurosurgery and Psychiatry.

Researchers from the Fundacio ACE, Institut Catala de Neurociencies Aplicades in Barcelona, Spain, and the University of Pittsburgh School of Medicine found that when used alongside medications to treat the disease, internet computer activities were even more successful than traditional exercises of mental stimulation commonly used with dementia patients.

"This study shows that tasks aimed at increasing or maintaining mental function have a place in treating Alzheimer's alongside pharmacotherapy," said Dr. Oscar Lopez, professor of neurology at the University of Pittsburgh School of Medicine, and a co-author on the study.

"While further study is needed, it is encouraging to find that an internet-based program can work for cognitive stimulation, making it easily available and accessible to many people," said Lopez.

Researchers looked at 46 Alzheimer's patients in an adult day-care centre in Barcelona. All were taking cholinesterase inhibitors, the most common drug treatment for the disease, for at least one year prior to enrolling in the study. All participants remained on the drug for the duration of the study.

Participants were placed into one of three groups. The first, the control group, received no cognitive therapy. They lived at home and didn't participate at the day-care centre.

Members of the second group were enrolled in a program that included 2.5 to 3.5 hours of cognitive stimulation tasks, musical therapy, arts and crafts, and physical activity.

The third group participated in the same activities as the second group but also used an interactive multimedia internet-based tool that allowed them to carry out a variety of different stimulation tasks at varying levels of difficulty throughout the day.

After 12 weeks of treatment, researchers found that the third group had improved scores as compared to the control group. These improvements were maintained at 24 weeks. The second group showed improvement over the control group at 12 weeks, but the effects decreased by 24 weeks.

"While Alzheimer's disease is a progressive degenerative condition, studies have shown that in the early stages, the brain is still able to learn and change. This indicates that increasing brain activity, especially in regards to memory and cognition, may help stave off cognitive loss in people with Alzheimer's," said James T. Becker, a professor at the University of Pittsburgh, and a co-author on the study.

The study was funded by Fundacio ACE, Institut Catala de Neurociencies Aplicades.


1331.Estrogen Plays Both Sides On Alzheimer's
Main Category: Endocrinology News
Article Date: 22 Oct 2006 - 9:00am (PDT)
http://www.medicalnewstoday.com/
Hormone replacement therapy can worsen Alzheimer's disease in older women but may prevent or delay the onset of the illness if started early, said Roberta Diaz Brinton, professor of molecular pharmacology and toxicology in the USC School of Pharmacy.

One of four panelists at a symposium on "The Aging Female Brain" at the 2006 annual meeting of the Society for Neuroscience, Brinton presented findings from her latest study, published online by the journal Endocrinology.

Brinton's research group set out to understand why HRT raises the risk of Alzheimer's for women 65 and older, as determined by recent large clinical trials.

In the process, the USC researchers found that HRT may lower Alzheimer's risk by as much as 50 percent in younger women.

"Essentially, they're being treated in a prevention mode," Brinton said. "If the [brain] cells are healthy, estrogen essentially promotes their survival. In unhealthy cells, cells that are degenerating, it's not great. It actually exacerbates the degenerative process."

Brinton added that HRT, when started early, appears to lower the risk of many other degenerative diseases.

"It's not that you don't age," she said. "You just age better."

To exploit estrogen's apparent protective mechanisms while minimizing its risks, Brinton's group is attempting to develop "brain-selective estrogens" that would benefit neural networks without activating cancer-related sites in the breast or uterus.

Also at the 2006 SFN annual meeting, Brinton is scheduled to become only the fourth recipient of the society's Science Educator Award, in recognition of her leadership in USC's STAR program, a neighborhood outreach effort that reaches nearly 1,000 middle and high school students every year and brings many of them into the university's laboratories for hands-on internships (www.usc.edu/hsc/USCSTAR).

A "very excited and very grateful" Brinton thanked USC's Good Neighbors program, which she said "has supported us at every step of the way."

Estrogen Plays Both Sides On Alzheimer's
Main Category: Endocrinology News
Article Date: 22 Oct 2006 - 9:00am (PDT)
http://www.medicalnewstoday.com/
###

USC groups present at Neuroscience 2006: Highlights from presentations by University of Southern California researchers at the Society for Neuroscience's annual meeting.

Contact: Carl Marziali
University of Southern California


1332.Vegetables May Boost Brain Power in Older Adults
Study found leafy, green veggies, but not fruits, slowed cognitive decline

By Rick Ansorge
HealthDay Reporter

MONDAY, Oct. 23 (HealthDay News) -- Want to preserve your mental edge as you age? Vegetables -- particularly green, leafy ones -- will do the trick if you eat three servings a day, new research shows.

But the research also suggests that the same effect is not found in those who eat lots of fruit.

"It's a modest effect," said Martha Clare Morris, associate professor at Rush University Medical Center in Chicago, and lead author of the study. "People who consumed two or more vegetables a day had a 35 to 40 percent decrease in the decline in thinking ability over six years. That's the equivalent of being five years younger in age."

The study results are published in the Oct. 24 issue of the journal Neurology.

Morris' team studied 3,718 research participants 65 or older who live in the south side of Chicago. Sixty-two percent were black, 38 percent were non-Hispanic white, and 62 percent were female.

"We used a complete food questionnaire of 139 different food items," Morris said. "We asked about their usual intake and assessed the frequency of intake." During the six-year study, the participants received at least two cognitive tests that measured their memory and thinking speed.

"By far, the association with a slower rate of decline was found in the group that ate high amounts of green, leafy vegetables," Morris said. Such foods included lettuce and tossed salad, spinach, kale and collards.

The study also found that the slowdown in cognitive decline was greatest in the oldest people who ate at least two more vegetable servings a day.

Because the cognitive tests measured overall thinking ability, the benefits of eating vegetables may translate into an easier time with such everyday tasks as remembering phone numbers and names and balancing checkbooks, Morris said.

Morris suspects that vegetables may help protect memory and thinking speed because they contain high amounts of vitamin E, an antioxidant that can help reduce the damage caused by free radicals, unstable oxygen molecules generated by normal metabolism that can damage neurons in the brain and contribute to dementia.

"We had found in previous studies that vitamin E in food protected against cognitive decline and the development of Alzheimer's disease," she said.

Her previous research also had shown that consumption of healthy fats, such as the polyunsaturated and monounsaturated fats found in foods such as olive oil, were similarly protective.

"When we eat vegetables, we tend to put the good fats on them, such as an oil-based salad dressing on salads, healthy-fat mayonnaise on cole slaw, and healthy-fat margarine on vegetables," Morris said. "Such fats help us to absorb the vitamin E, and perhaps are also beneficial to the brain. So that's one plausible explanation of why vegetables are good for you."

Morris' study also found that high consumption of fruit had no effect on thinking ability. A similar large-scale study, the Nurses' Health Study, also found that high vegetable consumption, but not high fruit consumption, was associated with a slower rate of cognitive decline.

One of the most common antioxidants found in fruit, vitamin C, has not been consistently shown to protect the brain, Morris said. Most of her study participants consumed fruit such as oranges, grapefruits, apples and bananas, which are high in vitamin C.

It's possible that some fruit may contain compounds that counteract antioxidants. Further studies are needed to determine whether fruit is brain-protective, she said.

As for eating vegetables, Morris said it's too soon to say for sure that they actually preserve the brain from age-related decline. "But it's encouraging to see that it appears to slow the rate of decline," she said. "We know that eating vegetables is important for chronic diseases. So this might be one more reason why you should eat your vegetables."

In her next study of the same group of Chicago residents, Morris hopes to examine whether high vegetable consumption helps protect against Alzheimer's disease. Results are expected in the next year, she said.

Dallas Anderson is program director for epidemiologic studies of Alzheimer's disease at the National Institute on Aging. "It may be premature to discount the role of fruit consumption in maintaining cognitive health," he said, citing recent research showing that weekly consumption of three or more servings of fruit and vegetable juices was associated with a reduced risk of Alzheimer's.

"Further research will be needed to take account of how the fruit is prepared, as peeling may greatly reduce the amounts of antioxidants available," Anderson said.

"I anticipate that further research will refine what we know about the relationship between fruit and vegetable consumption and cognitive function, helping to determine more definitively the types and amounts of foods that may preserve cognition," he added.

More information

To learn more about the health benefits offered by vegetables, visit the U.S. Department of Agriculture.

SOURCES: Martha Clare Morris, Sc.D., associate professor, Rush University Medical Center, Chicago; Dallas W. Anderson, Ph.D., program director, Population Studies Dementias of Aging Branch, Neuroscience and Neuropsychology of Aging Program, National Institute on Aging, Washington, D.C.; Oct. 24, 2006, Neurology

Last Updated: Oct. 23, 2006

Copyright (c) 2006 ScoutNews LLC. All rights reserved.


Source: Washington University in St. Louis Released: Mon 23-Oct-2006, 18:50 ET
Embargo expired: Tue 24-Oct-2006, 17:00 ET Printer-friendly Version

1333.Naturally Occurring Enzyme Can Break Down Key Part of Alzheimer's Plaques
Libraries
Medical News Keywords
ALZHEIMER'S, AMYLOID BETA, ABETA, BRAIN PLAQUES, MMP-9
Contact Information

Available for logged-in reporters only
Description

Scientists have identified a naturally occurring enzyme that can break down a key component of the brain plaques characteristic of Alzheimer's disease. The finding may provide researchers with new opportunities to understand what goes wrong in the brains of Alzheimer's patients and could one day help them seek new therapies.

Newswise - Scientists have identified a naturally occurring enzyme that can break down a key component of the brain plaques characteristic of Alzheimer's disease. The finding may provide researchers with new opportunities to understand what goes wrong in the brains of Alzheimer's patients and could one day help them seek new therapies.

Researchers at Washington University School of Medicine in St. Louis showed earlier this summer that the enzyme, matrix metalloproteinase 9 (MMP-9), degrades abnormally aggregated proteins known as amyloid fibrils, a main ingredient of brain plaques. In the brain, MMP-9 is made by support cells known as astrocytes.

MMP-9 is already well-known because of its links to cancer metastases, vascular disease, arthritis and other pathologies. Scientists called the new link to Alzheimer's encouraging, noting that previously identified enzymes only degrade a smaller, nonaggregated component of Alzheimer's plaques.

"We already knew of three enzymes that break down amyloid beta (Abeta), a protein fragment that clumps together with itself to form the fibrils," says Jin-Moo Lee, M.D., Ph.D., assistant professor of neurology. "But the thinking up until now had been that Abeta might be clumping together so tightly that the fibrils were indestructible."

In a new study, appearing October 25 in The Journal of Neuroscience, Lee's group found that disabling the mouse gene for MMP-9 increased levels of Abeta in the spaces between brain cells. The finding proves that MMP-9 contributes to clearance of Abeta from extracellular spaces and suggests its dysfunction could potentially contribute to the development of Alzheimer's.

"MMP-9 and other enzymes like it are secreted from brain support cells and active in the spaces outside of cells, and that's where we saw an increase in Abeta levels in the mice that lacked the gene for MMP-9," Lee notes. "That's relevant to Alzheimer's because all the amyloid plaques are extracellular, and the formation of the plaques seems to be related to an elevated level of Abeta that accumulates over time in those spaces."

In earlier studies, Lee's lab analyzed the production of MMP-9 in astrocytes. They found astrocytes close to amyloid plaques increased their MMP-9 production. Imaging studies also showed that MMP-9 levels increased around blood vessels laden with amyloid.


"Astrocytes become activated around plaques as they develop, and then eventually form a wall surrounding the plaques," he says.

Lee's results have led him to formulate a provocative but as yet unproven theory about an old mystery of Alzheimer's disease: why plaques continue to increase in number over time but only grow to a certain size.

"Even though everything we know about the fibrils suggests they should constantly grow, plaques reach a mature size and stop growing," Lee says. "It's possible that production of MMP-9 and other similar substances by support cells in the brain is establishing a balance that prevents the plaques from growing beyond a certain size."

To follow up, Lee plans to crossbreed mice lacking MMP-9 with a line of mice genetically modified to develop an Alzheimer's-like condition. Scientists want to see if removing MMP-9 causes the mice to develop Alzheimer's more quickly.
In a parallel project that will test MMP-9's potential as a therapeutic, Lee and his collaborators will use viruses to alter production of MMP-9 in the mouse model. Researchers want to learn if increasing levels of the enzyme present in the brain can delay onset of Alzheimer's.

Yin K-J, Cirrito JR, Yan P, Hu X, Xiao Q, Pan X, Bateman R, Song H, Hsu F-F, Turk J, Xu J, Hsu CY, Mills JC, Holtzman DM, Lee J-M. Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolism. The Journal of Neuroscience, Oct. 25, 2006.

Yan P, Hu X, Song H, Yin K, Bateman RJ, Cirrito JR, Xiao Q, Hsu F-F, Turk JW, Xu J, Hsu CY, Holtzman DM, Lee JM. Matrix metalloproteinase-9 degrades amyloid-beta fibrils in vitro and compact plaques in situ. The Journal of Biological Chemistry, June 20, 2006.

Funding from the National Institutes of Health, the National Institute of Neurological Disorders and Stroke and the American Health Assistance Foundation supported this research.

Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.


1334..Anaesthetics link to Alzheimer's in elderly
http://news.scotsman.com/ 26/10/2006

LYNDSAY MOSS
HEALTH CORRESPONDENT (lmoss@scotsman.com)
SOME general anaesthetics used during surgery may increase the risk of elderly patients developing Alzheimer's disease, research revealed yesterday.

Studies in the United States have shown that certain drugs may affect the growth of beta amyloid protein clumps - or plaques - in the brain, which are linked to the development of the disease.

Researchers hope the studies, which involved laboratory and animal tests, will mean the risks of individual anaesthetics are investigated urgently.

Alzheimer's campaigners in the UK also called for a prompt investigation into the possible links between anaesthetic use and dementia. New Scientist magazine reported the research, carried out by a team at the University of Pittsburgh in Pennsylvania.

The scientists found that two anaesthetics that are inhaled by patients - halothane and isoflurane - and the injected drug propofol encouraged the clumping of proteins.

Another study found that halothane interacts directly with beta amyloid to change its shape and increase the rate at which it binds to nearby proteins.

The American report said that just six hours of exposure to halothane was enough to trigger protein-clumping similar to that seen in people with Alzheimer's.

Halothane is popular in Asia and Africa because it is cheap, but it is rarely used in Europe and the United States. The other two anaesthetics studied are more widely used in Europe, but appear to take longer to have the harmful effects.

Experts said memory problems were seen most often in elderly patients who had long operations, such as heart bypass surgery or hip replacements.

Dr Pravat Mandal, who led the research, said the dangers and benefits of each anaesthetic needed to be studied.

"The main focus should now be using an anaesthetic that does not have any undesirable and deadly effects," he said.

Clive Ballard, the director of research at the Alzheimer's Society, said 10 per cent of older people given anaesthetic for major surgery experienced lasting problems with their memory and attention.

"It is not clear whether this decline may increase a person's risk of Alzheimer's disease, which is why this study and others in the area are so important. Further research to investigate these concerns is now is urgently needed," he said.

Dementia statistics
OF THE 62,000 people in Scotland who suffer from dementia, about 33,550 are believed to have Alzheimer's disease. Most patients are aged over 70 and the disease is uncommon in people under 60.


1335.Chronic drinking may damage brain, memory
By CHRISTINE DELL'AMORE
UPI Consumer Health Correspondent
WASHINGTON, Oct. 24 (UPI) -- Chronic, heavy drinking may damage the part of the brain related to learning and short-term memory, researchers have found.

In a recent study, alcoholic men had lower hippocampus volumes than men without a drinking history. A lower volume could mean a loss of tissue in that part of the brain.

"Although previous studies have shown a similar effect, this study was better controlled ... making the findings more believable," study author Dr. Gary Wand, a professor of medicine at Johns Hopkins University School of Medicine, said in a statement.

The study, led by Dr. Thomas Beresford of the University of Colorado Health Sciences Center, will be published in the November issue of Alcoholism: Clinical & Experimental Research.

Beresford and colleagues analyzed magnetic resonance imaging scans of eight adult male veterans who were also alcoholics, as well as eight veteran non-alcoholics. The researchers applied stringent criteria to their selection: The veterans had to be regular, chronic heavy drinkers -- at least five drinks a day at least three days a week -- recent heavy drinkers and alcohol-dependent.

The non-alcoholics were similar to the alcoholics by age and ethnicity, and were also selected for their low incidence of alcohol intake.

Likewise, the researchers were careful to exclude people with certain psychiatric illnesses, such as post-traumatic stress disorder, which some scientists believe may make the hippocampus smaller.

The hippocampus, responsible for the formation of new memory, is divided into two structures -- the right and the left, which are located in the right and left temporal lobes of the brain.

The researchers discovered total hippocampus volume, as well as the left hippocampus volume, shrank in the alcoholic men. The right hippocampus lost volume, but not as much as the left.

Previous research has shown alcohol impairs the ability to form new memory. For example, a person who can't remember his behavior after a night of drinking has experienced blocked hippocampus function.

It's unknown whether long-term drinking creates permanent damage, or kills hippocampus cells. Chronic alcoholics who are otherwise intelligent often have terrible memories, which "begs the question: if alcohol affects the hippocampus, does chronic drinking damage the hippocampus?" said Scott Swartzwelder, a professor of psychiatry at Duke University Medical Center.

Animal research has established a strong link between chronic alcohol intake and damage to the hippocampus, but observational studies in humans have remained inconclusive.

Many scientists cite poorly designed studies that have not excluded subjects with histories of other brain disorders as a possible reason.

Other conditions, such as chronic stress and Alzheimer's disease, are also associated with injury to the hippocampus.

Beresford's more exclusive study concluded that chronic, heavy drinking "exerts a unique and selectively injurious" effect on the hippocampus.

However, the study was observational, and it's still unclear whether heavy, long-term alcohol consumption really hurts the hippocampus.

There were also several limitations to the research. For one, the study sample size was small, and it did not include women.

Likewise, the study subjects were observed at one point of time: middle-age. It's unknown whether people with smaller hippocampi simply drink more, possibly due to a genetic proclivity.

Studying the men at various points in their lifetime would provide a better picture of what happens to the brain. For instance, animal research has shown the brain is most sensitive to alcohol during adolescence, and so chronic exposure during youth may cause more damage to the hippocampus, said Swartzwelder.

Overall, the study adds evidence to the hypothesis of long-term damage, he said.

"One of the nicest things about it is that it fleshes out a long-standing chunk of animal research and extends it to humans," he said.

Beresford and colleagues plan to continue studying the veterans, focusing on whether the hippocampus can heal itself after alcohol damage, and if so, what scientists can do to accelerate the healing process.


Last Updated: Thursday, 26 October 2006, 16:47 GMT 17:47 UK BBC

1336.Alzheimer's jab trial resurrected

Research into a vaccine for Alzheimer's disease, which was stopped early on safety grounds, is to be resurrected.
It was designed to reverse the disease's progression by clearing the beta amyloid protein that causes the disease.

But the trial was halted in 2002 when 6% of patients in the second phase of the study developed brain inflammation.

Southampton University researchers are to reassess 80 patients who took part in the initial phase of the study.

The vaccine is one of the most exciting treatments for Alzheimer's

Clive Ballard, Alzheimer's Society

They will look at whether features of the disease such as memory loss have been halted or reversed.

The vaccine, known as AN-1792, contains a synthetic form of beta amyloid protein.

It acts by stimulating an immune response to the protein.

Preliminary results from the trial showed the vaccine did clear the amyloid protein from the brain.

Vaccine 'realistic prospect'

James Nicoll, professor of neuropathology at Southampton University Hospitals NHS Trust, who is leading the research, said: "This study offers us a unique insight into whether immunisation against Alzheimer's is an effective solution to this devastating disease.

"We know that vaccination can reverse the processes of Alzheimer's to some degree - our challenge is to understand these processes better and translate them into real benefits for patients."

Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, said: "The prospect of a vaccine to protect against Alzheimer's is a realistic one because it is a disease, and not a normal part of ageing.

"Immunisation is an exciting area and we are delighted to be funding this groundbreaking study."

Clive Ballard, director of research at the Alzheimer's Society, said: "There are 25 million people worldwide with Alzheimer's disease and 100 000 people are diagnosed in the UK each year.

"This clearly highlights the urgent need to develop new ways of defeating dementia.

"The vaccine is one of the most exciting treatments for Alzheimer's and we are very please to see ongoing funding in the UK as part of a international effort to develop a vaccine for Alzheimer's disease."


1337.Behavior Problems in Moderate to Severe Alzheimer's Disease Improved With Combined Memantine and Donepezil: Presented at ANA
By Paula Moyer
DGDispatch
CHICAGO, IL -- October 10, 2006 -- Patients with moderate to severe Alzheimer's disease who are receiving a stable dose of donepezil (Aricept) have reduced behavioral symptoms when their regimen is supplemented with memantine (Namenda), according to findings presented here at the American Neurological Association (ANA) 131st annual meeting.

Patients receiving the adjunctive memantine performed significantly better on mood and psychosis subscales of the Neuropsychiatric Inventory (NPI), said Pierre N. Tariot, MD, director, Memory Disorders Center, Banner Alzheimers Disease Institute, Phoenix, Arizona. "This response suggests potential for memantine to provide specific benefits for behavioral symptoms."

In a presentation on October 8th, Dr. Tariot said the study was conducted to assess the effects of memantine on behavioral symptoms that are commonly associated with Alzheimer's disease. They conducted a post hoc analysis of behavioral outcomes in a study of 403 patients with moderate to severe Alzheimer's disease.

Patients had been diagnosed with probable Alzheimer's disease and had Mini Mental Status Examination (MMSE) scores of 5 to 14. All patients had been receiving donepezil for at least 3 months prior to randomization at doses of either 5 or 10 mg daily. They were then randomized to receive either memantine at a dose of 10 mg twice daily or placebo for 24 weeks.

Individual items of the NPI were aggregated into 4 subscales: 1) mood, which pertained to depression, anxiety, irritability, nocturnal exacerbations, and changes in eating habits; 2) psychosis; which encompassed delusions, hallucinations, and agitation or aggression; 3) frontal symptoms, which consisted of euphoria or elation and disinhibition, and 4) other common Alzheimer's disease symptoms, which consisted of apathy and aberrant motor behavior.

The 2 treatment groups had similar baseline characteristics. However, at week 24, the total NPI score was significantly lower for the memantine group than the placebo group. The placebo group had an increase, or worsening, of NPI scores, while the memantine-treated patients had a slight decrease (P < .01). Therefore, there were fewer behavioral disturbances and psychiatric symptoms in memantine-treated patients.

On the mood subscale, patients on combination therapy had an average improvement of 0.4 points at the end of the study, and those on monotherapy worsened by an average of 1.6 points.

Although both groups had some worsening of symptoms on the psychosis subscale, the increase was lessened in the patients on combination therapy compared with monotherapy (P = .008). Frontal symptoms were unchanged, and the slight worsening on the other symptoms were similar between the 2 groups, an average of 0.6 for the monotherapy patients and 0.1 for those on the combination therapy.

The investigators concluded that 6 months of treatment with memantine in combination with donepezil reduced behavioral symptoms of patients with moderate to severe AD, particularly symptoms associated with mood and psychosis.

Namenda is manufactured by Forest Laboratories, Inc., which sponsored the study.

[Presentation title: NPI Subscale Analysis of Memantine/Donepezil Treatment in Moderate-to-Severe AD. Abstract S-19]


1338.Britain developing new treatments for Alzheimer's

www.chinaview.cn 2006-10-27 08:11:56

LONDON, Oct. 26 (Xinhua) -- British scientists have created a new chemical compound that could be developed into a drug treatment for Alzheimer's disease.

UK researchers at the University of Liverpool have used a family of long chain sugars called Heparan Sulphates (HS), found on nearly every cell of the body, to produce a new compound that can prevent the formation of clumps of small proteins that form inthe brain, the science website Alpha Galileo reported on Thursday.

The clumps disrupting the normal function of cells leading to progressive memory loss which is characteristic of Alzheimer's disease, are formed from a small protein fragment called Amyloid-beta (A-beta) peptide released from its "parent" protein ? amyloid precursor protein (APP), and the process requires the action of an enzyme called beta-secretase (BACE), critical in clipping up the APP to form the smaller A-beta fragments.

The researchers have discovered that the HS sugars may play a key role in limiting the development of Alzheimer's disease. The sugars stick to the BACE enzyme and reduce its ability to "clip" the A-beta peptide, thus controlling the amount of A-beta peptide available to form damaging clumps in brain tissue.

"We have developed a new class of compounds called 'engineered heparins' that could possibly be developed into drugs to stop A-beta peptides in the brain from forming and for the first time treat the underlying cause of Alzheimer's," leading researcher Professor Jerry Turnbull was quoted as saying.

The compound, based on the blood thinning drug, heparin, has modified chemical structures designed to optimize their desired activities and reduce potential side effects, and the compounds work by blocking the beta-secretase enzyme, responsible for snipping proteins into smaller fragments, he said, adding that despite its central importance to the disease, there are currently no drug treatments which target this enzyme because it has proved difficult to find inhibitors using traditional drug discovery approaches.

The new compounds, based on the body's natural substances, may provide a novel route to effective treatments for this debilitating disease -- Alzheimer's, the researchers said.

A spin-out company, IntelliHep Ltd, has been founded to explorethe commercial opportunities of developing engineering heparans asnew drugs against Alzheimer's and other important medical conditions, according to the report.


1339.Activities of Daily Living Score Can Differentiate Mild Cognitive Impairment From Mild Alzheimer's Disease: Presented at ANA
By Paula Moyer
DGDispatch


CHICAGO, IL -- October 10, 2006 -- An assessment of a patient's ability to perform certain activities of daily living can help differentiate mild cognitive impairment from Alzheimer's disease, according to investigators who presented their findings here at the American Neurological Association (ANA) 131st Annual Meeting.

The researchers evaluated the Functional Activities Questionnaire (FAQ), which is commonly administered to the patient's caregiver and assesses the patient's ability to participate in 10 categories of instrumental activities of daily living. These included:
1) writing checks and maintaining other financial records;
2) assembling tax or business records;
3) shopping alone;
4) playing a game of skill;
5) making coffee or tea;
6) preparing a balanced meal;
7) keeping track of current events;
8) attending to and understanding a television program, book or magazine;
9) remembering appointments, family occasions, and medications; and
10) traveling out of the neighborhood.

The study required the caregiver to give the patient a score of zero to 3 on each activity, with 0 equaling normal independent participation in the activity, 1 indicating the patient's ability to do the activity alone but with difficulty, 2 indicating that the patient requires assistance, and 3 indicating that the patient is dependent on others to conduct the activity.

"Our findings show that analyses of individual assessments of activities of daily living, such as the FAQ, may be useful for diagnosing mild cognitive impairment," said principal investigator Edmond Teng, MD, PhD, fellow, Alzheimer Disease Center, David Geffen School of Medicine, UCLA, Los Angeles, California.

Although the FAQ scores in some domains overlapped between those with mild cognitive impairment and those with Alzheimer's disease, the scores on item 10, traveling out of the neighborhood, most effectively discriminated between those 2 groups (P = .001), Dr. Teng said.

Previous research has shown that people with mild cognitive impairment continue to have essentially intact functional abilities. However, other research has shown that such patients have declines in instrumental activities of daily living. Therefore, Dr. Teng and colleagues conducted their study to determine whether the FAQ could be used to distinguish subjects with mild cognitive impairment from those with mild Alzheimers disease.

The researchers analyzed FAQ responses for 65 normal control subjects, 42 with mild cognitive impairment, and 22 with mild Alzheimer's disease. They further categorized patients with mild cognitive impairment as those with memory deficits in a single domain, in multiple domains, or not having memory deficits, and subdivided mild Alzheimer's disease into possible and probable disease.

Total FAQ scores in mild cognitive impairment were similar across subtypes but significantly different from the control group and the mild Alzheimer's disease groups (P < .001 for each).

Dr. Teng indicated that the ability to manage transportation and travel outside of one's neighborhood most effectively discriminated between mild cognitive impairment and Alzheimer's disease. A cutoff of greater than 1 on this item yielded classification rates of 86% between all mild cognitive impairment and all Alzheimer's disease subjects. Further, on this score, there was a classification rate of 87% between those with mild cognitive impairment who had memory deficits across multiple domains and subjects with probable Alzheimer's disease.

The investigators concluded that a structured way to assess instrumental activities of daily living, such as the FAQ, could help physicians discern patients with mild cognitive impairment from those with mild Alzheimer's disease.

[Presentation title: Instrumental Activities of Daily Living in Mild Cognitive Impairment and Mild Alzheimers Disease. Abstract S-20]



Public release date: 27-Oct-2006
Contact: James Moyer, Jr.
jrmoyer@uwm.edu
414-229-3255
University of Wisconsin - Milwaukee

1340.UWM brain research supports drug development from jellyfish protein
Testing of aequorin yields promising results
With the research support from the University of Wisconsin-Milwaukee, a Wisconsin biotech company has found that a compound from a protein found in jellyfish is neuro-protective and may be effective in treating neurodegenerative diseases.

Testing of aequorin has yielded promising results, said Mark Y. Underwood of Quincy Bioscience located in Madison. Researcher James Moyer, Jr., an assistant professor at UW-Milwaukee, subjected brain cells to the "lab" equivalent of a stroke, and more than half treated with aequorin survived without residual toxicity.

Why does it work? Diseases like Alzheimer's are associated with a loss of "calcium-binding" proteins that protect nerve cells, said Moyer. Calcium is necessary for communication between neurons in the brain, and learning and memory are not possible without it. But too much of it leads to neuron death, interfering with memory and contributing to neurodegenerative diseases.

"There are ways in which cells control the influx of calcium, such as sequestering it by binding it with certain proteins," said Moyer. "If it weren't for these proteins, the high level of calcium would overwhelm the neuron and trigger a cascade of events ultimately leading to cell death."

Calcium-binding proteins decline with age, however, limiting the brain's ability to control or handle the amount of calcium "allowed in."

Aequorin, the jellyfish protein, appears to be a viable substitute.

Moyer, like Underwood, is interested in the "calcium hypothesis of aging and dementia," which is just one of many theories that attempts to explain what is going on in neuron degeneration.

He became interested in aequorin as an undergraduate at UW-Milwaukee, after reading an article that linked the stings of jellyfish with the symptoms of multiple sclerosis, a disease of the central nervous system that his mother has.

Aequorin was discovered in the 1960s and has been used in research for a long time as an indicator of calcium. But the protein has never been tried as a treatment to control calcium levels. Underwood believes his company is at about the 12-year mark in the typical 15-year cycle for a new drug to be developed.

Moyer's research centers on brain changes that occur as a result of aging. Specifically, he is interested in the part of the brain called the hippocampus, which is responsible for forming new memories. These capabilities not only deteriorate in neurodegenerative disorders such as Alzheimer's disease, but they also become impaired simply by aging.

Aging increases the number of "doors" that allow calcium ions to enter the cells, he said.

Moyer, who came to UW-Milwaukee from a post-doctoral position at Yale University, performs Pavlovian trace conditioning experiments to evaluate aging-related learning and memory deficits. These tasks first teach rodents to associate one stimulus with another and then test their memory of the association. During training, the stimuli are separated by a brief period of time, which requires the animal to maintain a memory of the first stimulus. The "stimulus free" period makes the task more difficult, especially for older animals.

Moyer's work also has implications outside of disease. He is able to show that at middle age, when the animal's learning ability or memory is not yet impaired, it already shows a drop in the number of neurons that contain an important calcium-binding protein.

"That cellular changes precede memory deficits indicates there is a window of opportunity for intervention before it's too late," he says. "Once the cells are lost, there is little chance of regaining normal brain function."


1341.Hope Remains For Alzheimer's Sufferers
Main Category: Alzheimer's / Dementia News
Article Date: 28 Oct 2006 - 2:00am (PDT)
http://www.medicalnewstoday.com/
The National Institute of Clinical Excellence (NICE), who last week rejected appeals to allow patients with mild Alzheimer's to receive the life-changing medication donepezil (Aricept?), will hopefully re-appraise their decision in 3 years time, according to neurologist Professor Robert Kerwin in an article published in the November issue of the medical journal Future Neurology.

Kerwin evaluated recent research published in the Lancet that may not have been taken into account by the NICE committee. In this study, nursing home patients with severe Alzheimer's disease were administered with donepezil, or a placebo drug, and were observed for 6 months. Those patients receiving donepezil treatment showed significantly improved cognitive function, compared with those patients not receiving the drug, despite recommendations by NICE not to prescribe donepezil to this patient group. Kerwin also evaluates recent data suggesting that the drugs are effective in patients with milder forms of Alzheimer's disease.

The recent 2005 NICE revised guidelines for cholinesterase inhibitors, the class of drug that donepezil and other Alzheimer drugs rivastigmine (Exelon?/Prometax?) and galantamine (Reminyl?) belong to, state that these drugs can only be administered to patients with moderate Alzheimer's, for whom NICE believe the evidence is strongest. At the same time NICE withdrew its recommendations for the use of these drugs for patients with mild-to-moderate Alzheimer's. Memantime (Exiba?), belonging to another class of drugs, is not recommended to Alzheimer's sufferers, but is restricted to ongoing clinical trials and may be possible treatment in the future.

"NICE's decisions are based upon the economic health calculations that they do, which are balanced against clinical benefit. Even though the drugs do work in the long-term, patients do progress to requirements of alternative care that do not necessarily lead to savings within the NHS." Commented Kerwin, who is a Professor of Clinical Neuropharmacology at the Institute of Psychiatry, London.

750,000 people are estimated to suffer from Alzheimer's disease in the UK alone, with 78,000 of these receiving rivastigmine, galantamine and memantine; a further 2-thirds of sufferers take donepezil. Since NICE's original 2001 guidelines that this family of drugs should be made broadly available within the UK NHS for mild-to-moderate Alzheimer's disease, prescriptions have risen sharply and many sufferers have experienced a welcome relief from the debilitating symptoms of memory loss and cognitive decline.

In 2005, NICE reviewed their previous decision based on the cost-effectiveness and clinical benefit of such drugs in mild- and severe-Alzheimer's sufferers, and ruled that the drugs should be limited only to patients with moderate forms of the disease. This is only applicable to newly diagnosed patients. Despite uproar from patient groups appealing this decision, NICE stuck by their guidelines and last week issued a statement over-ruling the appeal.

"It is a bizarre decision," continued Kerwin, "the economists in the appraisal may well have had sway over the clinicians in the appraisal, and the clinicians may, on the other hand, have said that the drugs do help mild patients to quite a significant degree. I personally think NICE would have made a mistake over this decision if it is dominated by health economists rather than clinicians, however I have no knowledge of the final deliberations of the NICE committee."

Kerwin, who once sat on the NICE committee appraising these drugs, points out that they would only have analysed current data in their review and that more recent data, published in the gap between the final draft of the appraisal and the appeal, would possibly not have been taken into account. NICE would only have evaluated their process and the methods used to reach such a decision.

"These drugs work in ways that are not predictable for severe Alzheimer's disease patients, which suggests there is an added mechanism. Mild patients will always do better, everybody knows that, but the economic sums don't quite fully add up in terms of cost. I believe that progression, when measured economically rather than clinically, may not be very impressive."

Despite the recent uproar, Kerwin remains hopeful that with new data, such as those analysed in his article on severe Alzheimer's disease patients, NICE could potentially reverse their decision due to their working principal of 'positive review' on a 3-yearly cycle.

###

Future Neurology is published by Future Medicine an imprint of the Future Science Group.

ABOUT FUTURE SCIENCE GROUP

Future Science Group Ltd, based in London has developed an innovative publishing portfolio to reflect post-genomic medicine. The sequencing of the human genome was a colossal milestone in the evolution of healthcare, with repercussions for all those involved in the healthcare chain. Through its imprints, Future Medicine and Future Drugs, Future Science Group Ltd provides healthcare practitioners and research professionals with a unique source of objective, cutting- edge information on exciting trends emerging in the light of these advances. Our flagship title Pharmacogenomics has evolved to become a leading source of commentary and analysis from international opinion leaders. Momentum toward an individualized approach to medicine is increasing as the value of linking diagnostic and therapeutic approaches becomes ever clearer.

For more information please go to:
http://www.future-drugs.com
and http://www.futuremedicine.com


1342.Into the fog: Alzheimer's numbers rising dramatically

Andrew Duffy, CanWest News Service
Published: Saturday, October 28, 2006
http://www.canada.com/saskatoonstarphoenix/index.html
OTTAWA -- On most days you'll fi nd Gerry McKee treading across the wide, polished floors of Ottawa's Bayshore Shopping Mall in the peaceful hour before the stores open.

His wife, Joan, is always beside him for what has become their morning ritual: a few laps around the mall with other members of the Bayshore walking club.

Married for 52 years, the McKees are closer than ever now. It's a state of affairs that refl ects both the strength of their relationship and the scourge that is Alzheimer's disease.

McKee, 73, has for five years lived with the brain disease that slowly corrodes an individual's mental, physical and social condition. In that time, he has grown progressively more dependent on his wife.

"My wife is a very strong person," McKee says, smiling. "She runs things now. I have nothing to do with anything." The disease affects everyone differently; McKee has experienced a slow onset. Still, his wife now manages their household, keeping close tabs on his medication and his whereabouts.

McKee can drive, but he has lost much of the internal map that once allowed him to effortlessly navigate the city. He can remember where he was the day Pearl Harbour was bombed -- sitting in a grade-school classroom in Montreal -- but he has trouble with the details of the day before yesterday.

He keeps a calendar on the kitchen table with everything he has to do and checks it two or three times a day.

"I've learned to write things down, which is how keep my memory," says McKee. "I can't contain it in my head the way I used to." McKee's journey into what British writer John Bayley called an "insidious fog" is one that more than a million Canadians will follow in the coming decades.

Canada faces a rising tide of Alzheimer's disease.

About 420,000 Canadians older than 65 now suffer from Alzheimer's or a related dementia. With the baby boomers poised to cascade into their retirement years, those numbers are projected to swell dramatically.

Canada's postwar baby boom produced 10 million children between 1947 and 1966. People at the front end of that human wave are about to enter their 60s.

Based on Statistics Canada projections, the number of seniors will rise from 4.3 million today to 5.8 million in 2016, 6.8 million in 2021 and eight million in 2026. (The fi gures assume a modest growth in life expectancy and a steady fl ow of immigrants.) By 2031, one of every four Canadians will be older than 65. The country will then have to manage the health problems of 9.3 million seniors.

Chief among those challenges will be Alzheimer's, a slow-moving, progressive disease that first attacks memory and then harms other brain functions.

Eventually, the disease robs its victims of their personality and independence.

Alzheimer's accounts for about 60 per cent of all dementias, a term used to describe the condition that results from Parkinson's, dementia of the Lewy body type, Pick's disease and other brain disorders.

About eight per cent of people over 65 suffer from some kind of dementia, according to a large Canadian study. If that rate remains steady, 744,000 Canadians will be living with Alzheimer's or a related dementia by 2031.

Those numbers raise some fundamental questions.

Will there be enough long-term care beds available for all those with dementia? Will there be enough doctors and nurses to care for them? Will Canada be able to afford that care? "There's a huge wave coming behind us and we need to get ready," said Scott Dudgeon, the 55-yearold director of the Alzheimer Society of Canada.

Alzheimer's has been the subject of concern for a century, ever since Dr. Alois Alzheimer told a German audience on Nov. 4, 1906, about the "peculiar disease of the cerebral cortex" that he had encountered in a patient who had gradually lost the ability to reason and to speak.

Today, the challenges posed by the disease have never been greater.

Dementia is the world's leading cause of disability among the elderly. Surveys show it is also the principal reason for nursing home admissions.

The risk of developing dementia doubles every fi ve years after the age of 65. As the journal Neurology Now recently noted: "Paradoxically, since age is the biggest risk factor for Alzheimer's, the very medical breakthroughs that doubled life spans over the past century have created a demographic time bomb." In Canada, plans to mitigate the suffering and expense wrought by Alzheimer's remain in their infancy.

The Advisory Council on Aging issued a report in October 2004 warning that "the challenges posed by dementia to individuals, communities and Canada's health and social care systems will be enormous." It urgently called for a strategy -- something that advocates continue to demand today.

"The current challenges related to Alzheimer's disease are serious," the council concluded, "but the real ones are ahead of us." Among the key challenges to come: - Housing. About half of all people with Alzheimer's disease live in nursing homes or other long-term care facilities. Yet many of the facilities are ill-suited to the needs of Alzheimer's patients and there are long waiting lists at the specialized units that are available.

- Affordability. The cost of caring for Alzheimer's patients promises to challenge families and governments.

For pensioned caregivers, the cost of respite care or qualified sitters can be difficult to manage. A bed in long-term care costs between $18,100 and $24,700 a year, but subsidies are available.

- Caring for caregivers. Surveys show most (75 per cent) of those who look after Alzheimer's patients at home are women; about one-third of them are employed. Many suffer their own health problems because of the physical demands and emotional stress of caring for a loved one with Alzheimer's.

- Health care staff. A study published last month in the Journal of the American Geriatrics Society estimated that Canada has fewer than 200 doctors who specialize in geriatric medicine. There is a demonstrated need, the University of Western Ontario study said, for three times that many geriatricians in Canada.

- Aggressive dementia patients. A Toronto inquest last year examined the deaths of two elderly residents at the hands of a confused dementia patient.

The inquest heard that 11 long-term care residents in Ontario were killed between 1999 and 2004 by fellow residents.

Assault cases in nursing homes rose precipitously during the same period.

That rise in violence, the inquest heard, was the product of more dementia patients entering nursing homes illprepared for the challenge.

- Research. A century after its imprint on the brain was first identified, Alzheimer's remains a mystery. Scientists have yet to discover precisely what triggers the disease, or how to halt its slow and steady progress.

Existing drugs have been shown to produce only modest, short-lived benefits for patients.

The federal government has, over the last five years, doubled the money it spends annually on Alzheimer's research to $18.7 million.

But many consider that woefully inadequate.

Dr. Peter St. George-Hyslop, a University of Toronto neurologist and molecular geneticist, said Alzheimer's research is in a similar position to cancer research two or three decades ago.

"The government is just beginning to recognize the problem, but its commitment to Alzheimer's is still nowhere near that of cancer." Alzheimer's is an imposing public@health challenge.

It usually begins with short-term memory loss. Once-simple activities -- driving, shopping, dressing and bathing -- become diffi cult, then impossible, to manage alone. An individual's sense of judgment and reasoning are corroded.

An estimated 60 per cent of people with Alzheimer's will take to wandering.

Some will get up in the middle of the night and leave their house or set out to fi nd people from their past.

Odd behaviour is common. People with Alzheimer's will often repeat the same question or make the same gesture over and over. They might fi dget, pace, shout or swear. They can hide keys and food, trail after their caregiver like toddlers, take their clothes off in public.

Other psychological problems, such as depression, aggression and hallucinations, can emerge.

Those with late-stage Alzheimer's are often unable to recognize spouses, family and friends. Many lose the ability to speak. They may become physically frail, confi ned to a bed or wheelchair.

They can have difficulty eating. Many lose bladder control.

The experience of Alzheimer's is different for each individual. For some, the disease will progress slowly over the course of a decade or more; others will deteriorate rapidly and die within two or three years.

Women tend to live with the disease for longer than men. In one U.S. study, which followed 521 Alzheimer's patients, women with the brain disease survived an average of six years after diagnosis; men survived an average of four years.

Alzheimer's is a costly disease to manage.

A study published by the Canadian Medical Association Journal in 1999 found that it cost an average of $38,257 a year to care for someone with advanced Alzheimer's in a nursing home.

Researchers now estimate the net economic cost of Alzheimer's tops $5.5 billion in Canada.

Some policy makers continue to peg their hopes on a treatment breakthrough, despite disappointing results so far.

In April, St. George-Hyslop and his colleague, Dr. Paul Fraser, published an article in the journal Nature announcing the discovery of a protein that inhibits the formation of the amyloid plaque that gums up the brains of those with Alzheimer's.

If the naturally occurring protein can be harnessed by drugmakers, it may be able to block the accumulation of plaque in the brain without harmful side-effects.

But many questions remain unanswered.

Researchers, for instance, don't know whether forestalling plaque formation will also halt the other major cause of Alzheimer's: the tangles that occur inside cells on which the plaque has formed. Or whether damage can ever be reversed.

aduffythecitizen.canwest.com - - - Warning signs Alzheimer's disease is a progressive, degenerative disease. Symptoms include loss of memory, diffi culty with day-to-day tasks, and changes in mood and behaviour. People may think these symptoms are part of normal aging, but they aren't. It is important to see a doctor when you notice any of these symptoms, as they may be due to other conditions such as depression, drug interactions or an infection.

If the diagnosis is Alzheimer's disease, your area Alzheimer Society can help.

Here are some warning signs to look for: - Memory loss that affects day-to-day function: It's normal to occasionally forget appointments, colleagues' names or a friend's phone number, and remember them later. A person with Alzheimer's disease may forget things more often and not remember them later, especially things that have happened more recently.

- Difficulty performing familiar tasks: Busy people can be so distracted from time to time that they may leave the carrots on the stove and only remember to serve them at the end of a meal. A person with Alzheimer's disease may have trouble with tasks that have been familiar to them all their lives, such as preparing a meal.

- Problems with language: Everyone has trouble finding the right word sometimes, but a person with Alzheimer's disease may forget simple words or substitute words, making her sentences diffi cult to understand.

- Disorientation of time and place: It's normal to forget the day of the week or your destination -- for a moment. But a person with Alzheimer's disease can become lost on their own street, not knowing how they got there or how to get home.

- Poor or decreased judgment: People may sometimes put off going to a doctor if they have an infection, but eventually seek medical attention. A person with Alzheimer's disease may have decreased judgment, for example not recognizing a medical problem that needs attention or wearing heavy clothing on a hot day.

- Problems with abstract thinking: From time to time, people may have difficulty with tasks that require abstract thinking, such as balancing a chequebook. Someone with Alzheimer's disease may have significant difficulties with such tasks, for example not recognizing what the numbers in the chequebook mean.

- Misplacing things: Anyone can temporarily misplace a wallet or keys.

A person with Alzheimer's disease may put things in inappropriate places: an iron in the freezer or a wristwatch in the sugar bowl.

- Changes in mood and behaviour: Everyone becomes sad or moody from time to time. Someone with Alzheimer's disease can exhibit varied mood swings -- from calm to tears to anger -- for no apparent reason.

- Changes in personality: People's personalities can change somewhat with age. But a person with Alzheimer's disease can become confused, suspicious or withdrawn.

Changes may also include apathy, fearfulness or acting out of character.

- Loss of initiative: It's normal to tire of housework, business activities or social obligations, but most people regain their initiative. A person with Alzheimer's disease may become very passive, and require cues and prompting to become involved.

Source: Alzheimer Society of Canada

? The StarPhoenix (Saskatoon) 2006


1343.Test will diagnose Alzheimer's before onset of symptoms
Mon 30 Oct 2006@http://news.scotsman.com/@
SCIENTISTS are a step closer to finding a blood test for Alzheimer's disease to diagnose people before they show symptoms.

In what has been hailed as a breakthrough in the fight against the debilitating disease, researchers found that levels of two types of protein found in the blood can indicate an increased risk of having the disease. Tests found that an increased level of these proteins was present only with patients suffering from the condition.

The discovery could prove important in the search to develop a blood test to diagnose the likelihood of developing the disease in later life.

Alzheimer's disease is a degenerative type of dementia that usually strikes in old age. The disease can severely effect the short and long-term memory of sufferers.

The study, based at the Institute of Psychiatry, King's College London, is due to be published today in the journal Brain. It compared protein levels in the blood of Alzheimer's sufferers and healthy older people. A cutting-edge process used by the team called proteomics found that the Alzheimer's patients tested had greater levels of certain proteins in their blood than the other people tested.

Professor Simon Lovestone, from the Institute of Psychiatry, who lead the project, said the results were encouraging.


1344.Naturally Occurring Enzyme Can Break Down Key Part Of Alzheimer's Plaques
30 Oct 2006@http://www.medilexicon.com/

Scientists have identified a naturally occurring enzyme that can break down a key component of the brain plaques characteristic of Alzheimer's disease. The finding may provide researchers with new opportunities to understand what goes wrong in the brains of Alzheimer's patients and could one day help them seek new therapies.

Researchers at Washington University School of Medicine in St. Louis showed earlier this summer that the enzyme, matrix metalloproteinase 9 (MMP-9), degrades abnormally aggregated proteins known as amyloid fibrils, a main ingredient of brain plaques. In the brain, MMP-9 is made by support cells known as astrocytes.

MMP-9 is already well-known because of its links to cancer metastases, vascular disease, arthritis and other pathologies. Scientists called the new link to Alzheimer's encouraging, noting that previously identified enzymes only degrade a smaller, nonaggregated component of Alzheimer's plaques.

"We already knew of three enzymes that break down amyloid beta (Abeta), a protein fragment that clumps together with itself to form the fibrils," says Jin-Moo Lee, M.D., Ph.D., assistant professor of neurology. "But the thinking up until now had been that Abeta might be clumping together so tightly that the fibrils were indestructible."

In a new study, appearing October 25 in The Journal of Neuroscience, Lee's group found that disabling the mouse gene for MMP-9 increased levels of Abeta in the spaces between brain cells. The finding proves that MMP-9 contributes to clearance of Abeta from extracellular spaces and suggests its dysfunction could potentially contribute to the development of Alzheimer's.

"MMP-9 and other enzymes like it are secreted from brain support cells and active in the spaces outside of cells, and that's where we saw an increase in Abeta levels in the mice that lacked the gene for MMP-9," Lee notes. "That's relevant to Alzheimer's because all the amyloid plaques are extracellular, and the formation of the plaques seems to be related to an elevated level of Abeta that accumulates over time in those spaces."

In earlier studies, Lee's lab analyzed the production of MMP-9 in astrocytes. They found astrocytes close to amyloid plaques increased their MMP-9 production. Imaging studies also showed that MMP-9 levels increased around blood vessels laden with amyloid.


"Astrocytes become activated around plaques as they develop, and then eventually form a wall surrounding the plaques," he says.

Lee's results have led him to formulate a provocative but as yet unproven theory about an old mystery of Alzheimer's disease: why plaques continue to increase in number over time but only grow to a certain size.

"Even though everything we know about the fibrils suggests they should constantly grow, plaques reach a mature size and stop growing," Lee says. "It's possible that production of MMP-9 and other similar substances by support cells in the brain is establishing a balance that prevents the plaques from growing beyond a certain size."

To follow up, Lee plans to crossbreed mice lacking MMP-9 with a line of mice genetically modified to develop an Alzheimer's-like condition. Scientists want to see if removing MMP-9 causes the mice to develop Alzheimer's more quickly. In a parallel project that will test MMP-9's potential as a therapeutic, Lee and his collaborators will use viruses to alter production of MMP-9 in the mouse model. Researchers want to learn if increasing levels of the enzyme present in the brain can delay onset of Alzheimer's.

Yin K-J, Cirrito JR, Yan P, Hu X, Xiao Q, Pan X, Bateman R, Song H, Hsu F-F, Turk J, Xu J, Hsu CY, Mills JC, Holtzman DM, Lee J-M. Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolism. The Journal of Neuroscience, Oct. 25, 2006.

Yan P, Hu X, Song H, Yin K, Bateman RJ, Cirrito JR, Xiao Q, Hsu F-F, Turk JW, Xu J, Hsu CY, Holtzman DM, Lee JM. Matrix metalloproteinase-9 degrades amyloid-beta fibrils in vitro and compact plaques in situ. The Journal of Biological Chemistry, June 20, 2006.

Funding from the National Institutes of Health, the National Institute of Neurological Disorders and Stroke and the American Health Assistance Foundation supported this research.

Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked fourth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.

Washington University in St. Louis
One Brookings Dr., Campus Box 1070
St. Louis, MO 63130
United States
http://wustl.edu


1345.Battle against Alzheimer's also a battle against time
By Cheryl Clark Monday, October 30 2006, 12:47 AM
http://www.paramuspost.com/
UNRAVELING ALZHEIMERfS

When neuroscientist Leon Thal first became interested in the puzzles of Alzheimer's disease 30 years ago, he didn't realize how tough they would be to solve.

After testing more than 100 drugs in thousands of patients, Thal and other researchers haven't found a way to stop the devastating loss of memory and function that afflicts 4.5 million Americans.

Only about four drugs seem to provide limited benefit, and they merely delay symptoms - not the disease process - by a few months to a year.

"This has turned out to be a much more difficult disease than anybody imagined," said Thal, whose $150 million, 15-year federal project to study Alzheimer's received an additional $52 million recently from the National Institute on Aging.

The money will be distributed through the University of California San Diego's Alzheimer's Disease Cooperative Study. It will fund a six-year research effort involving four studies with 70 test centers in the United States and Canada.

The battle against Alzheimer's is also a battle against time. As tens of millions of baby boomers age and life expectancy continues to grow, many more Americans will become Alzheimer's patients. More than half the population older than 85 has Alzheimer's, according to the institute.

For starters, Thal said, "we still haven't proved the cause of Alzheimer's."

The most prominent theory is that beta amyloid proteins promote plaque buildup in the brain and that a possibly related process disrupts "tau" proteins, resulting in a tangled maze of fibrous clumps.

One way to confirm that beta amyloid causes the disease is to prevent amyloid from forming and then see if a patient's memory improves, said Thal, who directs the university's Shiley-Marcos Alzheimer's Disease Research Center in San Diego.

Unlike people suffering other types of dementia, all Alzheimer's patients have short-term memory loss even to the point of forgetting events from moments ago. Also, Alzheimer's patients can't seem to plan or identify sequences of events.

Part of the difficulty is that Alzheimer's is only definitively diagnosed after death, when an autopsy reveals those amyloid plaques and tangles made of tau proteins.

Three of Thal's four new studies involve omega-3 fatty acid found in fish, intravenous immunoglobulin and lithium. Investigators will see whether these compounds can disintegrate beta amyloid or tau tangles.

The fourth effort will test whether Alzheimer's patients can answer questions about their well-being from their homes by phone, e-mail or computer.

If the experiment goes well, it might allow researchers to create more home-based Alzheimer's studies. Such an arrangement might allow recruitment of more patients for whom participation would otherwise be too time consuming, confusing and difficult.

Alzheimer's research has been slow, Thal acknowledged. He copes with its setbacks by weeding in the garden of his home and flying his single-engine prop plane out of San Diego County, once to Scotland by way of Iceland.

After decades of trials, Thal said, there is still no good animal model to test promising drugs. Second, it took many years to establish a way to categorize stages of Alzheimer's progression, which is necessary to determine whether certain drugs are working.

Third, Thal said, "it takes an enormous amount of work to recruit patients for studies." Those with early stages of mild cognitive impairment and their families often don't want to acknowledge the disease.

Fourth, many older patients take other medications, which excludes them from Alzheimer's research because of potential interactions with drugs under study.

Participants also must have a reliable support system of caregivers to help answer questions and provide transportation for study for several years, Thal said. That's why each test center will recruit just a few patients for the new project. For example, UCSD will have only 30 for the three upcoming drug trials.

"It has been frustrating," said Dr. Neil Buckholtz, head of the Dementias and Aging Branch of the National Institute on Aging. He enumerated many compounds for which high hopes turned to disappointment, such as estrogen and some anti-inflammatory drugs.

This month will mark the 100th anniversary of German neuropathologist Alois Alzheimer first describing Alzheimer's. But "only since the 1980s has there been any real focus" on research for the disease, Buckholtz said.

During the years, he and Thal recalled, there have been dozens of theories about the causes of Alzheimer's, some particularly bizarre. They include use of aluminum pots, pans and hair dye or exposure to petroleum, plastics and metals such as copper and zinc.

"You name it," Thal said.

But no connection has been found, nor has any association been made between Alzheimer's and any occupation or pastime. Geographic concentrations have not been identified either.

Some strong Alzheimer's risk factors are emerging. One is that people who are obese and have diabetes - a growing percentage of the U.S. population - are more likely to develop the disease.

Many theories circulate on how to prevent or delay symptoms. Daily exercise, large amounts of caffeine and maintaining intellectual pursuits are a few that are unproved.

On a positive front, researchers are excited about a few developments, Thal said. He is most energized by a new positron emission tomography imaging technique that can see plaque buildup in brains of living patients through the use of a special isotope "tag."

"It's pretty exciting," said Thal, who plans to use the imaging technique in some San Diego patients.

He is also hopeful about several compounds that may eviscerate amyloid and help patients get better or at least not get worse.

"If amyloid is actually toxic and you remove it, would cells that are marginally functional begin to recover?" asked Thal, who also is a staff physician at the San Diego Veterans Administration Medical Center. "If we could delay the onset of this disease by five to 10 years, that would be sufficiently satisfying."


1346.Nanogen Awarded Additional Patents for Diabetes, Alzheimer's Disease Biomarkers
Companies mentioned in this article:
Nanogen

10/30/2006 @ 7:36 AM http://www.freshnews.com/index.shtml

Nanogen, Inc. (NASDAQ:NGEN) , developer of advanced diagnostic products, announced today that it has been issued four patents by the U.S. Patent and Trademark Office for inventions related to diabetes and Alzheimer's disease biomarkers. The current patents are the most recent in a series describing biomarkers associated with these diseases.

U. S. Patent No. 7,125, 678, "Protein biopolymer markers predictive of type II diabetes," U.S. Patent No. 7, 097,989, "Complement C3 precursor biomarker predictive of type II diabetes," and U.S. Patent No. 7,094,549, "Fibronectin biopolymer marker indicative of insulin resistance," relate to the use of mass spectrometry and time-of-flight detection to identify biopolymers that characterize type II diabetes. These markers could potentially be used in applications of disease risk assessment and development of therapeutic avenues.

In addition, U.S. Patent No. 7,101,680 "Method for detecting the presence of monomeric brain associated human glutamine synthetase," relates to a method for detecting a biochemical marker, human glutamine synthetase, by immunoassay as a potential diagnostic for Alzheimer's disease. In addition, a method for distinguishing between AD and non-AD dementia is disclosed.

For information about licensing opportunities, contact Nanogen.

About Nanogen, Inc.

Nanogen's advanced technologies provide researchers, clinicians and physicians worldwide with improved methods and tools to predict, diagnose, and ultimately help treat disease. The company's products include real-time PCR reagents, the NanoChip electronic microarray platform and a line of rapid diagnostic tests. Nanogen's ten years of pioneering research involving nanotechnology holds the promise of miniaturization and continues to be supported for its potential for diagnostic and biodefense applications. For additional information please visit Nanogen's website at www.nanogen.com.


1347.Alzheimer's - from curiosity to worldwide disease By Joern Bender

dpa German Press Agency
Published: Monday October 30, 2006 http://www.rawstory.com/

By Joern Bender, Frankfurt/Tuebingen- On 3 November 1906 the psychiatrist Alois Alzheimer presented a paper entitled "Regarding a curious disease of the cortex." Alzheimer's colleagues did not immediately recognize the importance of his discovery. One century later, the name of Alois Alzheimer (1864-1915) is known across the globe.

In Germany alone, a country of 82 million people, between 700,000 to one million patients suffer from the brain disease named after the scientist. Worldwide over 20 million are said to have the disease.

A four-day conference starting in Tuebingen on November 2 intends to illuminate history and future of Alzheimer's research.

"When Alzheimer first announced his discovery, he only saw the final stage and had no idea about the dynamics of the illness. This has only been discovered afterwards," the host of the Alzheimer conference, Professor Mathias Jucker says.

To date, no cure has been found for the disease. "Even if we could find a way to stop Alzheimer from developing, and it would no longer pose a problem for society, the ageing brain remains a risk factor for a range of diseases," says the neurobiologist, who works at the Hertie Institute for Clinical Brain Research in Tuebingen.

"Not everyone gets Alzheimer, and it is not a normal consequence of ageing," Jucker insists in view of an increase of cases.

Alois Alzheimer's first patient with the diagnose, Auguste Deter, was only 51 years old when she was brought to the Frankfurt "Institution for lunatics and epileptics."

The woman said she had "lost herself." Alzheimer was puzzled by her memory loss. Up to this point the patient had been healthy, did not have a history of psychological troubles and had not experienced anything traumatic.

Alzheimer meticulously documented Auguste's memory loss on 31 handwritten pages. His notes include conversations held with "Auguste D."

"What is your name?" "Auguste." - "Surname?" "Auguste." "What is your husband's name?" "Auguste, I believe."

After the patient's death on April 8, 1906 at "1/4 to 6 in the morning," Alzheimer had Auguste Deter's brain sent to his lab. He discovered massive neuronal malfunction and deposits.

Half a year later, the physician from Tuebingen held a presentation at the "congregation of south west German alienists," where he declared "My case Auguste D. is deviant from all known disease patterns."

Since, scientist have understood that the disease is caused by a gradual degeneration of the neurones and usually sets on after the age of 65.

Many patients no longer recognise family members and friends, have orientation problems and struggle with speech.

"The presentation in Tuebingen did not necessarily get the hoped for attention," writes Alzheimer biographer Konrad Maurer.

100 years later, the situation has reversed. In view of an ageing society, Alzheimer's disease is regarded as the "widespread disease of the future."

The German Alzheimer Association expects that the number of Alzheimer patients in Germany will exceed two million by the year 2040.

Thomas Kunczik, manager of "Hirnliga," a German association of Alzheimer's researchers, hopes that the anniversary will boost prevention and therapy of brain diseases.

But Kunciyik is sceptical. "Alzheimer is still a frightening disease that many people prefer not to think about."

(c) 2006 dpa German Press Agency


Source: Saint Louis University Medical Center Released: Mon 30-Oct-2006, 15:50 ET
Embargo expired: Wed 01-Nov-2006, 00:00 ET Printer-friendly Version
1348.New Dementia Screening Tool Is More Sensitive
Libraries
Medical News Keywords
AGING COGNITIVE IMPAIRMENT ALZHEIMER'S DISEASE
Contact Information

Available for logged-in reporters only
Description

New research shows a screening tool developed by Saint Louis University geriatricians is more sensitive at detecting mild cognitive impairment than a commonly used clinical instrument.

Newswise ? A screening tool for dementia developed by Saint Louis University geriatricians appears to work better in identifying mild cognitive problems in the elderly than the commonly used Mini Mental Status Examination, according to a new study.

Physicians routinely administer the Mini Mental Status Examination (MMSE) to patients who they believe may have Alzheimerfs disease. Both the MMSE and SLUfs screening tool ? the Saint Louis University Mental Status Examination (SLUMS) ? indicate to doctors when they should pursue further testing in diagnosing dementia.

gThis early detection of mild neurocognitive disorder by the SLUMS offers the opportunity for the clinicians to begin early treatment as it becomes available,h says Syed Tariq, M.D., lead author and associate professor of geriatric medicine at Saint Louis University.

John Morley, M.D., director of the division of geriatric medicine at Saint Louis University, created the SLUMS to screen more educated patients and to detect early cognitive problems.

"There are potential treatments available and they slow down the progression of the disease," says Morley, who is a coinvestigator. "The earlier you treat, the better people seem to do. But families go through denial and sometimes miss diagnosing dementia until its symptoms are no longer mild."

The researchers found the new screening tool developed by SLU detects early cognitive problems missed by the MMSE.

gThe Mini Mental Status Examination has limitations, especially with regard to its use in more educated patients and as a screen for mild neurocognitive disorder,h Tariq says.

It takes a clinician about seven minutes to administer the SLUMS, which supplements the Mini Mental Status Examination by asking patients to perform tasks such as doing simple math computations, naming animals, recalling facts and drawing the hands on a clock.

Both screening tools work at detecting dementia, the research found.
gSLUMS has the advantage in that it can help the clinician identify patients with mild neurocognitive disorder on the initial visit compared to MMSE, which requires a follow up screening,h Tariq says.

Saint Louis University researchers used both screening tools to test 705 men who were at least 60 and treated at the Geriatric Research Education Clinical Center, Veterans Administration Hospitals in St. Louis in 2003. They found that while both tools detected dementia, only the SLUMS recognized a group of patients as having mild cognitive problems.

The SLUMS, which is free and currently used at many Veterans Administration hospitals, is available at this link
http://medschool.slu.edu/agingsuccessfully/pdfsurveys/slumsexam_05.pdf

The researchers cautioned that neither the SLUMS nor the MMSE screening tools substitute for clinical assessment and neuropsychological testing to diagnose cognitive problems and dementia.

The study appeared in the November issue of the American Journal of Geriatric Psychiatry.

Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first M.D. degree west of the Mississippi River. Saint Louis University School of Medicine is a pioneer in geriatric medicine, organ transplantation, chronic disease prevention, cardiovascular disease, neurosciences and vaccine research, among others. The School of Medicine trains physicians and biomedical scientists, conducts medical research, and provides health services on a local, national and international level.


1348.1Dementia before Death in Ageing Societies? The Promise of Prevention and the Reality

Carol Brayne1*, Lu Gao2, Michael Dewey3, Fiona E. Matthews2, Investigators Medical Research Council Cognitive Function and Ageing Study

October 31, 2006
http://medicine.plosjournals.org/

1 Department of Public Health and Primary Care, Institute of Public Health, Cambridge University, Cambridge, United Kingdom, 2 Medical Research Council Biostatistics Unit, Institute of Public Health, Cambridge, United Kingdom, 3 Institute of Psychiatry, King's College London, London, United Kingdom

Background

Dementia and severe cognitive impairment are very closely linked to ageing. The longer we live the more likely we are to suffer from these conditions. Given population increases in longevity it is important to understand not only risk and protective factors for dementia and severe cognitive impairment at given ages but also whether protection affects cumulative risk. This can be explored by examining the effect on cumulative risk by time of death of factors found consistently to reduce risk at particular ages, such as education and social status.

Methods and Findings

In this analysis we report the prevalence of dementia and severe cognitive impairment in the year before death in a large population sample. In the Medical Research Council Cognitive Function and Ageing Study (a 10-y population-based cohort study of individuals 65 and over in England and Wales), these prevalences have been estimated by age, sex, social class, and education. Differences have been explored using logistic regression. The overall prevalence of dementia at death was 30%. There was a strong increasing trend for dementia with age from 6% for those aged 65?69 y at time of death to 58% for those aged 95 y and above at time of death. Higher prevalences were seen for severe cognitive impairment, with similar patterns. People with higher education and social class had significantly reduced dementia and severe cognitive impairment before death, but the absolute difference was small (under 10%).

Conclusions

Reducing risk for dementia at a given age will lead to further extension of life, thus cumulative risk (even in populations at lower risk for given ages) remains high. Ageing of populations is likely to result in an increase in the number of people dying with dementia and severe cognitive impairment even in the presence of preventative programmes. Policy development and research for dementia must address the needs of individuals who will continue to experience these conditions before death.

Funding: The Medical Research Council Cognitive Function and Ageing Study is supported by the Medical Research Council, United Kingdom. All research has been undertaken independently of the funding bodies.

Competing Interests: The authors have declared that no competing interests exist.

Academic Editor: Willem Van Gool, University of Amsterdam, Netherlands

Citation: Brayne C, Gao L, Dewey M, Matthews FE, Investigators Medical Research Council Cognitive Function and Ageing Study (2006) Dementia before Death in Ageing Societies? The Promise of Prevention and the Reality. PLoS Med 3(10): e397 doi:10.1371/journal.pmed.0030397

Received: April 20, 2006; Accepted: July 26, 2006; Published: October 31, 2006

Copyright: ? 2006 Brayne et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abbreviations: CI, confidence interval; GMS, Geriatric Mental State; MMSE, Mini-Mental State Examination; MRC CFAS, Medical Research Council Cognitive Function and Ageing Study

* To whom correspondence should be addressed. E-mail: carol.brayne@medschl.cam.ac.uk

Editors' Summary
Background.
Severe cognitive impairment and its advanced form, dementia, are among the most difficult problems associated with aging in industrialized countries. Age-associated decline in mental functioning is also expected to become more common in developing countries as improvement of conditions that affect health leads to longer life expectancies. Although the risk of cognitive impairment is known to increase with age, the number of people who suffer from loss of mental abilities in the last years of their lives has not been well studied, as such persons are usually reported to have died from other causes. Further, because the very elderly are seldom included in prevention studies, it is not known whether factors found to reduce the risk of developing dementia by a given age will provide protection until the end of life.

Why Was This Study Done?
This study was designed to follow a representative population of aged people over several years to estimate the risk of developing cognitive impairment or dementia near the end of life and to determine whether factors such as education and social class, which may be protective earlier in life, can ultimately prevent decline in mental functioning.

What Did the Researchers Do and Find?
Using standardized assessments of cognitive status, the researchers interviewed people age 65 and over at six sites representing rural and urban areas in the United Kingdom. Interviews were conducted at regular intervals over ten years. Of approximately 12,000 study participants who had died by the time of this report, just over 2,500 had an assessment for dementia within one year before dying. Of this group, those who died between ages 65 and 69 had a 6% chance of dying with dementia, and those who died above age 95 had a 58% chance of dying with dementia. When moderate and severe cognitive impairment were considered together, the rate in people above age 95 reached almost 80%. Women were more likely to develop dementia than men, even after taking into account the fact that women tend to live longer than men. A higher level of education was associated with only a slightly lower risk of dementia before death.

What Do These Findings Mean?
According to these results, as the number of aged persons increases (with improved health care, preventive medicine, and healthier lifestyles), the chances of developing dementia in the last years of life will continue to increase. Factors believed to protect against dementia at earlier times may be of little effect at the end of life. Planning for aging societies must therefore include not only research into treatments and preventive efforts to reduce the impact of dementia at the end of life, but also realistic allocation of resources to support individuals and their caregivers who must deal with the difficulties of cognitive decline.

Additional Information.
Please access these Web sites via the online version of this summary at http://dx.doi.org/10.1371/journal.pmed.0030397.

Web site of the Medical Research Council Cognitive Function and Ageing Study
Web site of the Alzheimer's Association
Wikipedia entry on dementia (note: Wikipedia is a free Internet encyclopedia that anyone can edit)

Introduction
Changing global population structures require societies to face major issues raised by increasing numbers of the very old. Western societies have experienced sufficient change to be able to anticipate patterns of health and ill health in their ageing populations. These changes are likely to be echoed in a shorter time frame over the next decades in the less wealthy regions of the world because of their more rapid experience of demographic shift. This continuing change in life expectancy has been attributed to improved health and lower morbidity in early life, and to effective primary, secondary, and tertiary prevention in later life. Reductions in incidence have been seen in vascular disease, including cerebrovascular disease [1,2].

Increased life expectancy and improvement in many areas of health have been demonstrated, but sharp increases of morbidity with age are still observed in all populations [3]. Dementia and severe cognitive impairment are amongst the disorders with greatest increase with age in both incidence and prevalence [4,5]. Preventive action at the population level ideally eradicates risk of disease, but in reality much prevention reduces disease at a given age rather than eradicating its occurrence. The overall contribution of primary and secondary prevention to the reduction in cardiovascular disease mortality has been estimated at around half of the effect, with improved care for established disease resulting in the remaining improvement [6]. There is a global effort aimed at improving health in our older populations, and much of this effort hinges on the hope that extension of life expectancy will not be accompanied by increases in morbidity but by compression of morbidity [7].

Many of the factors that have been observed to be associated with reduced risk for chronic disease such as cancer and heart disease are also associated with lower mortality [8?10]. More recently such factors have also been studied in relation to Alzheimer disease and cerebrovascular disease and have been reported as associated with reduction in risk within the periods of follow-up [11]. These variables are often associated with social class and educational level, whose effects may be attributed to healthier lifestyles and health practices. Social class and education can be seen as proxies for these factors, and higher social class and more education have been shown in many studies to be associated with reduction in dementia outcomes [12,13].

At the same time as this attention to healthy ageing there is increasing attention to the end of life. Many people express a fear of dementia before death as well as a desire to remain independent up to the time of death rather than have prolonged periods of dependency. Quality of life in the period leading up to death is a relatively neglected area in the major emphases of most countries' health services, which tend, understandably, to focus on prevention and treatment. There is already clear evidence that individuals who have dementia and cognitive impairment have an excess mortality [14] and a shorter life expectancy [15] than individuals without. However, there is little information about the proportion of the population at any given age who die with dementia or severe cognitive impairment. Individuals at the end of life are likely to be underrepresented in studies of risk with infrequent follow-up as attrition is well known to be associated with cognitive decline and age [16]. Information on the dementia status of individuals from death certificates is inaccurate and cannot be used as a substitute [17]. More knowledge about the status of individuals in the period before and at death is important to assess the full implications of global population ageing and the potential for prevention of dementia and cognitive decline in the future. If we change risk in the population, can we expect to see different profiles in our very old population, including the period close to death? What is the association of dementia and cognitive decline with death (terminal decline), and how much can we estimate that we would avoid if all the preventive actions in place were able to effect a reduction in health inequalities? Longitudinal studies with sufficient follow-up and data on the mortality of all individuals are required to investigate dementia at death. Repeated interviews are necessary to correctly classify dementia at death. Notification of death for the whole cohort irrespective of continuing participation is also required.

The analysis presented in this paper investigates the prevalence of dementia and severe cognitive impairment in the period before death in the population-based Medical Research Council Cognitive Function and Ageing Study (MRC CFAS). It also investigates whether those who, on the basis of the literature to date, would be expected to have a relative advantage in risk for dementia at any given age are markedly less likely to die with dementia or severe cognitive impairment than those at greater risk.

Methods
Study Design and Population
MRC CFAS is a longitudinal population-based cohort study that involves six different study centres. The six centres were chosen because they represent the main national variation with regards to urban?rural differences, the north?south and east?west gradients, and variation in socio-economic levels and in known rates of chronic disease. All centres had existing researchers who were interested in population-based studies of the elderly. Urban sites included Liverpool, Newcastle, Nottingham, and Oxford. Rural sites included Cambridgeshire and Gwynedd, in North Wales. All centres have been used for this analysis.

The Liverpool study is described in full elsewhere [18]; a population stratified by 5-y bands over the age of 65 y was interviewed from 1989 onwards. Three full waves of follow-up (each 2 y apart) have been undertaken and used in the following analysis.

The full study design of the other five centres is described in detail elsewhere and is explained briefly here [4]. For these five centres, a total of 13,004 individuals aged 65 y and over were recruited, and interviewed at baseline (1990?1992) with a schedule including socio-demographic items, general health items, and cognitive items. Participants have been re-interviewed at various times, either the whole cohort or sub-samples stratified by centre, age, and cognitive state. Three types of interviews were used during the study. Baseline examination was conducted via a screening interview. A median of 3 mo after a screening interview, 20% of individuals had a diagnostic interview (assessment interview). The assessment interview consisted of a participant interview and an informant interview. The former consisted of the Geriatric Mental State (GMS), version B3, from which AGECAT [19] could be derived. The latter consisted of the History and Aetiology Schedule [20]. These are standardised psychiatrically based interviews to establish an algorithmic clinic diagnosis described below. Incidence screen and assessments and combined screen and assessment interviews were used during the follow-ups at 2 y, and combined screen and assessment interviews on all participants at 10 y. All interviews contained the Mini-Mental State Examination (MMSE). The Cambridge centre additionally interviewed the complete sample with a combined screen and assessment interview at 6 y. In Liverpool the whole population was interviewed with the full GMS AGECAT algorithm and the clinical version of the MMSE [21] on all these occasions. A study diagnosis of dementia and cognitive impairment can be derived from successful interviews.

All participants were flagged for mortality information. Death information was obtained from the Office of National Statistics up to the end of 2004. Version 8.0 of the five-centre identical data and version c4 for the Liverpool data have been used.

Definition of Dementia
The study diagnosis of dementia is based on the GMS AGECAT algorithm. This algorithm has been validated against clinicians and DSM-III-R [22]. In addition, for the analysis presented here, organicity level and memory defect rating at the last available interview before death were combined with ICD-10 diagnosis [23] (F00?F03, F29, F051, or G30) on the death certificate. Misclassification with organicity due to transient delirium is rare in the population studies [4].

Definition of Cognitive Impairment
MMSE scores were coded within each centre using identical methodology (ignoring backwards WORLD and coding gnot answeredh responses to incorrect). Some differences existed between the implementation of the questions (for example, apple, table, and penny in the five identical centres was any three items in Liverpool); however, examination of the distribution of the scores indicates that they have similar distributional properties at the lower end. The scores were grouped into severe cognitive impairment (MMSE < 18) or not, and moderate/severe cognitive impairment (MMSE < 22). Where the MMSE was missing at the last interview before death, a previous interview was used if cognitive impairment had already been demonstrated. In the analysis presenting cognitive impairment, the classification of dementia status on death certificates was ignored. Individuals with cognitive impairment were classified only from interview responses, and hence some individuals with dementia on death certificates were not classified as cognitively impaired.

Interview Waves
Only study waves where the complete population was interviewed were used in this analysis. Hence, information for Liverpool years 0, 2, and 4 and for the other five centres years 0, 2, 6 (Cambridge only), and 10 were used.

The dementia or cognitive impairment status required is the status at death for an individual, hence only those individuals whose last interview was within 1 y of their death were considered. A sensitivity analysis expanding this to deaths within 2 y has been undertaken, which is based on more deaths, but which underestimates the true amount of dementia/cognitive impairment.

Statistical Methods
Prevalence of dementia at death was calculated assuming binomial proportions with exact confidence intervals (CIs). Logistic regression analysis was used to investigate the relationships between confounders and prevalence of dementia at death. All analysis was undertaken using STATA version 8.0 (Stata Corporation, College Station, Texas, United States).

Results
Deaths
A total of 4,319 individuals from Liverpool (from an original sample 5,244) and 8,068 individuals from the other centres (from 13,004)?altogether 12,387 individuals?died by the time of this analysis. Of these, 12,286 deaths (99%) have information available from their death certificate. A total of 2,566 individuals who had a known dementia status at last interview died within 1 y of this interview, and 5,053 died within 2 y of this interview. A total of 2,555 individuals are included in the analysis of severe cognitive impairment, and 2,573 individuals in the analysis of moderate/severe cognitive impairment.

Dementia at Death
Table 1 shows a summary of dementia status at death classified by centre, sex, social class, education level, and age at death. Figure 1 shows a sustained increase in the proportion of individuals receiving a study diagnosis of dementia in the period before death with increased age at death (log). People who died between the ages of 65 and 69 y had a 6% risk of dying with dementia, but people who died above age 95 y had an over 58% risk of dying with dementia. There are wide confidence intervals around the estimate for the 31 individuals aged over 100 y at death, compatible with continued increase and stabilisation (42% demented, 95% CI 25%?61%).

Table 1.
Prevalence of Dementia at Death and Relationship to Potential Risk Factors for All Individuals Who Died within 1 y of Last Interview
Figure 1. Dementia or Cognitive Impairment by Age at Death with 95% CIs
There was a gender difference in risk, with women demonstrating an overall prevalence of dementia before death of 38%, almost double that of men. However, women have a longer life expectancy than men [24], and dementia prevalence increase with age [4]. Adjusting for age showed that women still had a higher absolute proportion of individuals with dementia than men (Table 1; Figure 2); however, there was no evidence that the effect of age differed in men and women (likelihood ratio test for interaction, ƒÔ2 = 7.6, p = 0.27). Dementia before death was less common in the non-manual-labour social classes than in the manual-labour group at all ages, but not after adjusting for other factors (p = 0.09) (Table 1; Figure 2). The absolute difference at death was 2%. A higher level of education was associated with slightly lower prevalence of dementia before death, even after adjusting for the other factors (p = 0.02) (Table 1; Figure 2). The individuals who had 10 y or more of full-time education had slightly lower dementia prevalence than individuals with less than 10 y of full-time education. The absolute difference between these educational levels was 6%. There was no evidence of any interaction between sex, education, and social class (likelihood ratio tests all had p > 0.2). An individual analysis investigated whether the age effect was partially explained by different patterns of dementia seen in different birth cohorts. There was no evidence that suggested there has been a change in the age and sex pattern by birth cohort after adjusting for all other covariates (likelihood ratio test, p > 0.2).

Figure 2. Rate of Dementia at Death by Sex, Education, and Social Class
Those participants who had an unknown social class and/or educational level (378, 15%) were more likely to have been demented at both baseline and follow-up (62% demented). A sensitivity analysis including these missing values as either the highest or lowest categories did not alter the findings.

Cognitive Impairment
The proportion of individuals with severe cognitive impairment before death was very similar to the proportion of individuals with dementia at death, with the same marked increase in cognitive impairment before death with age (Figure 1; Table 2). When individuals with moderate or severe cognitive impairment were included together, the rate was around 10% higher at all ages, with nearly 80% of individuals dying over 95 y of age having this level of cognitive impairment.

Table 2.
Prevalence of Moderate and Severe Cognitive Impairment at Death and the Relationship with Potential Risk Factors

The relationship between cognitive impairment and demographic risk factors was almost identical between the less and more inclusive levels of impairment and similar to the relationships with dementia at death, though the effects were all slightly stronger. The patterns were also similar if individuals with dementia were removed from the analysis (unpublished data). The absolute difference in severe cognitive impairment at death between social class groups was 5% and for educational levels was 7%. The absolute differences for moderate/severe cognitive impairment were 7% and 10%, respectively.

Centenarians
There were 31 centenarians in the study who died within 1 y of interview. Of these, 25 (81%) were female, 13 (42%) had dementia, and 13 (46%) had severe cognitive impairment (with three missing information).

Centre Effects
Although not the primary purpose of this analysis, centre was included as it may indicate unmeasured confounders. For dementia there were no differences between the centres once age and sex were accounted for. There were some small differences between centres for cognition before death, but no consistent pattern emerged.

Sensitivity Analysis
Including all individuals with an interview within 2 y of death did lower the proportions of individuals with dementia before death slightly (27% versus 30%). The proportion with dementia within 1 y of death (30%) was higher than that estimated for individuals seen between 1 and 2 y before death (23%; t-test for difference, p < 0.001), showing the proximity of much dementia to death. The findings in relation to age, sex, social class, and education were similar. Excluding individuals with limited information (such as screen-only data) did not indicate introduction of bias.

Population Impact
These results were combined with population projections for mortality. The number of deaths per year by age for England and Wales and the US [25,26] was combined with the prevalence of dementia at death. The prevalence rate of dementia was assumed to stay constant with time as there has been no apparent change with each successive 5-y birth cohort studied (year of birth ranges from 1888 to 1928). The results indicate that currently there are 114,000 individuals (95% CI 97,000?134,000) in England and Wales and 487,000 individuals (95% CI 362,000?503,000) in US who die with dementia each year. In 20 years' time, these numbers will have increased to 138,000 (95% CI 118,000?160,000) in England and Wales and 528,000 (95% CI 443,000?627,000) in the US.

Discussion
Summary of Findings
This 10-y longitudinal population study of people aged 65 y and over at baseline examines dementia and severe cognitive impairment status in the period before death and shows that the prevalence of dementia and severe cognitive impairment in the period before death rises steeply with age. Thus, by the time an individual aged 90 y dies, the risk of being demented or severely cognitively impaired is around 60%. Investigating whether higher education and social class?proxies for healthy exposures and lifestyles?protected individuals from dementia by the time they died showed that individuals with higher education and social class were at significantly reduced risk of dying with dementia or cognitive impairment. However, this reduction was limited: the reduction in dementia had an absolute value of only 2% and 7%, respectively, for higher social class and more highly educated groups; the reduction in cognitive impairment was 7% and 10%, respectively; and both high education and social class together conferred a reduction of 7% for dementia and 10% for cognitive impairment. Thus, the inequalities in healthy lifestyles and social advantage observed at given ages appear to be attenuated by the longer life expectancy of those individuals.

Critique of Findings
There are features of the study that need to be taken into account in interpreting the findings. The response rate at baseline and at each of the follow-up interviews was around 80% (see http://www-cfas.medschl.cam.ac.uk for details of audit trail). Some bias could be introduced into the analysis through this drop out due to death, refusal, and moving away. We know from earlier analysis of the dataset that individuals with cognitive impairment are at greater risk of death, so there is some potential to underestimate the prevalence of dementia at death given that we do not have cognitive status close to death in all respondents. We have taken this into account through the analysis of only those individuals who died within a relatively short period of being interviewed. If the analysis is conducted on the total sample for whom the last interview was more distant from death, a lower prevalence of dementia and cognitive impairment is found, as expected. However, individuals who dropped out from the study in the year preceding death were no more likely to be demented than those who undertook an interview in this time, indicating that the individuals analysed here are unlikely to be biased.

The measure for dementia in this study was GMS diagnostic algorithm organicity status, and for cognitive impairment was MMSE. Both of these will suffer from some misclassification bias. We have found severe MMSE and dementia states to be relatively stable, with only small proportions moving out of these categories in the extensive longitudinal data available. Limiting the analysis to subtypes of dementia such as Alzheimer disease or vascular dementia might indicate preventive potential for specific subtypes by death but would not reveal the true population picture, nor does cognitive impairment and dementia in the oldest old tend to fit into pure diagnostic categories [27]. Moreover, the concern many older people express is not about specific forms of dementia but that they will lose their independence and become cognitively frail. We have not addressed the mildest stages of impairment in this analysis.

Examining education and social class as proxies for healthy lifestyles could be seen as a crude approach, but these have been shown in their own right, in some studies, to be independently associated with lower rates of dementia. Certainly it would be desirable to expand this type of analysis to population studies with better lifestyle and health indicators?peak physical fitness, no smoking, moderate alcohol, good nutrition, and no hypertension, diabetes, or heart disease.

There are very few studies with which to compare these findings. One US study examined patterns of change in functional disability in the period before death [28]. Its goal was more to examine the predictive value of such patterns. It is already well established that cognitive impairment and dementia are associated with increased risk of death. We set out to examine how common dementia is by the time of death and whether those groups who are held to be at reduced risk of dementia and chronic disease during life appear to escape the risk before death. We have found that this is not the case, although there is a small diminution in risk before death, consistent with the absolute risk reductions reported for given ages in cohort studies. These findings confirm the finding of an earlier study by Bickel, who conducted a retrospective study of deaths by asking relatives about the status of the deceased before death and reported a prevalence of dementia-related conditions at death even higher than our estimates [29]. Our data also agree with findings on the health state of the very old, including centenarians. MRC CFAS reports odds ratios of incidence of dementia of over 25 for the 85-y-and-over age group compared to the 65- to 69-y age group [30]. In a study of 34 centenarians by Silver and colleagues [31], most (64%) were demented. Systematic reviews have shown that prevalence of dementia at this age is between 50% and 64% [32], with only 15%?25% estimated to have functionally intact cognition [33,34].

Implications and Conclusions
These data have serious implications for societies that are ageing. All public health services internationally will and should continue to promote healthy ageing through healthy lifestyles and optimal health care. It is important to continue to research treatments and preventive approaches for specific dementias aimed at lessening the devastation that dementia and cognitive impairment can cause. Substantial claims have been made for the prevention of dementia, and these need to be backed up by robust evidence of risk reduction through preventive strategies?not yet available as the evidence is based on observational studies. However, our findings suggest that preventive efforts are unlikely to be able to counteract the profound effects of age and proximity to death altogether. We will continue to examine early risk and track cognitive change, but the analysis presented here is about quality of life at the end of life. It may be that, although there will be a preventable component to dementia giving us a small and important absolute reduction in expectation of dementia at given ages, there is also a component that is not amenable to such types of prevention [35]. Researchers may be doing those who are ageing now and themselves a disservice in the future if they assume, and project to the public, that dementia and cognitive impairment can be prevented altogether during increasingly long lives. Given that the population of all deaths accounted for by people aged 85 y and over has increased from 8% in 1960 to 21% in 2003 in men and 16% to 41% in women in England and Wales, this is a matter of considerable importance [36]. Our data show that in the UK (and potentially in the US) the burden of dementia and cognitive impairment at time of death is substantial and is likely to become an increasing problem as the population ages. It is essential and urgent that societies invest in planning for (and researching) quality at the end of life for those with dementia and severe cognitive impairment [37?39], with sensible estimation of the likely increase in the numbers affected in the decades to come.

Acknowledgments
The MRC CFAS is supported by the Medical Research Council, UK. Thanks are due to the MRC CFAS team, our general practices, and most particularly to the respondents and their families. All MRC CFAS interviewing has been covered under local and multi-centre ethical approval.

Author contributions. CB conceived this analysis and led the study. LG and FEM designed and conducted the analysis. MD contributed at all stages. All authors discussed the results and commented on the paper. All MRC CFAS (corporate author) principle investigators and team were involved in the study and had an opportunity to comment on the paper.


1349.Human Spirit Stays Alive on Canvas in Alzheimer's Art Show
By Amanda Cassandra
New York
01 November 2006
http://www.voanews.com/english/portal.cfm
Cassandra report - Download 728K
Listen to Cassandra report

Experts in the medical and art communities recently gathered in New York to commemorate the 100th anniversary of the identification of Alzheimer's disease, a progressive brain disorder that gradually destroys a person's memory, and discuss the role of art in Alzheimer's disease. The lecture complemented the art exhibit "Portraits and Promises in Alzheimer's Disease."

The dementia associated with Alzheimer's disease was once considered a normal part of aging. It is now recognized as a progressive degenerative condition.

The disease, first identified by Dr. Alois Alzheimer in 1906, is a type of dementia that affects the brain. It causes memory loss, and eventually leaves its victim unable to communicate and perform normal daily functions. The U.S. National Institute of Health estimates four million Americans suffer from Alzheimer's.

President of the New York Chapter of the Alzheimer's Association, Lou-Ellen Barkan, says the threat posed by Alzheimer's disease is growing as the large baby-boom generation approaches age 65, when the chances of developing the disease increase.

"It will be the greatest health care crisis this country has ever known if nothing is done," Barkan said.

The lecturers discussed the work of William Utermohlen, an artist who suffers from Alzheimer's disease. The exhibit was developed as an innovative way to increase community awareness of the impact of Alzheimer's on the diagnosed individual, caregivers and loved ones.

Utermohlen was diagnosed with Alzheimer's in 1995. For the next five years, until 2000, he made portraits of himself in oil paints and pencil that gallery owner Chris Boicos says give a visual documentation of how and when certain abilities were lost.

"From the portraits that he painted, we can learn a lot about how someone suffering from the disease thinks about it, sees themselves inside, which is extraordinary as most Alzheimer's patients can't really express themselves verbally," he said.

In his series of self-portraits, Utermohlen gradually disappears on the canvas as his condition advances.

Eventually, the paintings take on a primitive style. They show few definitive facial lines and features, less color and vibrancy characteristic of his earlier works.

Boicos says Utermohlen's self portraits should be shown widely because they offer an alternative to the medical assessment of the disease.

"I think it is important that the pictures be exhibited and be exhibited in as many places as possible because they offer the public at large a more direct, perhaps more psychological and emotional apprehension of the disease and they can actually see someone who is ill retain his whole emotional capability," he said. "It's an apprehension of the disease that is not simply scientific or medical or dry or neutral. It is very much a human experience and I think this is really what the portraits best convey."

Many patients in the late stages of Alzheimer's lose the ability to communicate verbally, a function primarily controlled by the left side of the brain.

Dr. Bruce Miller studies artistic creativity in people afflicted with brain diseases. He says as Alzheimer's attacks the brain's verbal functions, even patients who had no previous inclination toward art began to express themselves visually.

"Sometimes these patients are compelled to draw," he said. "A woman from Malaysia came into my office and she said sit down. And I sat down and she just started drawing. This is one of the extraordinary things about some of these patients is this compulsion, this need to draw that comes on in the setting of this focal degeneration of the left anterior temporal lobe."

Miller says Utermohlen's work illustrates what he sees in many of his patients with dementia.

"I think you see in this story what you see with many people with Alzheimer's disease, which is that despite the illness, there's still life, genius, creativity and people express what they can with what's left," he said.

Lou-Ellen Barkan of the Alzheimer's Association says, while there is not yet a cure for Alzheimer's, the artwork offers hope.

"We know that one aspect of the human spirit is the capacity for self reflection and these paintings make it clear that even as Alzheimer's disease progresses, there is no immediate loss of self, that there are ways to stay connected to the world and to those we love. Life is not over with an Alzheimer's disease diagnosis, but getting that diagnosis is absolutely critical if people want to stay actively involved in the world," Barkan said.

Some doctors and advocates believe art may allow patients to emerge from the silence of the disease and find a way to communicate visually. Those pictures may be worth a thousand words, providing much needed insight for medical professionals, family and caregivers trying to understand how the disease attacks the brain, and how patients view themselves.


1350.Wine: good. Salt: bad. Fries
OK if nuked

Published: Thursday, November 02, 2006 @The Vancouver Sun

Drink red wine, microwave your french fries, and cut out the salt: That's the advice about a few of our guiltiest pleasures in three separate studies released Wednesday.

The wine research, done by American scientists, found compounds in red wine may not only offset the negative effects of high-calorie diets, but also extend life.

As for french fries, a study by Turkish scientists found a trip to the microwave before the frying pan can cut the levels of cancer-causing chemicals fries may contain.

And a third study, this time from Finland, found too much salt is associated with obesity -- with all the problems that entails.

Vancouver dietitian and nutrition coach Ramona Josephson called the studies fascinating.

"They bring into our own homes ideas that we can use to improve our health."

The U.S. study appears to be the first to suggest a compound in red wine, grapes and nuts -- resveratrol -- may increase the lifespan of mammals, just as it has previously been shown to prolong life 30 to 60 per cent in yeast, worms, flies and fish.

Resveratrol activates enzymes that regulate lifespan; the same enzymes are also involved in the response to a calorie-restricted diet.

"What we really would like to be the final answer, and can't quite say yet, is that resveratrol will mimic the effects of calorie restriction -- that it's going to trick your body into thinking that you're eating less calories by activating the same enzymes that get activated if you did eat less calories," said Joseph Baur of Harvard Medical School, referring to results from the study in mice released Wednesday in the journal Nature.

The wine research was led by scientists at Harvard Medical School and the U.S. National Institute of Aging.

The team used obesity as a model of premature aging since obesity shortens lifespan over all, says Baur.

"People appreciate it leads to diabetes and heart disease, but it's a little less appreciated that it increases your risk of cancer, of inflammatory diseases, of Alzheimer's disease and a lot of age-related diseases.

"We wanted to see if resveratrol could push back the progression of these diseases."

They used three groups of mice: one was put on a standard diet, another was fed a high-calorie diet, with 60 per cent of calories coming from fat, and the third was given the same high-calorie diet but also treated with resveratrol. The effective dose in mice was about 22 milligrams of resveratrol per kilogram of weight; one glass of wine contains just 0.3 per cent of that daily dose.

All the mice were about 52 weeks old, the equivalent of middle-aged humans. Mice on the high-calorie diet all got fat, but lived longer if they took resveratrol, with a median lifespan increase of about 14 per cent. While obesity can lead to diabetes, the treated mice were more sensitive to insulin.

"Generally, the more sensitive you are to insulin, the longer your predicted lifespan," Baur said.

As well, the livers of the high-calorie, untreated mice got large and fatty, but mice on resveratrol had fat-free

Pamela Fayerman, with a file from Sharon Kirkey, Vancouver Sun; CanWest News Service
Published: Thursday, November 02, 2006
Though resveratrol is available in supplements, the scientists don't endorse them since high doses could affect blood platelets, increasing the risk of bleeding if taken with blood thinners or nonsteroidal anti-inflammatory drugs.

Meanwhile, the Turkish study on french fries shows microwaving them before roasting or frying them cuts the level of acrylamides -- probable cancer-causing chemical compounds in foods like fries and potato chips that are baked, fried or broiled at high heats.

The research follows a report from Hong Kong earlier this week that inspections by the Hong Kong Consumer Council and Center for Food Safety in Hong Kong found that fries at McDonald's and KFC had the highest acrylamide content of snacks surveyed at fast food chains.

The Turkish study was prompted by a growing body of research that has found heating some foods, especially potatoes, to a temperature of at least 120 degrees C (248 F) can produce acrylamide.

Four years ago, researchers found that an amino acid called asparagine, combined with naturally occurring sugars in vegetables like potatoes, is a precursor to the formation of acrylamide at high cooking temperatures.

The relationship between acrylamide and cancer has not been studied in depth in humans. But based on animal research, a U.S. government agency stated recently that acrylamide can be "reasonably anticipated to be a human carcinogen."

In the Journal of the Science of Food and Agriculture, the Turkish team of food engineering professors said they compared potato strips without microwave treatment to those with prior microwave treatment.

"At all three frying temperatures, microwave pre-cooking resulted in lower acrylamide content ...in comparison to the control," they said.

There was a marked increase in acrylamide content as the frying temperature increased from 150 degrees C to 190 C.

Microwave pre-cooking didn't negatively affect the taste of the fries, so for french fry factories, microwave treatment is a smart strategy -- from a health and production line efficiency standpoint, they said.

Meanwhile, a Finnish study noted that salt intake in many parts of the world increased more than 50 per cent in the past decade and a half, and the amount of salt consumed is proportional to the amount of thirst.

Finnish scientists Heikki Karppanen and Eero Mervaala, in the journal Progress in Cardiovascular Disease, say there is an association between the amount of salt consumed in diets and obesity.

Salty foods induce thirst and people seem to reach for sweet beverages first, note the authors from the University of Helsinki and the University of Kuopio.

Calories consumed from sweetened beverages have steadily increased over the past three decades while milk consumption has dropped nearly 40 per cent.

Salt-induced thirst that is too often quenched by sweet drinks has "obviously remarkably" contributed to the increase of obesity, the article said.

Dr. Jean-Pierre Chanoine, a pediatric endocrinologist at B.C. Children's Hospital, said the association between salt and obesity is interesting and deserves more study.

Pamela Fayerman, with a file from Sharon Kirkey, Vancouver Sun; CanWest News Service
Published: Thursday, November 02, 2006
"It's a worthwhile hypothesis to explain the increase in obesity but I think there are many more factors at work like the fact that pop is less expensive than bottled water, that kids are getting less physical education in school and they're being driven to school because of safety concerns," said Chanoine, who focuses some of his research on childhood obesity.

pfayerman@png.canwest.com

This story can be heard online after 10:30 a.m. today at www.vancouversun.com/readaloud.

GUILTY PLEASURES

The health news is good, just go easy on the salt.

RED WINE

Overweight mice lived longer and better by consuming wine, grapes and nuts -- foods that contain resveratrol.

SALT

In a Finnish study, a one-third reduction in salt intake cut stroke and heart deaths and extended lifespans.

FRIES

Microwaving french fries before cooking them reduces levels of a cancer-causing substance.

? The Vancouver Sun 2006


1351.Massage May Help Dementia Patients With Agitation
Main Category: Alzheimer's / Dementia News
Article Date: 02 Nov 2006 - 0:00am (PST)
http://www.medicalnewstoday.com/
Massage could offer a drug-free way to treat agitation and depression among dementia patients, but there are still too few studies about the practice to know for sure, according to a review of recent research.

In two studies, hand massage and gentle touching during conversation helped ease agitation and restore appetite in dementia patients over short periods of about an hour.

"Although the available reliable evidence supports the use of massage and touch, it is so limited in scope that it is not possible to draw general conclusions about benefits in dementia," say lead authors Dr. Niels Viggo Hansen and colleagues.

"However, even if touch therapy aims only to reintroduce something which has been lost in the professionalization and institutionalization of care, it may still turn out to be a relatively effective, inexpensive and low-risk intervention," said Viggo Hansen, of the Knowledge and Research Center for Alternative Medicine, part of Denmark's Ministry of Health.

The review appears in the latest issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.

The Cochrane reviewers could only find two small studies, involving a total of 110 participants, of high enough quality to include in the review. Although the effect on behavior in the two studies was short-lived, some researchers and caregivers suggest that massage might also improve memory and cognition in those with dementia.

Cynthia Bologna, a Petaluma, Calif., massage therapist who works extensively with people with dementia, said she often works with patients to bring about short-term effects such as relaxation.

However, Bologna has noticed some long-term effects and said her clients "respond with recognition to the quality of my touch" even when they don't remember her name or recognize her from visit to visit. "So whereas I'm not sure about long-term cognitive memory, it seems as though their sensory memory is being enhanced," she said.

Viggo Hansen N, Jorgensen T, Ortenblad L. Massage and touch for dementia The Cochrane Database of Systematic Reviews 2006, Issue 4.

The Cochrane Collaboration is an international nonprofit, independent organization that produces and disseminates systematic reviews of health care interventions and promotes the search for evidence in the form of clinical trials and other studies of interventions. Visit http://www.cochrane.org for more information.


October 20, 2006 - 8:07 AM http://www.swissinfo.org/eng/index.html
1352.Scientists discover how memory gene works

Researchers at Zurich University have made an important step in improving understanding of how the human memory works.

They have for the first time been delving into the human genetic sequence to identify new memory-related genes.

One of their most important discoveries is the function of the Kibra gene, which helps regulate memory performance.

The scientists say the results of the study could help in the search for solutions to memory related diseases such as Alzheimer's and depression.

The research, headed by Andreas Papassotiropoulos and Dominique de Quervain from Zurich university's Division of Psychiatry Research - and done in collaboration with Dietrich Stephan from the Translational Genomics Research Institute in Phoenix, United States - is published in Friday's edition of the magazine, Science.

"The main objective of our research group is to identify the molecular underpinnings of human memory because very little is known about how memory works," Papassotiropoulos told swissinfo.

"Our work was to establish a new way of looking at things based on new information about the human genome. We hoped to identify novel and as yet undescribed memory-related genes in humans."

Genes

This is how the team was able to identify Kibra, a gene which had been previously pointed out but whose function was previously unknown in humans, said Papassotiropoulos.

To see how Kibra worked, scientists decided to do memory tests on around 350 people. They separated them into "good" and "bad" performers and then looked at their genetic blueprint or genome.

They also scanned brain activity during certain memory tasks. The Kibra gene was found to be linked to the hippocampus, which is crucial for memory performance and is often badly damaged in memory-related diseases.

"There are many diseases which affect memory such as depression or anxiety disorders," explained Papassotiropoulos.

"If you have a very good memory you can also have problems with, for example, post traumatic stress syndrome."

The professor said the team wanted to find out how normal memory works in humans because this would help with the development of drugs to target these types of illnesses as well as Alzheimer's.

New technique

Research using the genome differs from previous studies in that it does not with animals.

Usually researchers look for what is potentially important in memory in model organisms, such as rats or worms, and then see if there is a homologue gene in humans. The gene is then tested to see how important it is for memory performance in humans.

The genome-based approach was novel because it meant that the process was turned around, explained Papassotiropoulos.

"In fact we have identified Kibra and now the next step is to see whether this is related to basic mechanisms of memory and learning in flies and worms," he said.

In the future the team plans to examine genes related to memory performance and to re-scan the genome using better technology.

"We also want to understand why people remember emotional events better than neutral ones, which is a crucial question for psychiatric diseases," said Papassotiropoulos.

swissinfo, Isobel Leybold-Johnson


1353.Moderate Drinking May Boost Memory and Protect Against Alzheimer's
http://www.seniorjournal.com/index.html
Research grows saying what we eat, drink impacts dementia

November 2, 2006 - In the long run, a drink or two a day may be good for the brain, according to researchers who have found moderate drinking Ea couple of alcoholic drinks a day for humans E improved the memories of laboratory rats and say the discovery could have implications for Alzheimer's. The implications from this and other recent studies (see sidebar) is that drinking juice before dinner, then eating lots of leafy vegetables, with curry flavored fish and a couple of glasses of wine will offer considerable protection from Alzheimer's.

Matthew During, this study’s senior author and a professor of molecular virology, immunology and cancer genetics at Ohio State University, said “There is some evidence suggesting that mild to moderate alcohol consumption can protect against diseases like Alzheimer’s in humans. But it’s not apparent how this happens.E/p>

He and his colleague, Margaret Kalev-Zylinska, a postdoctoral researcher at the University of Auckland, in New Zealand, uncovered a neuronal mechanism that may help explain the link between alcohol and improved memory.

“We saw a noticeable change on the surface of certain neurons in rats that were given alcohol,EDuring said. “This change may have something to do with the positive effects of alcohol on memory.E/p>

The researchers presented their findings at the annual Society for Neuroscience conference in Atlanta.

During and Kalev-Zylinska designed a special liquid diet for the rats. One formulation included a low dose of alcohol, comparable to two or three drinks a day for a human, while the other diet included a much higher dose of alcohol, comparable to six or seven drinks a day for a human. A third group of rats was given a liquid diet without alcohol. All animals were given their respective diets daily for about four weeks.

The researchers measured the ratsEblood-alcohol levels three times throughout the study. Toward the end of the study, they subjected the rats to two different memory tasks.

For the first task, the rats were given several minutes to examine two identical, square plastic objects. After a certain amount of time, a researcher replaced one of the objects with a new, round object made of glass. The researchers measured the amount of time that each rat spent checking out the new object Ean indication that the animal recognizes it as a new object.

Rats given low doses of alcohol spent about three times longer examining the new object than did rats on the alcohol-free diet. Rats given the high dose of alcohol spent equivalent amounts of time checking out both objects, suggesting that they were unable to differentiate the old object from the new one.

For the second task rats were placed in a box with two chambers separated by a door. One chamber was well-lit, while the adjacent chamber was dark. After placing a rat in the well-lit chamber and then lifting the door, the researchers timed how quickly the rats entered the dark chamber (rats are nocturnal, and naturally prefer dark spaces.) Once inside the dark chamber, the rat received a mild electric shock to its feet.

The researchers repeated this same experiment 24 hours later, and kept track of how long it took the animal to enter the dark chamber. Many of the animals re-entered the dark area, yet the rats given alcohol waited anywhere from 2.5 to 4.5 times longer to enter the dark chamber than did the animals given the alcohol-free diet.

“The results suggest that both doses of alcohol moderately improved the animalsEability to remember this negative event, since they seemed hesitant to go into the dark area,EDuring said. “It also suggests that high levels of alcohol can reinforce bad memories.

“People who drink to forget bad memories may actually be doing the opposite by reinforcing the neural circuits that control negative emotional memory,Ehe continued.

At the end of the study, the researchers analyzed brain and liver tissue from each animal.

They found that low levels of alcohol increased the expression of a particular receptor, NR1, on the surface of neurons in a region of the brain, the hippocampus, that plays a role in memory. Researchers think that NR1 plays a role in memory and learning.


In a separate set of experiments, During and Kalev-Zylinska increased the number of NR1 receptors in another group of rats, and found that this boost improved the animalsEmemories to an extent similar to the improvement seen in the rats given low doses of alcohol. They also they used a new gene transfer technique to knock down the NR1 receptors in a group of rats given alcohol Ealcohol had no memory-enhancing effects on these animals.

“These experiments suggest that the effect of alcohol works through the NR1 receptor, at least where memory and learning are concerned,EDuring said.

“We didn’t see any toxic effects of low-level alcohol consumption on the brain or the liver,EDuring said. “It didn’t damage neurons nor did it cause liver damage during the short study. But the higher dose of alcohol damaged both.E/p>

The finding may have implications for serious neurodegenerative diseases.


DGNews

1354.Expert Panel Recommendations for the Treatment of Alzheimer's Disease and Related Dementias in Managed Care
NEW YORK, NY -- October 30, 2006 -- The consensus recommendations of a group of leading experts for the treatment of Alzheimer's disease and related dementias (ADRD) are published in a supplemental issue of the American Journal of Geriatric Pharmacotherapy (AJGP).

The panel of experts was convened by the Alzheimer's Drug Discovery Foundation to develop the recommendations for use by practicing physicians, other providers, medical directors and pharmacy directors in the managed care setting.

"Since previous clinical guidelines for ADRD were published, new treatment options have been developed. These include memantine, a N-methyl-D-asparate (NMDA) antagonist approved for moderate to severe Alzheimer's disease. Along with the cholinesterase inhibitors, treatment is now available for all stages of the disease, and combination therapy with both classes of drugs can be utilized," said lead author and international expert Howard M. Fillit, MD, Executive Director, Alzheimer's Drug Discovery Foundation and Institute for the Study of Aging.

With more than 5.8 million individuals now enrolled in Medicare Advantage managed care plans, and a total of 30 million Medicare beneficiaries having some type of drug coverage, the appropriate use of treatments for ADRD clearly has important implications for managed care. Considerable research has shown that anti-dementia therapies, including cholinesterase inhibitors and memantine, can treat the cognitive, function and behavioral symptoms associated with Alzheimer's disease, improve medical management and reduce healthcare costs.

Overall, Alzheimer's disease is the third most costly illness to U.S. society after heart disease and cancer, with direct and indirect costs estimated to be over $100 billion. Studies have also shown that Alzheimer's disease generates considerable excess costs in managed care. "Several studies have shown the pharmacoeconomic value of anti-dementia therapy. ADRD patients in managed care that are treated with FDA approved Alzheimer's medications have lower rates of hospital utilization and generate less annual costs," said Dr. Fillit.

"Alzheimer's treatment and care management has proven value for patients and caregivers. The recommendations of the panel represent the current standard of quality of care for ADRD," stated Rachelle Doody, MD, PhD, Professor of Neurology in the Department of Neurology at Baylor College of Medicine, a respected clinical expert in Alzheimer's disease and panel member. "It is important that patients and caregivers discuss these treatment and care management options for Alzheimer's disease with their physician."

The Recommendations
All of the recommendations noted are based on scientific evidence, FDA approved use of treatments, and expert opinion. The panel recognized that physicians, patients and caregivers need an open dialogue about the risks and benefits associated with treatment. The 20 recommendations include:

* Treatment of Alzheimer's disease should be determined by the stage at the time of diagnosis. Patients first diagnosed in mild stage should be treated with a cholinesterase inhibitor, patients first diagnosed in the moderate stage should be treated with a combination of a cholinesterase inhibitor and memantine; for patients who progress from mild to moderate, memantine should be added; patients first diagnosed with severe Alzheimer's disease should be treated with memantine as first line treatment, and combination therapy of a cholinesterase inhibitor can be added

* All patients should receive the same treatment options, regardless of their setting of care

* Newly diagnosed patients should be re-evaluated within two months, and then monitored at least every six months thereafter, to ensure appropriate treatment and care management

* Geriatric care management and counseling should be part of an integrated approach to treating patients with a diagnosis of Alzheimer's disease and their caregivers

* Cholinesterase inhibitors and NMDA antagonists should continue to be distinguished as two separate classes of drugs under Medicare Part D formulary guidelines, as patients need access to both classes

* Medicare managed care organizations (MCOs) should not discriminate against use of anti-dementia therapy through administrative burdens such as pre-authorization and appeals

About Alzheimer's Disease
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, resulting in loss of memory, thinking and language skills, and behavioral changes. An estimated one in ten persons over age 65 and nearly half of those 85 or older have Alzheimer's disease. Alzheimer's disease currently strikes approximately five million Americans; published reports project that by 2050 this number could more than triple to more than 16 million people in the United States.

SOURCE: Alzheimer's Drug Discovery Foundation


1355.The Big Question: It was discovered 100 years ago, but has treatment of Alzheimer's progressed?
By Jeremy Laurance, Health Editor
Published: 03 November 2006@http://www.independent.co.uk/

Why are we asking this now?

One hundred years ago today, on 3 November 1906, Alois Alzheimer, psychiatrist and pathologist, presented the first case of the disease that later came to bear his name in Tubingen Germany. The patient, Auguste D, developed dementia in her 50s and was so restless and confused that doctors prescribed balneotherapy - day long immersion in a lukewarm bath - to soothe her. When she was at her worst they knocked her out with chloroform.

Today, treatment has changed, but little else. Alzheimer's disease is estimated to affect 25 million people worldwide, and the numbers are rapidly rising as the population ages. Doctors no longer use lukewarm baths, but may try soothing them with music, aromatherapy, pet therapy or a variety of cognitive and behavioural techniques.

Despite extraordinary medical advances in the last 100 years, there is not much to celebrate in relation to Alzheimer's. The quality of care depended then, as now, on the skill of the clinical team. The main change has been the introduction of drugs to control the worst symptoms, such as agitation and restlessness. But a cure remains a distant dream.

A review of the disease published in The Lancet today concludes: "Although the practice of care may have changed the core principles have remained the same."

What is Alzheimer's disease?

It is a condition you would not wish on your worst enemy. It strips people slowly of their memory, their personality and eventually their humanity. It is a progressive, neurodegenerative disorder that is incurable and irreversible.

Iris Murdoch and Ronald Reagan are among the best known sufferers. Murdoch's last novel, Jackson's Dilemma, published a year before she was diagnosed in 1996, showed early signs of the disorder with a dwindled vocabulary and simpler grammar when compared with the rich language of her earlier novels Under the Net and The Sea, The Sea.

The condition is caused by an accumulation of "plaques and tangles" - protein deposits - in the brain which may interfere first with the semantic system, causing "word-finding difficulty". No one is quite sure what causes the plaques and tangles or why they produce the typical symptoms of dementia - loss of memory, confusion and agitation.

Dementia affects over 750,000 people in the UK. More than half (55 per cent) have Alzheimer's disease. A further 20 per cent have vascular dementia caused by mini-strokes which disrupt the blood supply to the brain. Vascular dementia is commonest in people with heart disease and high blood pressure.

The remaining 25 per cent of cases of dementia have a range of causes, some of which are rare. In all there are 200 types of dementia which are commonly misrepresented by the common label Alzheimer's disease.

How is it distinguished from the ordinary effects of ageing?

With difficulty. The test for Alzheimer's is examination of the brain for the presence of plaques and tangles - which can only be conducted post mortem. Accurate diagnosis while the patient is living therefore depends on the clinical skill of the doctor.

As a rule of thumb, anyone whose memory starts to cause them problems with the activities of daily living should see their GP. There is likely to be a medical reason such as depression, vitamin deficiency or the effects of other medications. If so, the effects can be reversed - and can result in a miraculous improvement.

If the cause is not obvious, the GP may refer the patient to a memory clinic for further investigation, where a diagnosis of Alzheimer's may be made on the basis of memory tests. A major problem is that people are so terrified of Alzheimer's that they don't go to the GP - even though many, whose memory loss has other causes, could be helped.

Can I do anything to prevent it?

Wear a nicotine patch. Studies have shown that nicotine, the addictive drug in cigarettes, can help prevent Alzheimer's. Taking up smoking is not recommended, however, as it increases the risk of heart disease and stroke, raising the likelihood of vascular dementia which would more than cancel out the reduced incidence of Alzheimer's.

More seriously, eating a diet rich in fruit and vegetables, taking plenty of exercise and keeping mentally active are all recognised effective strategies against Alzheimer's and other forms of dementia. A large US study published in April concluded that eating a Mediterranean diet reduced the risk of the disease by 40 per cent.

Playing chess, Sudoku or similar games are thought to offer protection, but the evidence is limited. Staying socially engaged, with friends or family, is seen as a more important way of keeping alert. Drinking alcohol in moderation and keeping blood pressure under control are also important. "What is good for the heart is good for the brain," says The Alzheimer's Disease Society.

What treatments are available?

This is a touchy issue. Four drugs, which have been available for a decade, are claimed to halt the progression of the disease. In 2001 they were approved for use on the NHS by the National Institute for Clinical Excellence and an estimated 54,000 patients are currently taking them.

In 2005 Nice reviewed its earlier decision and last month ruled that three of the drugs - cholinesterase inhibitors called donepezil (Aricept), galantamine (Reminyl) and rivastigmine (Exelon) - should be withheld in the early and late stages of the disease and only prescribed to those with "moderate" disease. The fourth drug memantine (Ebixa) was banned altogether.

The decision provoked uproar among patients' groups who protested that it was taken on cost grounds. Although the drugs appear relatively cheap at ?2.50 a day, they only work in one in five patients and it is impossible to say in advance who will benefit. The Alzheimer's Disease Society says: "These drugs make an amazing difference to some people's lives and those who benefit should not be penalised because they don't help everyone."

What hope is there for a cure?

There are two stages to finding a cure. The first is to halt the progression of the disease, the second is to reverse it. Some, limited progress has been made on the first (see above). The second is an aspirational target rather than a realistic goal as the brain has no capacity to repair itself.

A number of drugs are in final Phase III trials. The latest hope is the development of a vaccine that might halt the disease in its early stages. First trials in humans had to be abandoned after side effects emerged, but a modified vaccine is under development. A blood test for Alzheimer's is also being developed which would aid early diagnosis, identify patients for treatment and help research.

Scientists one day hope to stimulate stem cells to replace neurones lost as a result of the disease. A recent study provided the first evidence that stem cells are active in the brain in response to changes caused by the disease. But the research is in its early stages and scientists say it is too soon to predict the outcome.

Alzheimer's Society Dementia Helpline 0845 3000 336 www.alzheimers.org.uk


1356.Alzheimer's cure in Ayurveda!
http://www.dailyindia.com/
From ANI

By Mike Lockey

London, Nov 4 (ANI): A team of British and Indian scientists have been testing the 5,000 year-old traditional healing medicine Ayurveda in the search for a cure for Alzheimer's disease, and researchers have already announced that Ayurveda can be as effective as prescription drugs in boosting the mental agility of patients.

Ayurvedic medicine uses a variety of everyday herbs and spices, such as aloe vera, basil, garlic, ginger and turmeric, as well as yoga exercises, and this mix has proved to be beneficial to many people in the treatment of both physical and psychological problems.

The researchers studied five of the plants used in the production of Ayurvedic medicine, but, as one of the British members of the team, Professor of Pharmacognosy at King's College London, Peter Houghton, pointed out: "The work is still at the lab stage and nothing has been tested on humans as yet. No clinical studies have been done and just because we get interesting results from the lab doesn't mean people will be cured."

Nevertheless, the scientists, including experts from Jadavpur University in Kolkata, have found that the five plants they concentrated on helped prevent the breakdown of neurotransmitters in the brain, so improving the memory and concentration of people suffering from Alzheimer's.

The next stage is for the scientists to identify the chemical compounds in the plants. Once they have achieved that aim, and it is an aim that, sadly, could take years, then it should be possible to develop effective drugs incorporating those chemical compounds.

If those innovative drugs can be developed, then, at last, there will be real hope of a lasting cure for a disease that afflicts an ever-growing number of people across the world.

Until that happens, the usual therapies, as well as a selection of existing drugs, will continue to be used in the treatment of the disease to try and stimulate the patient. These range from simply encouraging people to reminisce about their past in order to reduce their depression, to art therapy and music therapy.

Meanwhile, the team of British and Indian scientists will continue with their quest, possibly, along with a cure for cancer, the holy grail of medical research. (ANI)

Copyright ANI


1357.New Alzheimer's drug shows promise
By SooToday.com Staff
SooToday.com
Saturday, November 04, 2006

GEORGETOWN UNIVERSITY
Alzheimer's expert Aisen leads research on novel treatment

Washington, DC - The only drugs currently available for Alzheimer's patients are those that alleviate symptoms, but a team of scientists led by Paul Aisen, MD, director of the memory disorders program at Georgetown University Medical Center, is testing a new class of drugs that actually target the molecule believed to cause the disease.

Aisen and his colleagues report that a compound called tramiprosate reduced levels of a marker for the progression of Alzheimer's disease in a Phase II clinical trial in the November 1 electronic version of Neurology.

"Everyone wants to figure out how to create an Alzheimer's treatment that attacks the amyloid peptide, which is considered to be the molecular cause of the disease," said Aisen. "This is the most advanced anti-amyloid treatment that exists ? it has the potential for slowing down progression of the disease."

Aisen and his team are currently in the midst of Phase III clinical trials on tramiprosate (manufactured by Neurochem, for which Aisen is a scientific advisor, as ALZHEMED?) and hope to have results by early next summer.

About Georgetown University Medical Center

Georgetown University Medical Center is an internationally recognized academic medical center with a three-part mission of research, teaching and patient care (through our partnership with MedStar Health).

Our mission is carried out with a strong emphasis on public service and a dedication to the Catholic, Jesuit principle of cura personalis ? or "care of the whole person."

The Medical Center includes the School of Medicine and the School of Nursing and Health Studies, both nationally ranked, and the world renowned Lombardi Cancer Center.


1358.Alzheimer's still somewhat a mystery

By SAM GANDY, M.D.
http://abcnews.go.com/
Nov. 3, 2006 ? If I turned back the clock 100 years to Nov. 3, 1906, and happened to be sitting, surrounded by psychiatrists in a small stone auditorium in the village of Tubingen, Germany, I might see on the program the name of a speaker, Dr. Alois Alzheimer.

Alzheimer actually spoke in this German auditorium in 1906, and he described a patient named "Augusta" who, in her middle 50s, had developed the seemingly unfounded delusion that her husband was unfaithful.

This delusion blossomed into full-fledged paranoid psychosis, and Alzheimer continued to care for Augusta in the hospital until she died.

Alzheimer then personally conducted her autopsy.

During the autopsy, he noticed something very wrong with Augusta's brain, which he called "a peculiar disease of the cerebral cortex."

Alzheimer used that phrase as the title of his presentation at Tubingen.

He had thought, at the time, that Augusta's "peculiar disease" was a rarity.

But, in fact, half of our current population older than the age of 85 is affected by the same disease.

Today, we call it Alzheimer's disease.

Alzheimer might be astonished to learn that nursing homes and psychiatric hospitals in developed nations have gradually filled with millions of patients suffering from the still-baffling illness that now carries his name.

A Slow Discovery

Doctors didn't often use the diagnosis of Alzheimer's disease until very recently.

The syndrome of dementia ? literally, the loss of the ability to think or mentate ? was long blamed on the narrowing of blood vessels in the brain, but the narrowing blood vessels weren't severe enough to explain the problems with thought and reasoning.

Over time, though, medicine evolved and people lived longer.

As life span increased, and as the brains of our elders began to be examined, two things happened.

First, highly functional 80- and 90-year-olds ? think pianist Vladimir Horowitz or cellist Pablo Casals ? defied the myth that late-life brain failure was inevitable; in other words, dementia wasn't something that "normally" happened, doctors realized.

Then, by comparing patients' medical histories with their autopsies, doctors realized that the brains from most elderly patients with dementia were "gunked up" with abnormal proteinlike structures, both inside and outside nerve cells.

That gunk between nerve cells, called amyloid plaque, is now considered one sign of Alzheimer's disease.

So, doctors gradually began to recognize the disease, but the truth is, doctors aren't certain that these plaques cause Alzheimer's disease, and doctors don't know what usually causes those plaques.

In some ways, Alzheimer's disease is still a mystery, much as it was 100 years ago.

When Will There Be a Cure?

OK, then, so, what do doctors and scientists know for sure about Alzheimer's?

Certainly, several things happen in the brain before the first signs of Alzheimer's appear:

Levels of a key brain chemical plummet: The technical name for this substance is acetylcholine.

Levels of two substances rise: The technical names are amyloid and tau.

Standard lab animals never develop Alzheimer's unless they are given a gene with a mutation that causes human Alzheimer's. Then, they develop some, but not all, features of the human illness.

Doctors know for sure they can cure mice with some of the features of Alzheimer's.

Some people with Alzheimer's get a little better for a little while with medicines like Aricept, Exelon and Razadyne. Those medicines help the brain compensate for the loss of acetylcholine.

These medicines will not stop the progression of the basic cause of Alzheimer's.

Alzheimer's develops in people with Down's syndrome and in people with rare genetic mutations.

Knowing anything "for sure" about Alzheimer's is a great leap forward, especially considering that the very first Alzheimer gene was only discovered 15 years ago!

But, what does the flip side look like? What do experts not know that we wish we did know?

Experts do not know for sure:

What causes the most common form of Alzheimer's.

Whether the medicines that work for mouse models will work for humans.

When Alzheimer's begins.

Who has Alzheimer's until the brain is examined under a microscope, which usually is only done after death, during an autopsy. It is technically possible to examine the brain while a person is still alive, but because Alzheimer's disease isn't treatable, that isn't a justifiable thing to do.

Exactly how to recommend diet and lifestyle modifications that will definitely lower a person's risk for Alzheimer's.

If or how rapidly brain function will decline once the very first memory change is noticed by someone or by his or her family.

Understanding Progress

How are doctors moving forward? What is being done to get the information to treat or prevent Alzheimer's?

Medicines and vaccines that work in mouse models are being tested in people with Alzheimer's. More than 100 Alzheimer's trials are listed at www.clinicaltrials.gov as being open for enrollment.

Local chapters of the Alzheimer's Association (www.alz.org) are now assisting patients to find details on trials in your area.

The very first brain scans have been developed with the promise of diagnosing and/or predicting Alzheimer's so that doctors can test new medicines at the very earliest stages of the disease. These tests undergo quality control as quickly as possible so that they can hopefully become widely available.

President Bush has cut Alzheimer's research for the first time in history. Each research study that initially asked for government funding now has less than a one in 10 chance for success.

Reconnecting With the Original Dr. Alzheimer

"So," doctors might say to Alzheimer if he were teleported here to the present.

"A hundred years have passed since you told us about your patient, Augusta. And in 100 years, we have learned so much about your disease, but we have also learned so little."

"Do you think the drugs we are currently testing will be effective? Were we right to bet on the genetic forms of Alzheimer's to teach us how to treat common forms of the disease? And will our research enterprise survive or collapse?"

The professor might take a few draws on his pipe and say, "Some things change over 100 years. Some things do not. These are the same questions that scientists in my day thought about, too ? all day, every day."

"But, Dr. Alzheimer," doctors might say. "Do you realize that dementia alone will soon consume our country's entire health-care budget? That there will be no money left for people with any other diseases?"

With a knowing glance and an air of enthusiastic determination, Alzheimer might once again set himself to the task.

"What are we waiting for? We have work to do!" he might say, and away the doctors would all go to the bedside, where Alzheimer would pick up where he left off, trying to unravel the secrets of a disease that still baffles and frustrates us.

Dr. Sam Gandy is a professor and director at the Farber Institute for the Neurosciences of Thomas Jefferson University in Philadelphia. Gandy is also chair of the Alzheimer Association's National Medical and Scientific Advisory Council.


1359.Changing minds in Alzheimer's research
Scientists have moved away from plaque and tangles in the brain toward developing better treatments for the disease.
By Greg Critser, GREG CRITSER, the author of "Fat Land and Generation Rx," is working on a book about neural aging and postwar America.
November 5, 2006 http://www.latimes.com/

THIS WEEK, major scientific and medical societies concerned with Alzheimer's disease are marking the central event in the evolution of this modern malady: the centennial of the case of Auguste D as presented by Dr. Alois Alzheimer at a medical conference in November 1906.

Something else will not be marked as loudly: the slow but gradual end of Alzheimer's as we know it - and the Americanization of dementia science.

It was Alois Alzheimer who gave us the basis of the modern conception of the disease, that of a dementia caused by a buildup of plaque between neurons and fibrous tangles inside brain cells. This he did through his examination of a 51-year-old woman named Auguste D, who came to him at a hospital at Frankfurt am Main. He found her anxious, disoriented, apathetic, unable to care for herself, often delusional and unable to remember key personal details of her life. As Auguste told Alzheimer at one point: "I have lost myself." Slices of her brain at autopsy showed that Frau D's brain had extensive plaque and tangles.

Yet Auguste D's case was hardly tidy. Yes, she had plaque and tangles; no, she did not have brain lesions (dead areas) and artery problems normally associated with brain dysfunction.

For a century, most of neuroscience used Alzheimer's observations to, essentially, reason backward. What causes the tangles, which seem to starve brain cells? What causes the plaque, which seems to mix up neural communication? And how do such changes lead to dementia? The focus on plaque and tangles has led to important discoveries about how brain disease develops, including inflammation, infection, chromosomal aging and beyond. But that narrow focus also has yielded no major therapeutic advances.

In many ways, it took a presence like Ronald Reagan, a perpetually sunny Californian, to wrest the disease from the grim determinism of fin de siecle Germany's model of Alzheimer's. The late president's candor about his condition, and wife Nancy's energetic dedication to the cause, helped transform dementia science. The result is a number of new approaches that, while more promising than classic plaque-and-tangles theory, require a leap of faith. Stem cells are one such tack. If you can grow new neurons, you might be able to rewire demented brains.

More radical: What, for example, if one abandoned "reasoning backward" from plaque and tangles altogether? That is the bombshell dropped last summer in the pages of the journal Alzheimer's & Dementia. After studying Alzheimer's patients who were given experimental doses of the diabetes drug Avandia, Allen D. Roses, head of the neurological drugs lab at GlaxoSmithKline, and Ann M. Saunders theorized that what causes Alzheimer's dementia is not plaque and tangles. Instead, the disease results from a "dysfunction" in the way brain cells of a certain genetic stripe use glucose, leading to destroyed dendrites, neurons' main way to communicate. Roses did not leave the implications of his theory hanging. Targeting impaired glucose - not plaque and tangles - should be a priority for early detection and treatment.

On the other end of the new research wave are academic entrepreneurs who are asking: Can we find a public health intervention that can slow the growing dementia rates in large populations? To that end, the National Institutes of Health has begun trials on omega 3 oils. But it is California - and particularly Los Angeles - that is at the leading edge of such work.

A number of promising experiments are underway, including the work of Greg Cole, a professor of medicine and neurology at UCLA, on the use of curcumin, a spice in curry powder, and its ability to retard dementia-linked changes in Alzheimer's-prone rats. USC has a number of experiments underway as well, many inspired by the pacesetting work of Caleb Finch, arguably the world's leading gerontological thinker.

Instructively, dementia and cognitive impairment, not Alzheimer's, have been the hot topics at the major Alzheimer's conventions in recent years. And for good reason. Not all dementia is caused by plaque and tangles (stroke is a leading cause), and not all plaque and tangles lead to dementia. Aging does not inevitably lead to dementia either.

Where gerontological wisdom once held that anyone who lived to 110 or older would be demented and/or afflicted with plaque and tangles, such has turned out not to be the case. Jeanne Calment, the Frenchwoman who lived to age 121, was cognitively unimpaired to the end. And gene science and brain scanning are showing that dementia is hardly the linear disease that Alzheimer and his successors proposed. Environment catalyzes genes, genes catalyze environments. Reagan's dementia has become a hot topic among researchers for this reason. What role did the environment created by his neglectful alcoholic father and emotionally absent mother play in the origins of his disease? Did the fact that he was easily able to quit smoking indicate a shortage of certain, later critical, brain receptors?

But whether caused by plaques, tangles, genes or childhood experience, there is clearly a huge dementia wave coming. We as a society are getting older, and we are doing so in a uniquely American way - as big-time consumers of fat, sugar, booze and drugs - legal and illegal. And so the boomer pattern of neural aging slowly but surely emerges. Boomers might come in with "normal aging issues," said Annette Swain, a San Fernando Valley clinician. "But on closer examination, they have a significant 'other' problem - the untreated diabetic with brain issues because of uncontrolled blood sugar. Or long-term pot users - in their 50s and early 60s - who are utterly puzzled by the fact that they have slower reaction times. The same with alcohol abuse and bad eating patterns, or improper use of prescription drugs."

She pauses. "What they don't seem to get is that it matters how you've lived your life."

Instead, the boomer ethos has turned to - what else? - gadgets and games, Sudoku and Brain Age. It's true that such brain teasers can impart small increments of "cognitive reserve," and they're fun. But they hardly address the real issues. "I am afraid we are going to get into the habit, you know, of sitting around the pool and debating whether Sudoku or Brain Age is better for making our brains healthier, while as a society we resist dealing with real medical issues and their detection, everything from mild cognitive impairment to dementia," said J. Wesson Ashford, who sees demented patients at the Stanford/VA Alzheimer's Research Center of California. "Only about one-half of dementia patients are ever diagnosed as such. We have got to get better at that."

To do so, Ashford and his colleagues recently issued an international call for annual screening for dementia in people older than 75, and a baseline "dementia discussion with your physician" at age 50. It is a bold initiative, considering that there is no treatment for Alzheimer's. It is also a generational challenge. Ashford believes that the benefits of anxiety reduction for those who discover they are not at risk, along with risk reduction and symptom reduction for those who are, are worth it.

The response to his call? "So far, there's really only one word," he said. "Apathy." It's a symptom worth attending to. Do it for the Gipper.


1360.Can caffeine protect against Alzheimer's?
Updated 11/6/2006 9:46 AM ET@http://www.usatoday.com/

By Kathleen Fackelmann, USA TODAY
Connie Lesko's not looking for the jolt that a cup of hot java offers.
Instead, she's hoping new research that shows caffeine may protect against Alzheimer's pans out: The 56-year-old from Wimauma, Fla., has two parents with this incurable disease.

KIM PAINTER: Good news, coffee lovers

"I've never been much of a coffee drinker," she says. "But now I'm thinking ? what the heck ? I'll have a cup."

Lesko and others are betting on research suggesting that caffeine will offer protection not just against Alzheimer's, but also against Parkinson's. Together these degenerative brain diseases affect about 6 million people in the USA. Cases of both diseases are expected to explode in the next few decades.

"Boomers are coming of age, and large numbers of them will develop neurodegenerative diseases," says Zaven Khachaturian, president and CEO of the Lou Ruvo Brain Institute in Las Vegas and the former director of the Alzheimer's unit at the National Institute on Aging.

The coming epidemic has fueled a search for drugs and other interventions that might slow the onset of these diseases, he says. If research by Gary Arendash and others holds up, boomers might be able to get some protection simply by enjoying an espresso.

"Caffeine is the most widely used psychoactive drug in the world," says Arendash, a researcher at the Byrd Alzheimer Institute in Tampa. "We think it might protect against Alzheimer's."

The research on caffeine ranges from a just-released mouse study by Arendash and colleagues to large-scale trials of coffee and tea drinkers. Such research might lead to the development of better drugs, Khachaturian says. Right now drugs for Alzheimer's and Parkinson's treat the symptoms but can do nothing to stop the underlying damage, he says.

Scientists like Arendash are searching for ways to stop diseases like Alzheimer's at an early stage.

At later stages, Alzheimer's destroys the memory centers in the brain, leading to severe forgetfulness and confusion. Arendash and his colleagues wondered if caffeine, the stimulant in coffee and tea, would slow this process in mice bred to develop an Alzheimer's-like disease.

Arendash gave young Alzheimer's mice either plain water or water spiked with caffeine ? the human equivalent of about five cups of coffee a day.

Months later Arendash and his colleagues gave the older mice a series of brain challenges. They found that Alzheimer-stricken mice that had guzzled caffeine could easily find their way through a maze. Mice that got just water had more signs of brain disease and got confused in the maze, he says. The team just published the study online in the journal Neuroscience.

The human research seems to suggest that caffeine might shield the brain from subtle problems with forgetfulness ? a possible early sign of Alzheimer's.

?A study of more than 600 men published in the August European Journal of Clinical Nutrition suggests that coffee drinkers may be protected from mild memory and thinking problems that come with old age.

?A 2002 study in the European Journal of Neurology found that people who consumed more caffeine in midlife appeared to be protected from developing Alzheimer's later on.

Studies on caffeine and Alzheimer's are just starting to roll in, but the literature on Parkinson's is well established:

?A study of more than 8,000 men in the Journal of the American Medical Association by G. Webster Ross and colleagues found that those who drank the most coffee (more than three cups a day) were the least likely to get Parkinson's.

?Another large study, published in 2003 in the Journal of Neurological Sciences, found that tea and coffee drinkers were protected from Parkinson's.

The list of large human studies linking caffeine to a reduced risk of Parkinson's keeps growing, says Caroline Tanner, director of clinical research for The Parkinson's Institute in Sunnyvale, Calif.

The evidence on caffeine and Parkinson's makes a strong case for coffee, but it still falls short of scientific proof, Ross and others say. To get a more solid picture of caffeine's potential benefit, researchers will need to do much larger human studies of caffeine, then watch for early signs of Alzheimer's or Parkinson's, Khachaturian cautions.

So where does that leave people like Lesko?

Ross, a neurologist at the Honolulu Department of Veterans Affairs in Hawaii, says in most cases, drinking coffee and other caffeinated beverages can't hurt. But people with high blood pressure or a history of sensitivity to caffeine should first talk to their doctor.

Lesko says she knows enough about Alzheimer's to take a chance on caffeine. She says that her father can still discuss current events, but her mother has more advanced disease and sometimes cannot remember family members, including Lesko.

That pains Lesko and brings up worries about the future. "If you've lived with this disease ? if it is part of your life ? you can't help but be fearful," she says.

So Lesko now drinks more caffeinated beverages, including coffee and several cups of black tea every day. The prospect of staving off this disease even by a little has pushed her to change her habits.

"It's worth a shot," she says.

Posted 11/5/2006 8:52 PM ET
Updated 11/6/2006 9:46 AM ET


Source: Wake Forest University Baptist Medical Center Released: Mon 30-Oct-2006, 13:25 ET
Embargo expired: Mon 06-Nov-2006, 18:00 ET Printer-friendly Version

1361.Study Suggests Underlying Cause of Dementia after Cancer Treatment
Libraries
Medical News Keywords
WHOLE-BRAIN IRRADIATION, DEMENTIA, COGNITIVE DEFICITS
Contact Information

Available for logged-in reporters only
Description

Researchers at Wake Forest University School of Medicine have identified changes in brain chemistry that may be associated with the dementia that many cancer patients develop after whole-brain radiation treatment.

Newswise ? Researchers at Wake Forest University School of Medicine have identified changes in brain chemistry that may be associated with the dementia that many cancer patients develop after whole-brain radiation treatment.

gBy identifying exactly how radiation causes these side effects, our hope is that we can find a way to prevent or reverse them,h said Lei Shi, M.D., Ph.D., lead author and a research fellow.

Whole-brain radiation is widely used to treat recurrent brain tumors as well as to prevent breast cancer, lung cancer and malignant melanoma from spreading to the brain. About 200,000 people receive the treatments annually. Starting at about a year post-treatment, up to one-half develop progressive memory problems.

Researchers donft know precisely how radiation injures the brain, but suspect it causes changes in the brainfs communication system. To test this theory, Shi and colleagues evaluated rats that had been treated with radiation and developed learning and memory impairments.

Today, at the annual meeting of the Radiation Research Society in Philadelphia, the researchers said they found changes in brain receptors for glutamate ? a neurotransmitter, or molecule that carries signals between nerve cells. They said the receptors change in composition as a result of whole-brain irradiation and that the changes seem to be associated with cognitive deficits.

These findings are significant because they may lay the groundwork for developing new therapies to prevent or reverse these potentially devastating impairments induced by whole-brain irradiation.

gThere is a growing concern about the cognitive consequences of whole-brain radiation,h said Judy Brunso-Bechtold, Ph.D., a professor of neurobiology and anatomy and senior researcher. gOur findings suggest that very subtle changes may be critical and that glutamate receptors may be one of those changes.h

The researchers focused on middle-age rats because middle-age adults are most prone to the cancers that require whole-brain irradiation treatment. Half of the rats received doses of whole-brain radiation similar to what humans receive. The other half received gshamh treatments that involved no radiation. One year later, researchers tested the ratsf learning and memory using a water maze.

The rats that had received radiation performed significantly worse than the untreated animals. Additional experiments were conducted to determine if these deficits were associated with cell-to-cell communication in the hippocampus, a region of the brain associated with learning and memory.

The scientists specifically looked at glutamate receptors that lie on cell membranes. There are several different subtypes of the receptors that differ in the types of brain chemicals that most readily bind to them. They found that the composition of these subtypes was different in the animals receiving whole-brain irradiation.

gThis shift in composition could impair synaptic communication and lead to the spatial learning and memory deficits measured in the treated rats,h said Shi.

Next, the researchers will see if the chemical changes also extend to the synapses themselves. They also want to focus on why some animals ? and people ? experience cognitive deficits while others donft. Eventually, they hope to test drug therapies that may prevent the effects.

Shi received the 2006 Marie Curie Award from the Radiation Research Society for the research.

The research is supported by a recently funded grant from the National Institutes of Health and is part of a broad collaboration among researchers led by Michael Robbins, Ph.D., in the Department of Radiation Oncology. Other co-researchers were Michelle Adams, Ph.D., Michelle Nicolle, Ph.D., William Sonntag, Ph.D., and Kenneth Wheeler, Ph.D., all from Wake Forest.


Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the universityfs School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in family medicine, 20th in geriatrics, 25th in primary care and 41st in research among the nation's medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.


1362.Samaritan Seeks FDA Nod For Human Testing Of Alzheimer's Drug

2006/11/06 15:05:37

(financialwire.net via COMTEX) -- November 6, 2006 (FinancialWire) Drug developers Samaritan Pharmaceuticals Inc. and Samaritan Pharma Ireland, Inc. (AMEX: LIV) have submitted an investigational new drug application with the U.S. Food and Drug Administration to evaluate its lead compound, Caprospinol, as a pharmaceutical treatment for Alzheimer's disease.
If approved, the company will test Caprospinol on humans as a potential memory-saving Alzheimer's drug.
Unlike drugs currently used to treat Alzheimer's that alleviate symptoms, Caprospinol seeks to be a viable treatment for the disease itself.
Samaritan's preclinical studies have shown that Caprospinol targets and binds to the beta-amyloid protein, washing out beta-amyloid plaque from the brain. The beta-amyloid protein is what most researchers believe is the cause of Alzheimer's disease.
After preclinical testing to show the biological activity of a compound against a targeted disease is completed, a company then files an IND with the FDA to begin testing of the drug in people.
Scientists at Samaritan Laboratories at Georgetown University led the preclinical studies for Caprospinol, while Samaritan's Drug Development executives amassed the seven thousand pages of data to formulate the IND submitted to the FDA.
PharmaPlaz, Ireland, Samaritan's collaborative manufacturing partner, led the chemistry, manufacturing and controls section of the submitted IND.
Las Vegas-based Samaritan is a small-cap biotechnology firm whose focus is to discover, develop and commercialize innovative therapeutics' for AIDS, Alzheimer's, Cancer and Heart disease patients.
For up-to-the-minute news, features and links click on http://www.FinancialWire.net
FinancialWire is an independent, proprietary news service of Investrend Information, a division of Investrend Communications, Inc. It is not a press release service and receives no compensation from any company for its news or opinions. Other divisions of Investrend, however, provide shareholder empowerment platforms such as forums, independent research and webcasting. For more information or to receive the FirstAlert daily summary of news, commentary, research reports, webcasts, events and conference calls, click on http://www.investrend.com/contact.asp
For a free annual report on a company mentioned in the news, please click on http://investrend.ar.wilink.com/?level=279
To become an investor monitor of independent research for a company in which you are invested, go to the not-for-profit Shareholders Research Alliance, Inc. website by clicking on http://www.shareholdersresearch.com/
The FinancialWire NewsFeed is now available in multiple formats to your site or desktop, free. Click on: http://www.investrend.com/XmlFeeds?level=268

URL: http://www.financialwire.net

(C) 2006 financialwire.net, Inc. All rights reserved.


1363.Neurochem Receives Recommendations from Data Safety Monitoring Boards to Continue Phase III Clinical Trials for Tramiprosate (Alzhemed)

LAVAL, November 06, 2006 /PRNewswire-FirstCall/ - Neurochem Inc. , announces that it has received recommendations from both the North American and European Data Safety Monitoring Boards (DSMB) to continue its two Phase III clinical trials currently ongoing for tramiprosate (ALZHEMED(TM)), Neurochem's investigational product candidate for the treatment of Alzheimer's disease (AD).



The two DSMBs are made up of independent clinical experts who monitor and evaluate the safety of patients taking part in the tramiprosate (ALZHEMED(TM)) Phase III clinical trials. In North America, this fifth recommendation by the DSMB was based on the recent review of the available safety data from 1,052 patients who have been on study medication for an average of 12.9 months. The Company announced previous recommendations by the North American DSMB in February 2006, and April, June and October 2005.

In Europe, this first recommendation by the DSMB members was based on their recent review of the available safety data from 333 patients who have been on study medication for an average of 1.8 months.

Tramiprosate (ALZHEMED(TM)) is a small, orally-administered molecule known as an amyloid (B) antagonist, which crosses the blood-brain-barrier, binds to soluble A(B) peptide and interferes with the amyloid cascade that is associated with amyloid deposition and the toxic effects of A(B) peptide in the brain.

About the Phase III Clinical Trials for tramiprosate (ALZHEMED(TM))

Neurochem is currently conducting a multi-center, randomized, double-blind, placebo-controlled and parallel-designed, 18-month Phase III clinical trial in 1,052 mild-to-moderate AD patients, which is being carried out at close to 70 clinical sites across the United States and Canada. The trial is scheduled to be completed in January 2007. To date, 542 patients have completed 18 months on study medication. All patients who complete the North American Phase III clinical trial are eligible to receive tramiprosate (ALZHEMED(TM)) in an open-label extension study.

Neurochem is also actively advancing an 18-month Phase III clinical trial for tramiprosate (ALZHEMED(TM)) in Europe, which was initiated in September 2005. The ongoing European Phase III clinical trial, an international, multi-center, randomized, double-blind, placebo-controlled and parallel-designed study, is progressing on schedule and is designed to investigate the safety, efficacy and disease-modifying potential of tramiprosate (ALZHEMED(TM)). Some 930 mild-to-moderate AD patients are expected to take part and enrollment is expected to be completed in fall 2006.

About Alzheimer's Disease

Alzheimer's disease (AD), associated with specific brain pathologies, is a progressive form, and the most common cause, of dementia. It impairs a person's cognitive and motor functions, affects their ability to undertake basic daily activities, alters their behavior and gradually destroys their brain.

Current treatments for AD provide benefit to patients through the alleviation of symptoms; however, the underlying disease is not directly affected. Research is now capitalizing on advanced knowledge about the biochemistry of A(B) and the pathway by which it is produced. The goal is the development of disease-modifying therapies with the capacity to slow or arrest the progression of AD.

Almost five million individuals in the United States alone currently suffer from the condition. The U.S. Alzheimer's Association estimates that by the year 2025, over 22 million people worldwide will be afflicted.

About Neurochem Inc.

Neurochem Inc. is focused on the development and commercialization of innovative therapeutics to address critical unmet medical needs. Eprodisate (KIACTA(TM)) is currently being developed for the treatment of AA amyloidosis, and is under regulatory review for marketing approval by the U.S. Food and Drug Administration and European Medicines Agency. Tramiprosate (ALZHEMED(TM)), for the treatment of Alzheimer's disease, is currently in Phase III clinical trials in both North America and Europe and tramiprosate (CEREBRIL(TM)), for the prevention of Hemorrhagic Stroke caused by Cerebral Amyloid Angiopathy, has completed a Phase IIa clinical trial.

To Contact Neurochem

For additional information on Neurochem and its drug development programs, please call the North American toll-free number 1 (877) 680-4500 or visit our Web Site at www.neurochem.com.

This news release contains forward-looking statements regarding tramiprosate (ALZHEMED(TM)) as well as regarding continuing and further development efforts. These statements are based on the current analysis and expectations of management. Drug development necessarily involves numerous risks and uncertainties, which could cause actual results to differ materially from this current analysis and these expectations. Analysis regarding the results of clinical trials may not provide definitive results regarding safety, tolerability or therapeutic benefits. Even if all the endpoints sought in the clinical trials were met (which is not certain), there is no certainty that regulators would ultimately approve tramiprosate (ALZHEMED(TM)) for sale to the public. Risks and uncertainties may include: failure to demonstrate the safety, tolerability and efficacy of our product, the expense and uncertainty of obtaining regulatory approval, including from the FDA, and the possibility of having to conduct additional clinical trials. Further, even if regulatory approval is obtained, therapeutic products are generally subject to: stringent on-going governmental regulation, challenges in gaining market acceptance, and competition. Neurochem does not undertake any obligation to publicly update its forward-looking statements, whether as a result of new information, future events, or otherwise. Please see the Annual Information Form for further risk factors that might affect the Company and its business.

For further information, please contact:
Lise Hebert, Ph.D.
Vice President, Corporate Communications
(450) 680-4572

lhebert@neurochem.com

CONTACT: Lise Hebert, Ph.D., Vice President, Corporate Communications,(450) 680-4572, lhebert@neurochem.com

Ticker Symbol: (Toronto:NRM.),(NASDAQ-NMS:NRMX)

Terms and conditions of use apply
Copyright ? 2006 PR Newswire Association LLC. All rights reserved.
A United Business Media Company


1364.Diabetes and Alzheimer's: Insulin resistance increases risk
Mayo Clinic Nov 6, 2006

Diabetes increases your risk of Alzheimer's. Reduce this risk by controlling your blood sugar. Diet and exercise can help.
Public health officials were already concerned about the projected increase in the number of Alzheimer's cases that will occur simply because the aging baby boom generation is so large. Now they worry there may be even more Alzheimer's cases than expected.

That's because diabetes ? a strong risk factor for dementias like Alzheimer's ? also becomes more common with age. Type 2 diabetes, which is by far the most common form of the disease, often occurs in people who weigh too much and exercise too little ? a group that includes a large proportion of baby boomers.

Luckily, type 2 diabetes can often be prevented if you maintain a healthy weight and exercise regularly. And if you already have diabetes, controlling your blood sugar with diet and medication, if needed, appears to decrease your risk of Alzheimer's.

How diabetes accelerates dementia
Your body changes the food you eat into glucose, the sugar that fuels all your cells. People who have type 1 diabetes don't produce enough insulin, a hormone that makes it possible for glucose to enter your cells. People with type 2 diabetes produce enough insulin, but their cells resist the hormone's action and fail to take up enough glucose.

Scientists have identified several ways in which the abnormal insulin and blood sugar levels in diabetes could promote the brain damage that causes dementia. These proposed mechanisms are closely related, so they all may operate in concert. Here are the leading possibilities.

High blood sugar and blood vessel damage
When your blood sugar is too high, it damages your blood vessels. This damage may first become evident in the tiny vessels of your eyes and feet, but it can also affect your brain. Small-vessel damage in the brain often contributes to vascular dementia.

While vascular dementia and Alzheimer's disease are separate types of dementia, they often occur together. Some scientists have suggested that vascular dementia may deplete a person's cognitive reserve, making Alzheimer's symptoms appear earlier.

Insulin in the brain
Before full-blown type 2 diabetes develops, your body becomes less responsive to insulin. The result is elevated blood sugar, a condition sometimes referred to as prediabetes. Your body compensates by producing more insulin.

A modest increase in insulin makes more glucose available to brain cells, resulting in improved memory. But if you're insulin resistant and the level of insulin in your bloodstream remains high, the brain takes measures to slow the transport of insulin across the blood-brain barrier. That reduces the amount of insulin in the brain, making less glucose available to nourish brain cells.

Researchers have found that some people with Alzheimer's experience improved memory when they use a nasal spray containing insulin. The nasal spray bypasses the bloodstream to deliver the insulin directly to the brain.

Insulin, amyloid and inflammation
Excessive insulin in the bloodstream may trigger increased production of beta-amyloid, a segment of a protein the body normally makes. In Alzheimer's disease, beta-amyloid builds up in the brain, forming clumps, or amyloid plaques. Excess insulin may also be responsible for brain cells' failure to clear beta-amyloid.

This whole process appears to be worsened by inflammation, another side effect of high levels of insulin in the blood.

Reduce your risk
You can counter insulin resistance through modest weight loss and exercise. If you have prediabetes, you can cut your risk of developing type 2 diabetes in half by losing 5 percent of your body weight ? 10 pounds for a 200-pound person ? and exercising 30 minutes most days of the week.

In addition to reducing your risk of diabetes and Alzheimer's, these lifestyle changes can also help protect you from heart attacks and strokes.

more information By Mayo Clinic Staff
Nov 6, 2006
c 1998-2006 Mayo Foundation for Medical Education and Research (MFMER). All rights reserved. A single copy of these materials may be reprinted for noncommercial personal use only. "Mayo," "Mayo Clinic," "MayoClinic.com," "Mayo Clinic Health Information," "Reliable information for a healthier life" and the triple-shield Mayo logo are trademarks of Mayo Foundation for Medical Education and Research.


1365.Medivation to Host Conference Call on November 15 to Provide Clinical Development Update for Lead Product Candidate Dimebon(TM)
Posted on : Wed, 08 Nov 2006 21:04:00 GMT | Author : Medivation, Inc.
News Category : PressRelease
http://www.earthtimes.org/

Dimebon, an orally available small molecule, has been shown to inhibit neuron (nerve cell) death in preclinical models of Alzheimer's disease and Huntington's disease, making it a novel potential treatment for many neurodegenerative diseases.

In a six-month, randomized, double-blinded, placebo-controlled Phase 2 clinical trial of 183 patients with mild to moderate Alzheimer's disease, announced in September 2006, Dimebon was well tolerated and met all five efficacy endpoints with strong statistical significance compared to placebo. An extension study of the Phase 2 trial, which allows patients to continue treatment for up to 12 months in the same treatment group to which they originally were randomized, is currently ongoing. Medivation is also evaluating Dimebon in an ongoing Phase 1-2a trial in patients with Huntington's disease in collaboration with the Huntington Study Group.

Teleconference/Webcast Details

A telephone replay will be available beginning approximately two hours after the completion of the call through November 22 by dialing 800-642-1687 from the U.S. or 706-645-9291 internationally. The replay passcode is 1678449. A replay of the webcast will be available on the company's website for 30 days.

About Medivation

This press release contains forward-looking statements, which are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements involve risks and uncertainties that could cause actual results to differ significantly from those projected. You are cautioned not to place undue reliance on the forward- looking statements, which speak only as of the date of this release. You are also cautioned that none of the Company's product candidates have been approved for sale, that significant additional animal and human testing is required in order to seek marketing approval for any of its product candidates, and that Medivation cannot assure you that marketing approval can be obtained for any of its product candidates. Medivation's filings with the Securities and Exchange Commission, including its Annual Report on Form 10-KSB for the year ended December 31, 2005, and its Quarterly Reports on Form 10-QSB for the quarters ended March 31, 2006, and June 30, 2006, include more information about factors that could affect the Company's financial and operating results.
Medivation, Inc.

Copyright ? 2006 PR Newswire. All rights reserved.


1366.Phytopharm Preliminary Results for the Year Ended 31 August 2006
http://www.engelpub.com/

CAMBRIDGESHIRE, England, Nov. 8, 2006--Phytopharm plc (PYM: London Stock Exchange) (gPhytopharmh or the gCompanyh, or the gGrouph) today announces its preliminary results for the year ended 31 August 2006.

Key Points ? Pharmaceutical Products

? Good overall safety and tolerability demonstrated in 256 patient Phase IIa clinical study for Cogane? in mild to moderate Alzheimerfs disease patients.

? Demonstration of a trend for slower disease progression in patients with more moderate Alzheimerfs disease taking Cogane? compared with placebo.

? Detailed assessments and due diligence now in progress for Cogane? and Myogane? with suitable licensing partners.

Key Points ? Functional Foods

? Successful completion of the first stage and progression into second stage of the Joint Development Agreement with Unilever for our weight management product, Hoodia gordonii extract. Clinical studies underway.

? Commitment by Unilever to pay up to ?3.5 million (?0.66 million already received) to support the second stage of the development programme. The balance of this payment is expected during the next financial period (FY 2007).

? Exclusive global marketing and distribution agreement for Phytopica? with Schering-Plough Animal Health (Schering-Plough). Product launched in UK and plans underway to launch in multiple European territories.

Key Points - Financial

? Revenue of ?1.88 million (2005 ?7.38 million)
? Loss of ?5.64 million (2005 ?3.33 million)
? Cash balance of ?6.00 million (2005 ?11.64 million)

Key Points ? Board

? Appointment of Mr Sandy Morrison and Dr Peter Blower as Non-Executive Directors
? Retirement of Mr Gordon Stevens as Chairman and Dr Trevor Flanagan as Non-Executive Director
? Appointment of Dr Paul Whitney as Chairman

Dr Richard Dixey, Chief Executive of Phytopharm, said:

gThe highlights of the year were the successful progression of our functional food products with our partners Unilever and Schering?Plough. The market launch of Phytopica? is a real milestone for us. Our business strategy of combining the development of functional foods with speciality pharmaceuticals is consolidating rapidly, and we look forward to positive developments in both sides of the business over the coming period.h

Enquiries:

Phytopharm plc Tel: 01480 437697
Dr Richard Dixey, Chief Executive Tel: 01480 437697
Dr Daryl Rees, Chief Operating Officer Mobile: 07710 479626
Financial Dynamics
David Yates / Ben Atwell Tel: 0207 831 3113

Please see the attachment for the complete press release.
Downloads
20061108-3180-7144B964.doc


1367.Touch, massage may aid dementia patients
Wed Nov 8, 2006 2:31pm ET

By Amy Norton

NEW YORK (Reuters Health) - Gentle massage therapy shows some promise for easing dementia patients' agitation and anxiety, though there have been too few well-conducted studies to recommend the treatment yet, according to researchers.

In a review of two clinical trials, Danish researchers found that hand massage helped calm dementia patients' agitation levels, while gentle touch and "verbal encouragement" at mealtime improved their food intake.

The findings suggest that human touch could help allay the agitation, anxiety and other behavioral and emotional problems that come with Alzheimer's disease and other forms of dementia.


However, so few well-designed studies have looked into the question that it's hard to draw conclusions for now, according to Dr. Niels Viggo Hansen, a researcher at the Knowledge and Research Center for Alternative Medicine, which is part of Denmark's Ministry of Health.

Indeed, Hansen told Reuters Health that he and his colleagues were disappointed to find only two clinical trials of high enough quality to include in their review.

Their findings appear in the Cochrane Library, a publication of the Cochrane Collaboration, an international organization that evaluates medical research.

The behavioral and emotional effects of dementia -- including wandering, difficulty with eating and bathing, anxiety, confusion and agitation -- are challenging for caregivers, and there is growing interest in whether therapeutic touch can bring some short-term relief from these problems.

The two studies Hansen and his colleagues reviewed included a total of 110 nursing home residents with dementia. In one study, researchers used gentle touch and verbal encouragement to help residents stay calm at mealtime. They found that those who received actual contact ate more than residents who received verbal encouragement alone.

In the second study, researchers found that hand massage, with or without calming music, helped soothe dementia patients' agitation levels for a short period.

What's needed now are larger, longer-term studies with more rigorous designs, Hansen said. This, he noted, includes giving a precise description of the touch therapies being used, so that the findings can be "useful and repeatable elsewhere."

In general, there is reason to believe that massage and other forms of touch could prove helpful for dementia patients, according to Hansen. On the physiological level, touch could affect the release of hormones that regulate anxiety and agitation, for example.

Then there's the "commonsense psychological level," Hansen noted. Physical contact, he explained, is a basic form of human communication that often gets lost once people are mature enough to use words instead.

But for people with dementia, Hansen said, human touch may again become the easiest way, or even the only way, to communicate.

SOURCE: Cochrane Library, online October 18, 2006.


1368.No Link Between Mild Thyroid Disease and Cognitive Dysfunction, Mood Disorders

Medscape

Subclinical thyroid dysfunction is not associated with depression, anxiety, or cognitive dysfunction in the elderly, a new study has found.

Caroline Cassels
Medscape Medical News


November 7, 2006 \ Subclinical thyroid dysfunction is not associated with depression, anxiety, or cognitive dysfunction in the elderly, a new study has found.

"This study shows fairly conclusively there is no justification for screening for mild thyroid disease on the basis that we can influence patients' cognitive dysfunction, anxiety, or depression," the study's principal investigator, James Parle, MD, from the University of Birmingham in the United Kingdom, told Medscape.

The study is published in the October 17, 2006 issue of Annals of Internal Medicine.

While there is a well-established association between overt thyroid disease, cognitive dysfunction, and mood disorders, the evidence demonstrating a similar association with mild disease has been inconclusive, said Dr. Parle.

Widespread Testing

"If you have a patient with severe thyroid failure, their cognitive function will very likely be impaired. The concern is that clinicians infer from this that milder degrees of thyroid failure are also associated with milder cognitive impairment and mood disorders. And while this is a reasonable inference, it is still only an inference and not scientific evidence," he said.

In the meantime, he said, the advent of highly sensitive tests for thyroid hormones and thyroid-stimulating hormones and ensuing widespread use of such tests have led to a substantial increase in the diagnosis of mild thyroid dysfunction, particularly among elderly patients.

"In the United Kingdom there is quite a strong opinion within the medical community that one needs to be sure screening is going to be beneficial to the patient in the long run. Just because you have the means to do a particular test doesn't necessarily mean it should be done. So our goal was to find out whether such testing is justified," he said.

Unexpected Result

The community-based, cross-sectional study included 5865 elderly patients aged 65 to 84 years recruited from 20 primary-care practices in central England.

Serum thyroid-stimulating hormone and free thyroxine were measured. In addition, the Hospital Anxiety and Depression Scale was used to measure anxiety and depression, and cognitive functioning was assessed using the Middlesex Elderly Assessment of Mental State and the Mini-Mental State Examination. Comorbid conditions, medication use, and socioeconomic status were also recorded.

A total of 295 patients met the criteria for subclinical thyroid disease. Of these, 127 were hyperthyroid and 168 hypothyroid.

After adjusting for medication use, age, sex, and socioeconomic deprivation, the investigators found no association between mild thyroid disease and cognitive dysfunction, depression, or anxiety \ a result that was unexpected.

"Based on the effect of overt disease on cognitive function and mood, we expected to find a small but statistically significant association with mild thyroid disease, so we were a little surprised when no association was found," said Dr. Parle.

Exceptions to the Rule

The study's findings, he added, indicate population-based screening for subclinical thyroid dysfunction should not be done for the purposes of modifying cognitive decline or mood outcomes in the elderly.

However, he said, symptomatic patients presenting with cognitive dysfunction or other neurological symptoms that could be attributed to thyroid dysfunction should be tested.

Furthermore, he said, population-based screening for thyroid dysfunction may be warranted in areas where there is a higher-than-average incidence of thyroid disease. For instance, he said, thyroid dysfunction is more common in individuals from certain parts of Eastern Europe, Africa, and Asia.

New Paradigm?

Adding to the complexity of thyroid testing, said Dr. Parle, is the fact that criteria for determining clinical and subclinical thyroid dysfunction are "purely arbitrary." In an attempt to address this issue, he said, the United Kingdom is moving toward an individualized risk-assessment approach, similar to that used to assess heart disease risk.

"If we move toward this paradigm, it would mean the diagnosis of thyroid dysfunction would at least be determined based on its effect on other systems. This model would allow physicians to determine whether to test and/or treat a particular patient based on their unique combination of risk factors," he said.

Ann Intern Med. 2006;145:573-581.

Medscape Medical News 2006. (C) 2006 Medscape


1369.Alzheimer's disease evolving, but remains a mystery

By DEANNA LEE-SHERMAN - Staff Writer
Friday, November 10, 2006 3:54 AM EST
http://www.harlandaily.com/
It is often said that words alone cannot describe some of life's most challenging obstacles.

That is true for Jane Karst, an only child whose mother was diagnosed with Alzheimer's disease at 60. Because Karst's mother hadn't reached her 65th birthday when her symptoms began to appear, her case is considered to be early-onset - what more and more health professionals are seeing today.

While developing Alzheimer's is not a normal process of aging, there are reportedly more than four million Americans age 65 and older who have been diagnosed with the disease, which is still largely the mystery it was upon its discovery a century ago.

It's an irony that many can't quite put their fingers on, including those who have first-hand experience with the disease.

In Karst's case, she went through many of the same emotions that Alzheimer's patients experience upon their diagnoses. There was denial, an overwhelming amount of anger and plenty of confusion.

Despite some of the most explicit signs of Alzheimer's, the Catrons Creek resident said it just didn't register that her mother, a healthy Sunday school teacher and an active community leader, could be suffering from the most common type of dementia.


Even when her mother, a sharp woman with a successful furniture and accessories business in Harlan, would stop and ask directions to places in her native county that she'd been countless times before. Even when she began to forget the names of some of her closest acquaintances.

gShe could tell me all about them and where they lived. But she couldn't tell me their name,h said Karst.

Karst said she grew concerned but thought that perhaps her busy mother was on her way to a gbreakdown.h

gShe tried to tell me that she was OK. She would say, eI'm just not myself today.' She knew something was happening to her. I just thought she had her plate too full and needed a break.

gThen someone mentioned dementia. ... I was in denial,h said Karst.

Her mother's case progressed so quickly that Karst can't quite seem to describe all that followed.

gIt happened so fast. It was like it was almost overnight. That's how bad it was,h she said.

Karst's experience was much the same for family member Pat Sellers, a Teetersville resident who said she also couldn't accept that her cousin, who was more glike a sister,h had Alzheimer's.

gShe was as smart as a whipper-snapper. We really had a hard time believing it,h said Sellers, who is active in the local Alzheimer's Association Memory Walk, an early autumn event held each year in Harlan.

Although each case of Alzheimer's is individual, research does suggest that the disease progresses more quickly in those who are diagnosed at a younger age, said Tonya Cox, vice president of education and programs for the Lexington Regional Office of the Alzheimer's Association.

gEarly-onset does seem to progress more quickly for a good majority,h said Cox, adding that other health problems can also affect progression.

According to the association, early-onset Alzheimer's can strike someone as early as their 30s and new data indicates there may be half a million Americans younger than 65 who have dementia or cognitive impairment that is consistent with dementia.

But technology and new therapies are redefining the face of the disease, according to the Alzheimer's Association. Research has enabled earlier diagnoses and, therefore, earlier treatment - which is maximizing the quality of life for those suffering from Alzheimer's.

Research has also shown that a healthy lifestyle may help prolong or even possibly prevent Alzheimer's. That can be somewhat difficult to digest for some families, including Karst's. Karst said her mother, a social butterfly, had no health problems and was extremely active.

And while it is still unknown how much of a role family history plays in Alzheimer's, Karst said there was no other trace of the disease in hers.

Research has shown, however, that a strong genetic link exists in early-onset Alzheimer's.

gWhat we see most often is sporadic (Alzheimer's) - no traceable family history,h said Cox. In familial cases, parents have a 50 percent chance of passing the disease on to their children, she said.

Karst also said her mother, who has ghad a battleh with different medications, didn't revert back to her childhood, something health officials see often in Alzheimer's patients.

gThey can tell you very detailed information about their childhood, but they can't remember what they had for breakfasth - a classic symptom of long-term memory loss, Cox said. Short-term memory loss, minor forgetfulness that steadily progresses, is the most striking early symptom of Alzheimer's.

Cox said she can't emphasize how gindividualh each case of Alzheimer's is. No matter what the family background may be or what lifestyle has been led, it's something that can happen inevitably.

gSome people do everything right and still get the disease,h Cox said.

Individuals should be concerned, she said, when memory loss begins to interfere with daily life or familiar tasks.

There are an estimated 74,000 Kentuckians and approximately 4,000 Cumberland Valley residents who are suffering from Alzheimer's, Cox said. The state's estimate is expected to jump by 30 percent over the next 20 years, she added.

The irreversible disorder affects men and women of all races and ethnic groups in all walks of life: gNo one group doesn't suffer from it,h said Cox. The duration of the illness varies from three to 20 years; the average life expectancy is eight years from the time of diagnosis, she said.

Those who have concerns about Alzheimer's should gknow your resources,h Cox advised. Information about the disease, as well as toll-free numbers, are readily available on the Internet or through countless organizations such as the Alzheimer's Association, she said.

As for Karst, she said she tries not to feel frightened by the mystery of Alzheimer's. She has two girls herself and prefers to focus on the here and now.

gI have concerns, but I try not to think about that,h she said.

Still, every now and then, when she hears how helpful her mother has been to community members and churches, her emotions get the best of her.

She's not sure if her mother knows who she is.

gShe'll smile when she sees me,h said Karst, explaining that her mother can't talk much anymore. gBut I've seen her smile at others, so I don't know that she knows who I am.

gIt's just sad. You never know. But you don't know what tomorrow holds. ... You just have to not have regrets about what you should've said or didn't say,h she said.

To talk with a representative of the Alzheimer's Association, call the organization's toll-free helpline anytime at 1(800)272-3900. For more information, visit www.alz.org.


Posted on Sat, Nov. 11, 2006email thisprint thisreprint or license this
1370.Nursing homes take residents back to ethnic roots
Associated Press
CLEVELAND - Nursing homes, aware that residents sometimes remember their childhoods better than what happened yesterday, are turning to ethnic roots to help residents stay in touch.

At the Lorantffy Care Center, paintings of heroes and legends of Hungary, including Queen Lorantffy, stare from the walls, Gypsy music fills the air and a staff member speaks in soft Hungarian to check on meals.

Lorantffy, a family-run nursing home outside Akron, stands at the crest of a trend to help the aging cope with memory loss by providing familiar ideas from years ago, often in a person's native tongue from an overseas homeland.

America's overwhelmingly white and female nursing-home population is growing larger and more diverse like the country.

"I don't know, maybe this is the ideal," said Gabriella Nadas of Canton, whose parents-in-laws, Julias and Ibolya Nadas, live at the Lorantffy home.

A typical nursing home can be a foreign, frightening place to people who do not understand the staff or do not like what they're fed. One response, culturally competent care, calls for offering elders their language, their ethnic dishes and their cultural traditions.

"That's an approach that's going to become more popular," said Peter Reed, senior director of care service for the national Alzheimer's Association.

"It's an idea that's gone from intuitive to practical," said Dr. James Campbell, chairman of family medicine and geriatrics at MetroHealth Medical Center in Cleveland. He hopes to import cultural care concepts into a senior home and wellness center scheduled to open in 2008 in the former Deaconess Hospital in Cleveland.

The region's Latino community is growing older, he notes. So are the Asian Indian, Chinese and Arab communities - ethnic groups not yet widely represented in area nursing homes.

"We have to plan for a multicultural population," Campbell said.

Residents of the Slovene Home for the Aged in Cleveland, about half of whom are of Slovenian heritage, receive the same basic services as residents at other long-term-care facilities. But they also tap their feet, and sometimes spin their wheels, to live polka music.

At the Menorah Park Center for Senior Living in Beachwood, there are two full-time rabbis, a kosher kitchen and Torah study for its 800 residents, some of whom speak only Yiddish.

The Eliza Bryant Village in Cleveland caters to black seniors with southern roots. Greens and cornbread are on the menu, jazz and gospel music play, and art evokes African-American life and times.

"It helps people feel more comfortable, at peace, to go back to memories that were important to them," said executive director Harvey Shankman.


1371.'Lifesaver' Helps Locate Lost Alzheimers Patients
wfrv.com
http://www.topix.net/
November 12, 2006

The recent change of seasons in Northeast Wisconsin isn't normally a cause for too much conern. But for families of Alzheimers and Dementia patients, the dip in temperatures causes additional concern and worry.

"A lot of families don't realize how dementia develops and it can progress into their loved ones wanting to get away and so wandering becomes a big issue," says Bonnie Warren of the Alzheimer's Association

Families can turn to the Alzheimer's Association for tools to protect loved ones, including the popular 'Safe Return' program.

"Patients wear a bracelet. It's gonna provide information. It's gonna provide identification and notification of what to do if someone is lost," says Warren.

The program has been been very successful, but to return these patients, first the person has to be found.

The Brown County Sheriff's Department receives training regarding dementia cases. "What we've learned through our training is that once a person gets disoriented they may try to hide somewhere, not knowing what's going on," said Lieutenant Keith Barth.

However, a new program called Project Lifesaver is helping to make it easier to locate patients who may be lost. Like Safe Return, Lifesaver patients wear a bracelet. But in this case, the bracelet contains a tiny chip that sends out radio frequency waves that can be used to track the location of the bracelet, and its patient. Each bracelet emits a unique frequency, making it possible to locate a specific bracelet.

Warren believes this new project helps shorten the time to locate patients. "The Safe Return program covers a lot of area, but the Project Lifesaver is one that's going to give us actual rescue services," she said. "A family is devastated when something like this happens.. so we want to find that person as quickly as we possibly can. And by using this service.. it's going to cut down the time immensely."

Project Lifesaver is being offered in Brown County, and has been shown to reduce search times from days and hours.. to only minutes. Lt. Barth says that their equipment allows them to track the signals from a mile away, but can be detected from over three miles from the air, and Eagle III and County Rescue Services have agreed to assist the Brown County Sheriff's Department in 'Safe Return' cases. And when someone's lost in the elements, disoriented, not sure where to go, that can mean the difference between life and death.

Copyright ? 2006 wfrv.com, All Rights Reserved.

Hosted by: Topix.net Publisher Platform (beta)


1372.How to prepare for the Alzheimer's wave
http://www.canada.com/vancouversun/index.html
Published: Saturday, November 11, 2006
A compilation of key recommendations made by Alzheimer societies, advisory councils, coroner's inquests and physicians:

- Develop a federal strategy to coordinate preparations to improve the diagnosis, treatment and care of dementia patients.

- Invest more in research now, as the baby boomers are about to enter their 60s -- the decade when the risk of Alzheimer's begins to spike; a breakthrough treatment could save the country billions of dollars related to their future care.

- Expand the federal income-support policy to provide working Canadians with the ability to better care for loved ones with chronic diseases such as Alzheimer's. The existing program allows Canadians to collect unemployment benefits for up to six weeks to care for a gravely ill child, spouse or parent who is at risk of dying within six months.

- Develop a provincial strategic plan to manage the expansion of the long-term care system over the next two decades and the introduction of more home care, respite care and housing options for those with Alzheimer's.

- Introduce more geriatric medicine into undergraduate physician and nursing programs, since today's graduates will ultimately have to treat a growing population of seniors.

- Establish a centre to share best practices in the care of Alzheimer's patients and to translate new research into useful strategies.

- Create specialized, well-staffed units within provincial long-term care systems to manage physically aggressive Alzheimer's patients.

- Ensure all staff who feed, clothe, bathe and groom residents in long-term care systems receive special training in dementia care.

- Mount a public-education campaign to encourage those with noticeable memory problems to seek early medical help.

? The Vancouver Sun 2006


1373.Easing the agony of Alzheimer's
Specialist offers guidance to caregivers
By Robert Knox, Globe Correspondent | November 9, 2006
http://www.boston.com/
Everything we know about the world, says Suzanne Faith Baybutt, a psychiatric nurse consultant, we know because of memory.

A person suffering memory loss is like a stranger in a foreign country. "You don't speak the language, or know the currency, or where you are," Baybutt says. Without memory, she adds, "you are living truly in the moment." But that's a very hard way to live -- and frightening to both the person who is living that way and those trying to care for him or her.

Memory impairment is the cardinal symptom of Alzheimer's disease, a progressive, degenerative disease of the brain that gradually destroys mental capabilities. It affects an estimated 4.5 million Americans, a number that has more than doubled since 1980.

Baybutt, who has worked in Alzheimer's care for 20 years, will lead a program called "Understanding Alzheimer's Disease: Becoming a Better Caregiver " from 7 to 8:30 p.m. Monday at the Plymouth library. Through specializing in the management of Alzheimer's and related dementias, Baybutt said she has learned that caregivers need education in how to care for a loved one with the disease.

Memory impairment through Alzheimer's or dementia is qualitatively different from, and much worse than, simple forgetting. In Alzheimer's, she said -- borrowing an image from computers -- the "file" where the information is stored is erased and you can't get it back. "If you've lost the file, lost the connection, you don't know what it is." The person with Alzheimer's "is always living with an undercurrent of anxiety, never really sure where they are, or who they are, in any moment of time."

Alzheimer's and dementia are not the same. Alzheimer's is a specific disease, while dementia is a wider term for a group of 70 medical conditions that produce similar symptoms. Memory loss is a consequence of both.

But it's a mistake to attribute all memory impairment to Alzheimer's, and one of Baybutt's first advisories for caregivers is to make sure they get a medical diagnosis. Some dementias are reversible. Some are associated with depression and are treatable with antidepressants. If the diagnosis is Alzheimer's, one sad consequence is inevitable: it does get worse.

Family caregivers face the challenge of learning new ways to communicate with loved ones suffering from memory loss, Baybutt said. They have to "undo all the usual patterns of communication and learn new patterns of communication," such as nonverbal language, "to help the person feel good" and avoid bringing on more anxiety in the sufferer by insisting on old patterns.

"This is the biggest problem," she said. "Family members continue to want their parent and spouse to live in our world. And they can't anymore."

The "horrendous behaviors" people are likely to hear about people with Alzheimer's have often been prompted by caregivers, she said. An elderly relative, for example, looks out the window and sees someone. There's no one out there, the caregiver tells her; "you're out of your mind."

The person with Alzheimer's becomes afraid. Since they no longer "orient to reality," Baybutt urges the caregiver to "join them in their reality. You let them live in their world." Doing that, she acknowledges, is "very difficult," and caregivers can't do it without education and support.

Support is available through groups, many of them sponsored by state grants because the state recognizes that working with caregivers is better than letting them flounder until a crisis leads to admission to a nursing home -- less comfortable, more expensive. For more information on family resources visit traincaregivers.com.
"The worse thing to do," she said, "is to isolate yourself."
The Plymouth library's Outreach/Senior Services Department is sponsoring Monday's program at 132 South St., its ninth annual event in recognition of Alzheimer's Awareness Month. The event is free; light refreshments will be served. Reservations are requested and may be made by calling the library's Sharon LaRosa at 508-830-4250, ext. 219, or by TTY at 508-747-5882. The library is fully accessible, but contact LaRosa in advance if you need special accommodations to attend.
Robert Knox can be contacted at rc.knox@gmail.com.
? Copyright 2006 Globe Newspaper Company.


11/14/06
1374.Supreme Court upholds $13M verdict against Beebe
http://www.capegazette.com/index.html
By Laura Ritter
Cape Gazette staff
The Delaware Supreme Court has upheld a juryfs $13 million award to the family of an Alzheimer patient who was locked in a freezer at Lewes Convalescent Center and later died as a result of her injuries.

In a unanimous decision released Thursday, Nov. 9, the Supreme Court unanimously denied an appeal of the juryfs award brought by the Beebe Medical Center and its insurance carrier. The decision upholds the largest jury verdict in state history in this type of case, according to attorneys for the patientfs family.

Julie Bailey had worked as a nurse at the medical center before a diagnosis of Alzheimerfs disease limited her mental capacity. In December 2002, after treatment at the hospital, she was released to the nearby convalescent center. Unnoticed by convalescent center employees, she wandered into a food locker, became trapped there and suffered frostbite injuries that led to her death.

Juliefs husband, Tony Bailey said after he heard the verdict, gI slept for three days. A great load has been taken off me.h

In an interview Monday, he said while hefs glad the Supreme Court has ruled, he still worries the case might not be over. gI feel extremely relieved that we got a unanimous decision from the Supreme Court. Itfs been quite consuming ? and thatfs an understatement,h he said from his home in Lewes.

The case, which originally sought both compensatory and punitive damages, went before Superior Court Judge E. Scott Bradley in March 2005. In the course of the trial, the jury heard testimony that applied to both compensatory and punitive claims, a fact that would become a central issue in the appeal after the punitive damage claim was settled privately before the case went to the jury.

In a statement released Thursday, medical center chief executive officer Jeffrey Fried wrote, gBeebe Medical Center and the Lewes Convalescent Center continue to regret the death of Mrs. Julie Bailey, our patient, former co-worker, and friend who died while in our care in January 2003. During the trial we publicly took full responsibility for her death and privately we settled the punitive damages claim with the family in the amount of $5 million, which the family accepted independent of the compensatory damages award.h

Attorneys for both sides could file motions for reconsideration of the Supreme Court verdict. John Elzufon, one of the attorneys who represented both the hospital and its insurance carrier, said at the direction of his clients, he had no comment on the case.

Attorney Chase Brockstedt, who has represented the Bailey family since 2001, said every time the case took a new turn, the family has been forced to relive all of the anguish surrounding Julie Baileyfs death. gThey can now move forward with the grief process and begin to put this behind them,h Brockstedt said.

Brockstedt also said large verdicts are unusual in Delaware, but gby affirming this verdict, the Supreme Court is recognizing that juries have the ability to evaluate the facts of the case and appropriately compensate the families.h

In an earlier appeal, Brockstedt said, gJudge Bradley ruled that this verdict was not unreasonably inflated by the testimony from the punitive damages case. So in affirming that ruling, the Supreme Court has said itfs not an inflated verdict. Theyfre saying a Delaware jury got it right.h

The opinion, which quotes extensively from the trial records, finds that the trial judge did not abuse his discretion by not ordering three separate trials of the various claims, and that because of the way the trial unfolded, Beebe had waived its right to limit the familyfs claims for mental anguish. The court also found that the judgefs instructions to the jury were sufficient for the jury to render a fair verdict.

Fried could not be reached for comment Monday. But in his prepared statement, he wrote, gBeebe Medical Center subsequently entered into an agreement to sell its nursing home, but not the building, to a group of private investors who have extensive experience in the ownership and operation of Delaware long-term care facilities. The investors are building a new 120-bed long-term care facility on Route 24 west of Long Neck Road.h

Fried said Lewes Convalescent Center will continue to operate until the new facility is complete.


1375.Assisted Living, Erratic Regulation
With No Federal Regulation And Limited State Laws, Negligence Cases Are Growing
Nov.13, 2006
(CBS) Dennis Camarata lost his father in a way no child could imagine.

At age 83, Mike Camarata was healthy and active ? but dementia had turned him almost childlike. So his family placed him in an assisted-living facility in Michigan because it would feel more like home, CBS News chief investigative correspondent Armen Keteyian reports.

"They encouraged you to wander around," says daughter-in-law Mary Camarata. "He would go in the refrigerator and drink orange juice out of the jug."

In April 2004, Mike Camarata drank from a jug he found in an unlocked kitchen cabinet. But he wasn't drinking juice ? it was a toxic, industrial dishwashing detergent containing lye.

"The chemical just literally burned his entire mouth and then burned him all the way down," says Dennis.

Four days later, Mike Camarata died what Dennis calls "a horrific death."

So how could a toxic chemical be stored, unlocked, in an Alzheimer's wing? One reason: Unlike nursing homes, the nation's 36,000 assisted living facilities ? places designed for seniors who don't need constant medical attention, just a little extra help ? are not subject to any kind of federal regulation. A CBS News investigation has found that state laws are literally all over the map.

For example, only 32 states require CPR and first aid certification. Just 24 require a nurse on staff, and Alabama is the only state in which the medical director must be a doctor.

"No real policies. No real sanctions. No accountability," says
Jules Olsman, an elder-care attorney.

And no way, say elder-care experts and industry insiders, to track what they say are a growing number of negligence cases.

In Pennsylvania, 69-year-old Angelita Torres was an Alzheimer's patient who wandered away from an assisted living facility. She was found drowned in a nearby canal.

In Georgia, 70-year-old Ann Wideman should have been moved from assisted living to a nursing home after she became bedridden. Instead, the facility kept her; she developed a massive bedsores and died from the infection.

"They knew and they didn't do anything about it," says Toni Godfrey, her daughter. "They let her die."

In Michigan, where Mike Camarata died, facilities outnumber inspectors 100-to-1. There is no requirement that staff members for Alzheimer's residents receive any special training. As for regular caregivers, they must be "awake and fully dressed."

Keteyian asked Marianne Udow, the woman in charge of assisted living in Michigan, who writes the laws that basically say "awake and fully dressed" is enough in some people's mind to provide resident care.

"Those are probably old regulations," she says. When told that they date from March 2006, she adds that the laws "probably been in place for many, many years and have not been updated."

When asked if families know what the quality or lack of quality of some of the care is in the state's assisted living facilities at the moment, she says, "I think they don't."

After Mike Camarata's senseless death, the state's only response was a letter, asking the facility if a "corrective active plan" was implemented.

"So you're father's death boils down to a 'don't do this again' memo?" Keteyian asks.

"Pretty sad, isn't it," says Dennis Camarata.

Correction: This story was updated Nov. 14, 2006, to reflect new information from the state of Minnesota. Minnesota recently implemented laws specific to assisted living that include background checks for all staffers and a nurse on-call at all times; last week the state confirmed to CBS News it had no staff requirements.

?MMVI, CBS Broadcasting Inc. All Rights Reserved.


1376.Complaints About Memory Are Associated With Alzheimer-Related Brain Damage
http://www.engelpub.com/

Memory complaints could offer an early warning system for Alzheimerfs disease

CHICAGO, Nov. 14, 2006--Researchers at Rush University Medical Center found that having complaints about memory problems is associated with changes in the brain related to Alzheimerfs disease. They reported their findings in the November 2006 issue of Neurology.

The researchers looked at the association between memory problems reported by study participants and signs of disease found in their brains after death. The study looked at autopsies of 90 older adults from the Rush Memory and Aging Project. The study included both participants who had been diagnosed with Alzheimerfs disease (23) and those that showed no clinical signs of the disease (67).

gOne of the most interesting findings of the study was that individuals who had yet to have any clinical symptoms of Alzheimerfs disease still showed a strong link between their self-reported memory complaints and brain pathology associated with Alzheimerfs disease,h said Lisa L. Barnes, PhD, from the Rush Alzheimerfs Disease Center. gThis information may allow us to use memory complaints as a measure to intervene at an early point in the disease process.h

To measure memory complaints participants were asked two questions:

How often do you have trouble remembering things?
How is your memory [now] compared to 10 years ago?
The researchers combined the answers to these two questions to create a scale to measure the severity of memory complaints. They used the memory scores taken closest to time of death. They also adjusted for confounding factors that might be related to memory problems like age, sex, and level of education.

The researchers then compared this scale with the levels of damage to the brain revealed during autopsy. The damage specifically looked at was the amount of amyloid plaques and tau tangles in the brain at the time of death. These plaques and tangles are the type of damage most closely linked to Alzheimerfs disease.

The researchers found that each unit of Alzheimer-related pathology was associated with one point higher score on the memory complaint scale. gOur results suggest that older persons with and without dementia possess some insight to their level of functioning, and this insight is related to actual changes in the brain,h said Barnes. gThe data suggests that if youfre having complaints therefs probably something going on. In other words, if mom notices that therefs something different about her memory, we need to listen closely and investigate further.h

The study shows that memory complaints should be taken seriously and not seen as just part of the aging process. gIn my opinion, it is possible to preserve your memory into old age,h said Barnes. gMemory loss is not an inevitable consequence of aging.

In fact, if you think you are having memory problems, you should probably see your doctor. As Barnes noted, galthough not all memory complaints will lead to Alzheimerfs disease, our data support the idea that memory complaints in older adults may represent the presence of significant Alzheimerfs disease pathology in the brain.h

gI donft want to cause concern for people who experience occasional memory loss, like losing their keys or forgetting their wifefs birthday,h said Barnes. gThe important point in our study was that the people who hadnft developed Alzheimerfs disease by the time they died, but complained about their memory performance, already had Alzheimerfs pathology in their brains. We donft know whether they might have eventually developed the disease had they lived longer. The data suggest, however, that memory complaints may be an early sign of disease in some people.h

The researchers at Rush are grateful for the remarkable dedication and altruism of the volunteers participating in the Rush Memory and Aging Project. The research was supported by grants from the National Institute on Aging, which leads the Federal effort to support and conduct basic, clinical, and social and behavioral studies on aging and on Alzheimerfs disease.


1377.Doctor to detail Scripps research
Possible approach to treating Alzheimer's Disease focus of talk by Malcolm Leissring at Beach Club.

By DAVID ROGERS
Daily News Staff Writer

Monday, November 13, 2006
http://www.palmbeachdailynews.com/
Dr. Malcolm Leissring has a interesting way of explaining the mechanisms responsible for the development of Alzheimer's disease.

The disease, which progessively damages memory and cognitive functioning, typically occurs when cells in the brain overproduce a protein called amyloid-B, or beta amyloid, and create a damaging plaque material.

To stop the development of Alzheimer's disease, scientists must create a medication that inhibits beta amyloid production, increases cells' ability to rid the brain of that protein, or both. That is, they have to turn off the faucet and open one or two chemical "drains" to solve the problem.

Stopping beta amyloid over-production cannot be the only potential solution, he said.

"That only represents about 5 percent of all Alzheimer's cases," he said. "And we know that in most cases, the 'faucet' is not turned up. That leads to the other possibility which is that one or more 'drains' are clogged. So you get the same effect but for a different reason."

Leissring, two other Scripps Florida scientists, and three Florida Atlantic University undergraduates are performing research on this type of dementia.

The scientist ? formerly of Harvard Medical School and its teaching affiliate, Brigham and Women's Hospital ? will discuss "The Forgotten Side of Alzheimer's" at 6:30 p.m. Friday at the Beach Club.

The talk is part of an educational dinner seminar presented by the Institute of Science and Health and the Arthur R. Marshall Foundation.

Yuequan Shen of the University of Chicago, colleagues there and with Argonne National Laboratory, also in Illinois, recently identified the structure of insulin-

degrading enzyme. That bivalve-shaped enzyme helps neutralize beta amyloid.

If a molecule can be created to trigger its latch, the enzyme could increase its release of beta amyloid-

inhibiting chemicals by 40-fold, according to Leissring.

For many years, much of Alzheimer's research focused on stopping beta amyloid production. Now, with the University of Chicago/Argonne National Laboratory discovery, scientists are working to activate IDE.

The Scripps Florida team is focusing on that approach.

Leissring has studied this angle with his former Brigham and Women's Hospital colleague Dennis Selkoe, a leader in Alzheimer's disease research. The two scientists reviewed and wrote commentary about the Shen and company breakthrough for the online edition of the journal Nature.

"Selkoe could win the Nobel Prize for his Alzheimer's research," Leissring said.

"Our group was the first to show that if you increase the drainage system by increasing the amount of these proteases that degrade beta amyloid, we could completely prevent Alzheimer's disease inside an animal model," Leissring said. Proteases start and stop enzymatic activity by cutting the molecular link between amino acids.

Scripps scientists are aided by a $10 million Kalypsys research robot that can quickly screen thousands of chemical compounds a day for potential drug uses. Scripps is the only academic facility with such a device, he said. The institution, however, needs more funds to keep its laboratories running.

"I was over budget the day I walked into the lab. Currently government funding is at record lows. It's just tragic because there are so many new opportunities that have emerged in the last five to 10 years. We really should be accelerating," he said.

"So this robot, I liken it to a NASCAR race car just sitting there in your driveway. All we need is some gas to fill up the tank. It's not going anywhere unless we get some money to use it."

The cost to attend Friday's dinner is $150. For more information, call Teresa Dailey at 969-7519.


1378.Elder Abuse Resources
How To Spot Elder Abuse, And What To Do About It
NEW YORK, Nov. 14, 2006
(CBS) Each year hundreds of thousands of older persons are abused, neglected, and exploited by family members and others. Of the known cases of elderly abuse and neglect, researchers say 89 percent happened in private homes, and more than half at the hands of children or other relatives.

Many victims are people who are older, frail, and vulnerable and cannot help themselves and depend on others to meet their most basic needs.

What is elder abuse?

Elder abuse is an umbrella term referring to any knowing, intentional, or negligent act by a caregiver or any other person that causes harm or a serious risk of harm to a vulnerable adult.

What makes an older adult vulnerable to abuse?

According to the National Center on Elder Abuse, social isolation and mental impairment (such as dementia or Alzheimer's disease) are two factors that may make an older person more vulnerable to abuse. But, in some situations, studies show that living with someone else (a caregiver or a friend) may increase the chances for abuse to occur. A history of domestic violence may also make a senior more susceptible to abuse.

What should you do if you see or hear of abuse?

If you see someone being physically hurt or threatened with a weapon, call a law enforcement emergency line such as 911. Be part of their "safety plan," the National Clearinghouse on Abuse in Later Life recommends. A safety plan is created by the victim with the help of a professional. The intent is to plan for a victim's safety needs before another violent episode erupts. If you believe they are in immediate danger, call 911.

Are there criminal penalties for the abusers?

It is a violation of State and Federal law for any person, including facility staff, volunteers, visitors, family members or guardians, or another resident, to neglect or abuse a resident. The National Academy of Elder Law Attornies can help.

Although there are variations across the country, in most states there are several laws that address criminal penalties for various types of elder abuse. Laws vary state to state. Some states have increased penalties for those who victimize older adults. Increasingly, across the country, law enforcement officers and prosecutors are trained on elder abuse and ways to use criminal and civil laws to bring abusers to justice.


1379.Omega-3 fatty acid may slash dementia risk - study

By Stephen Daniells
http://www.nutraingredients.com/
15/11/2006 - Increased bloods levels of the omega-3 fatty acid docosahexaenioc acid (DHA) could slash the risk of dementia and Alzheimerfs disease, suggests a new study from the US.

gSubjects with baseline plasma PC DHA levels in the upper quartile experienced a significant 47 per cent lower risk of dementia compared with participants with levels in the lower three quartiles,h wrote lead author Ernst Schaefer, from Tufts University, Boston.
The research adds to a growing body of science linking intake of the omega-3 fatty acids, mainly DHA, to improved cognitive function and slower cognitive decline.

Indeed, only last month scientists from Karolinska University Hospital Huddinge in Sweden reported in the same journal that supplements of omega-3 fatty acids may slow mental decline in people with very mild Alzheimers disease, but no effect was observed in people with more advanced forms (Archives of Neurology, Vol. 63, pp. 1402-1408).

Alzheimer's disease is the most common form of dementia and currently affects over 13 million people worldwide. The direct and indirect cost of Alzheimer care is over $100 bn (? 81 bn) in the US alone. The direct cost of Alzheimer care in the UK was estimated at ?15 bn (? 22 bn).

The new prospective follow-up study, published in the November issue of Archives of Neurology (Vol. 63, pp. 1545-1550), looked at the association between DHA levels and dementia in the blood of 899 men and women (average age 76) who were part of the population-based Framingham Heart Study.

The participants, who were free of dementia at the start of the study, provided blood samples and underwent neuropsychological testing, while subgroup of 488 also filled out a semi-quantitative 126-item food frequency questionnaire (FFQ) to assess their diet, including fish consumption.

After an average of nine years of follow-up, the researchers documented 99 cases of dementia, including 71 with Alzheimer's disease.

After controlling for other known risk factors for dementia, including age and homocysteine levels, and dividing the study population into quartiles based on levels of DHA, the researchers found that men and women in the quartile with the highest DHA levels had a 47 per cent lower risk of developing dementia and 39 per cent lower risk of developing Alzheimer's disease than the other three quartiles with lower DHA levels.

Among the participants who completed the FFQ, those in the top quartile of blood DHA levels reported that they ate an average of 0.18 grams of DHA a day and an average of 2.9 fish servings a week, while participants in the other quartiles ate substantially less fish (between 1.3 and 2.3 servings per week).

"In our study, the correlation between [blood] DHA content and fish intake was significant, indicating that fish intake is an important source of dietary DHA," wrote the authors.

The researchers did not perform a mechanistic study to elucidate the beneficial effects of the DHA. It has previously been reported, however, that DHA is involved in the membrane of ion channels in the brain, making it easier for them to change shape and transit electrical signals.

The study, does have several limitations that should be noted, including only taking DHA measurements on one occasion, and having dietary data on only a subset of participants.

"In the future, it will also be important to determine whether combined dietary supplementation with DHA can decrease further mental deterioration in patients with established dementia," concluded the researchers.

In an accompanying editorial, Martha Clare Morris, from the Rush University Medical Center, Chicago, said the study was an gimportant contribution to a young field of study on diet and neurodegenerative diseasec [and] provides the first evidence that direct measure of DHA in human plasma is related to lower Alzheimer disease risk.h

Morris also noted that, while fish consumption was correlated with DHA levels, there was no significant link between eating fish and Alzheimer's risk, possibly because the study was underpowered to fully observe such an effect, if such a relationship existed.

The risk of pollutants from oily fish, such a methyl mercury, dioxins, and polychlorinated biphenols (PCBs) have led to some claims to reduce fresh fish intake, especially for pregnant women who may damage the development of their babies.

gThe only way to resolve the risk-benefit question is to examine, directly in humans, mercury intake from fish and its effect on various health outcomes relative to the beneficial effects of the omega-3 fatty acids consumed,h said Morris.

Such concerns has seen the number of omega-3 enriched or fortified products on the market increase. Most extracted fish oil are molecularly distilled and steam deodorised to remove contaminants.

According to Frost and Sullivan, the European omega-3 market was worth around ?160m (?108m) in 2004, and is expected to grow at rates of 8 per cent on average to 2010.

E-mail this page to a colleague
Print in friendly format
Market reports, buy online now!


Tuesday November 14, 05:27 PM
1380.World's largest study into Alzheimer's launched
By 7News@http://au.news.yahoo.com/
Scientists are calling for volunteers to take part in the world's biggest study into Alzheimer's disease.
The study led by the CSIRO, was launched in Melbourne today and will involve 1,000 people over three years.

They are confident of finding a cure for a disease that affects 200,000 Australians. ADVERTISEMENT

Researchers will look at lifestyle, diet and genetic factors; basically anything that could provide clues as to the cause of this disease.

They will also examine brain scans of all volunteers, to determine if a particular protein found in the brains of Alzheimer's patients triggers the condition..

"It looks like some of the people who are going to get Alzheimer's have some of this protein accumulating in their brain and we think this might mean they are going to get the disease in the future," said Professor Ames.

One of the first trial participants will be ACCC chairman Graham Samuel.

His 83-year-old mother, Shirley, died from Alzheimer's three weeks ago after a 15 year battle.

"She had not known our names or been able to identify with us for many many years," he said today.

Some 200,000 Australians now suffer dementia. That figure is tipped to explode to more than 700,000 within 50 years, making it the number one cause of death in this country.
But researchers are confident that within 20 years they will have developed a preventative drug to treat the early stages of the condition.


1381.Alzheimer's death toll soaring
LOS ANGELES, Nov. 15 (UPI) -- Death rates from Alzheimer's disease are soaring, making it a top cause of death, according to new data released by California officials Wednesday.

In fact, for the first time, Alzheimer's has claimed a spot on the list of Top 10 causes of death in Los Angeles County, said officials from the Alzheimer's Association of Los Angeles and the County of Los Angeles Department of Public Health.

According to the data, from 1994 to 2003 death rates from diseases such as breast cancer, HIV/AIDS, stroke and lung cancer were down in Los Angeles County, while the death rate from Alzheimer's disease jumped by a stunning 220 percent.

Statistics from the 2003 report of Mortality in Los Angeles show Alzheimer's disease has rocketed to the eighth leading cause of death for Los Angles County residents, between colorectal cancer and breast cancer, officials said.

Adjusting for race groups, between 1994 and 2003, the death rates from Alzheimer's increased among all populations in Los Angeles County, rising 233 percent for whites, 200 percent for Hispanics, 138 percent for blacks and 100 percent among Asian/Pacific Islanders, they said.

"With the enormous size of the Baby Boomer generation, which is getting older and living longer, the impact of Alzheimer's disease is escalating at a dramatic rate and is only going to get worse," said Peter Braun, executive director of the Alzheimer's Association of Los Angeles. "It is also clear that many more people suffer from Alzheimer's than we know, since the cause of death is often listed as pneumonia or another illness that accompanies Alzheimer's. We need to realize that unless something changes, the toll on society brought on by the epidemic of Alzheimer's disease will be profound and devastating."


1382.Analysis: Bracing for Alzheimer's avalanche
By LAURA HEATON
UPI Correspondent
WASHINGTON, Nov. 15 (UPI) -- Preparing for the crush of an estimated 7.7 million Americans who will be afflicted with the debilitating mental disorder Alzheimer's disease by 2030, leaders from science, business, government and caregiving must join to create a "road map" to meet the crisis head-on, health policy experts said this week.

Speaking at a forum in Washington entitled "Preparing the Country for the Alzheimer's Epidemic," Newt Gingrich, founder of the Center for Health Transformation, said Alzheimer's disease is "rivaling diabetes and cancer as one of our greatest challenges."

He called for the development of a "road map" that would lay out a comprehensive approach to dealing with the societal costs of the devastating illness, expected to affect one in 10 people over the age of 65 and half of individuals who live to be 85 and older.

Gingrich said he hopes this road map will lead to a congressional hearing and concrete measures by the legislative and executive branches. Legislators need to mobilize for Alzheimer's the way they have for HIV/AIDS and avian flu, Gingrich said.

However, on the positive side, scientists and doctors say there is real potential to harness the progress made in the field of medicine and apply it effectively toward finding a cure for Alzheimer's, or at least improve treatment.

Molecular medicine is "catalyz(ing) a transformation in health, healthcare, and the health delivery system," said Andrew von Eschenbach, acting commissioner of the Food and Drug Association.

He said the emergence of molecular medicine has revolutionized the way diseases are treated. In the old model, diagnostics and therapeutics were separate, whereas in the new model they are congruous, he said.

"(We are witnessing) a metamorphosis of medicine," said von Eschenbach. Therefore, the way we think about healthcare needs to change."

Von Eschenbach cited in particular his hope that his agency will "deliver the fruits of those discoveries and developments to the patient."

Highlighting the advantages of molecular medicine, forum participants also stressed the role of preventative care, which can be especially effective now that patients can screen to see if they have a predisposition for diseases like Alzheimer's.

This is a disease that "begins its corrosive march through a brain up to 20 years before symptoms appear," Gingrich said, and patients can incorporate preventative and early-detection methods into their lives.

One challenge now, however, is the fact that "people at large don't see Alzheimer's disease as an epidemic," said Robert Essner, CEO of Wyeth Pharmaceuticals. He suggested that a sense of urgency in combating Alzheimer's is "very much needed" and advocated for a "coordinated response" to this disease.

"(Alzheimer's) could be like HIV/AIDS -- a disease that, for most sufferers, went from a lethal diagnosis to a treatable chronic condition within six years of its discovery," he said.

But the question of funding still looms.

"We don't have a business model," said Eschenbach. He said he took on responsibility in his role at the FDA for "developing the business case" to promote collaborative efforts to prepare for the Alzheimer's epidemic.

Given the power shift in the U.S. Congress, the task of securing funding may not be quite as difficult as it was last year, some observers say, when Bush's budget for fiscal year 2007 decreased funding for research and eliminated funding for several Alzheimer programs.

Ironically, Gingrich noted, the prevalence of Alzheimer's is a consequence of medical breakthroughs that have made an increased life span possible in the United States. "Alzheimer's is a disease of success," he said.


1383.On Alzheimer's 100-Year Anniversary, Scientists Warn Aging Boomers Will Multiply the Number of New Cases

http://journalism.berkeley.edu/ngno/

By Jessica Meyers, November 15, 2006 04:48 PM


SAN FRANCISCO-Alzheimer's disease isn't going away. It's increasing and scientists say as the baby boomers age, it could lead to the collapse of the nation's healthcare system in coming decades.

"If nothing is done to reduce the number of cases in the next decade, it could bankrupt the healthcare system," Dr. Ronald Peterson, the director of the Mayo Alzheimer's Disease Research Center said in a telephone interview.

Four and a half million Americans are currently affected by the degenerative disorder that attacks the brain's nerve cells. Treatment costs have reached at least $100 billion annually, according to estimates by the Alzheimer's Association and the National Institute on Aging. Up to 16 million people will have the disease by 2050.

Although the past 15 years have shown considerable advancements in the field, what will make the difference now is money, said Bill Fisher, CEO of the Alzheimer's Association's Northern California & Northern Nevada chapter. The last federal budget had a $7 million decrease in the National Institute of Health's additional research funding.

"One of the things it will take is a more robust investment on the part of the federal government," he said adding that he would like to see an additional $350 million coming from the new Congress. "This really is a tremendous opportunity and we have some of the brightest scientists working on the issue."

Dr. Lennart Mucke said study of the disease has come a long way since 1906 when German doctor Alois Alzheimer discovered abnormal brain tissue in a woman who died from an unusual mental illness.

Mucke, a professor of neurology and neuroscience at the University of California, San Francisco and director of its Gladstone Institute of Neurological Disease, spoke Wednesday at San Francisco's Commonwealth Club.

He said clinical and technological advances have made it possible to identity the disease while people are still alive. Furthermore, scientists have recently identified ways to reduce detrimental proteins like amyloid beta peptides that deplete memory.

"Proof is in the pudding," said Mucke. "The outcome of the trials are still being awaited but early detection is the key and that is where the field is heading."

Alzheimer's disease begins with simple forgetfulness like misplaced car keys but gradually destroys memory and the ability to function to the extent that patients can no longer feed themselves. Increasing age and family history are the greatest risk factors for Alzheimer's, but scientists are uncertain why some 65-year-olds get this form of dementia and other 85-year-olds never do. Once it hits, a person will live an average of eight years.

"The disease likes to strike like a sniper from a rooftop," said Mucke, whose grandfather suffered from Alzheimer's. "This illness is truly wicked in that it robs people of the image of who they really are."

Although positive about the latest developments, Peterson cautioned against too much overconfidence. "We have a greater understanding of the underlying pathology of what it means to have the disease," he said. "I think it is quite likely we are going to get lucky with the amyloid process but it's another issue whether it's going to eliminate the disease."

Hal Waterman, 70, listened attentively to Mucke. He's unsure there's enough funding anywhere to appease his concerns. "I have a father who died of Alzheimer's," he said. "If you can't remember that you scrubbed your legs in the shower, do you have Alzheimer's?"


1384.Science Journal: Alzheimer's research makes dramatic shift
Friday, November 17, 2006
http://www.post-gazette.com/
By Sharon Begley, The Wall Street Journal


For any normal field of science, the conclusion that "there is more to (fill in a disease) than (fill in leading but unproved hypothesis) alone" wouldn't cause anyone to bat an eye. After all, science is supposed to consider all reasonable ideas. But Alzheimer's disease is not your normal field of science.

Proponents of the leading theory of Alzheimer's have been in pitched battle with scientists who have other ideas about this awful neurodegenerative disease. For more than 20 years, the leading theory has held that sticky blobs in the brain called amyloid plaques cause Alzheimer's. Because that idea has numerous problems, doubters argued that the plaques might be innocent bystanders to the real, "upstream" culprit. If so, targeting the plaques, or the rogue protein called beta-amyloid that forms them, would do nothing to help the 4.5 million Americans who suffer from Alzheimer's.

You might think this debate would play out with each side conducting research, in a "may the best science win" approach. But as I've written before, many scientists whose work challenges the amyloid dogma have been unable to publish in top journals, and their grant proposals, "go down in flames," as Mark Smith of Case Western Reserve University School of Medicine told me. "Among the major journals and funding agencies, the attitude was, 'if it isn't amyloid, it isn't AD.'"

Hence the impact of that "there is more to" statement. It is the focus of a paper in the October issue of the journal Alzheimer's & Dementia reporting on a "research roundtable" convened by the private, nonprofit Alzheimer's Association. Finally, academic scientists and leaders in biotech, medical imaging and big drug companies recognize "there is more to AD than B-amyloid alone," the paper concludes. Which is why the roundtable's goal "was to address, primarily, strategies that do not hinge on directly modulating levels of B-amyloid" (my emphasis).

It's a remarkable turnaround. "This is the first concerted effort by the Alzheimer's Association to focus on things beyond beta-amyloid," says John Trojanowski of the University of Pennsylvania, who has done pioneering work on the role of so-called neurofibrillary tangles in the disease.

To get a sense of what a sea change this is, consider the Alzheimer's drug pipeline. Five drugs have been approved in the U.S. One (tacrine) causes liver toxicity, so is rarely prescribed anymore. None of the other four treat what anyone considers the real cause of the disease. Instead, they nibble around the edges, using strategies to maintain the brain's "cognitive reserve" so that when Alzheimer's sets in you don't become senile quite so fast. None of the drugs provides more than marginal benefit, if that, and help only some patients. And the disease keeps marching through the brain.

Some of the estimated 100 Alzheimer's drugs in clinical trials also nibble around the edges, such as by trying to lower cholesterol or inflammation (thought to worsen Alzheimer's). But of those that aim at a suspected cause of the disease, "the pipeline is full of antiamyloid therapies," says William Theis, vice president for medicine and science at the Alzheimer's Association. "The field was lulled into a false sense of confidence that beta-amyloid was the culprit," says Dr. Trojanowski. "But there is a great deal of uncertainty that the beta-amyloid hypothesis will be validated, although some stalwarts still strongly believe in it. We need to have a balanced portfolio of targets."

Thankfully, there are other suspects for what causes the disease. This month marks the 100th anniversary of Alois Alzheimer's report on his senile patient, Auguste D.: Her brain had stringy tangles inside neurons and "senile plaques" around them. The tangles, it turns out, are made of a protein called tau that gets transformed in such a way that strands of it stick together like cold pasta. The plaques are those globs of beta-amyloid. For many reasons, including the discovery of genes having to do with amyloid, the search for causes and treatment focused on that.

But when you think about it, concluding that B-amyloid and plaques cause Alzheimer's is like believing a scab on your knee causes pain. The scab is the body's response to an earlier injury. Similarly, there is evidence that amyloid plaques don't cause Alzheimer's.

Some elderly people who die with the disease don't have senile plaques. Some who show no sign of dementia do. When an Alzheimer's brain has plaques, they often are not where neurons have died, casting doubt on their toxicity. Also, in people with early Alzheimer's, tau tangles sometimes form before plaques, suggesting that plaques are a response (and maybe a therapeutic one), not a cause. If so, ridding the brain of plaques could cause harm.

"I definitely think it's time to think along other lines of treatment, and that's finally becoming more widespread," says Robert Mahley, president of the nonprofit J. David Gladstone Institutes, San Francisco, and a leading Alzheimer's researcher. "Big pharma has had all its eggs in (the amyloid) basket, and is starting to worry about that."

As a result, there is new emphasis on finding pathologies that lie upstream of beta-amyloid and plaques, or that have nothing to do with them. Next week, I'll discuss some of these ideas and experimental treatments based on them.


Public release date: 17-Nov-2006

Contact: Paul Francuch
francuch@uic.edu
312-996-3457
University of Illinois at Chicago

1385.Yeast model shows promise as Alzheimer's test
A century ago this month, German psychiatrist Alois Alzheimer formally described characteristics of the neurodegenerative disease which ultimately came to bear his name. While international efforts to learn about Alzheimer's disease and develop treatments have progressed significantly in recent years, a cure remains an elusive goal.

A new research tool developed by Susan Liebman, distinguished university professor of biological sciences at the University of Illinois at Chicago, may ultimately provide a means for treating the earliest stage of Alzheimer's, thereby stemming its progression.

Alzheimer's disease is characterized by the formation of plaques in the brain largely composed of fibers made from a peptide called beta-amyloid, or A-beta, for short. There is abundant evidence to support the hypothesis that accumulation of A-beta peptide triggers the appearance of Alzheimer's. But while earlier research suggested the A-beta fiber caused Alzheimer's, recent research points at much smaller aggregates of the peptide as the culprit.

"We've developed a yeast model system in which A-beta small aggregate formation can be detected," said Liebman. "The system employs a fusion of the human A-beta peptide to a functional yeast protein, called a reporter protein, which is only active in allowing cells to grow on test media if the fusion does not form aggregates."

Liebman said the yeast model system can be used to develop a high throughput assay to screen small molecules to find those that inhibit the A-beta dependent aggregation. "We'll screen a library of drugs and compounds, looking for ones that allow our yeast with the reporter protein to grow."

She said after the assay conditions are perfected, the screen will be ready for an automated process that will allow for fast testing of many compounds. Medicinal chemists would then study the structures of compounds that pass the screen and design compounds that enhance the activity without being toxic. Animal and human trials would follow.

"One promising, emerging approach for treatment of Alzheimer's disease is to prevent these smaller aggregates from forming," said Liebman. "Disruption of these small aggregates rather than the larger fibers seems prudent since inhibition of A-beta fiber formation might cause the smaller aggregate species to accumulate, and since inhibiting smaller aggregate formation should also prevent the initial formation of the fibers."

###
The findings were reported in BMC Biology. It was the journal's most viewed article this past month. UIC graduate student Sviatoslav Bagriantsev worked on the project in Liebman's laboratory and co-authored the paper.


1386.Problems possible in Alzheimer treatment
CLEVELAND, Nov. 16 (UPI) -- U.S. researchers have determined an enzyme that produces a toxic protein involved in Alzheimer's disease is also important for nerve cell myelination.

The finding by Riqiang Yan and colleagues at the Cleveland Clinic suggests targeting the BACE1 enzyme as an Alzheimer disease treatment might produce significant adverse side effects.

Most nerve cell axons are wrapped with a layer of myelin, which acts as an insulator to allow nerve impulses to travel more quickly to their destination. Riqiang Yan and colleagues studied mice with a deletion of the BACE1 gene.

The researchers found the thickness of the myelin sheath in the mice was reduced along axons throughout the brain and spinal cord. Those effects were visible as early as 15 days following birth and lasted into adulthood.

The mice also exhibited lower pain thresholds and decreased grip strength -- both typical signs of demyelination.

The researchers concluded that although inhibition of BACE1 may reduce the conversion of amyloid precursor protein into the plaques deposits seen in Alzheimer disease, the study's results suggest that as a therapeutic technique, it should be approached with caution.

The research is presented in the December issue of Nature Neuroscience.


1387.Occupational Therapy Helps Those With Dementia
11.16.06, 12:00 AM ET
http://www.forbes.com/
THURSDAY, Nov. 16 (HealthDay News) -- Occupational therapy -- training to do simple things around the house -- improved the lives of people with dementia such as Alzheimer's disease, as well as the people who care for them, a Dutch study found.
The results of the study, reported in the Nov. 18 British Medical Journal, could help change the attitude of health insurance companies and Medicare about paying for occupational therapy for persons with dementia, one expert said.

"I like the validation of what I knew instinctively," said Elicia Dunn Cruz, an assistant professor of occupational therapy at the University of Texas Medical Branch, Galveston.

Medicare sometimes refuses to pay for such therapy because of a belief that people with dementia "don't have a good rehabilitation potential," Cruz said, an attitude also shared by some, but not all, health insurers. "I think this article counters that," she said.

In the study, researchers at the University Medical Center Nijmegen divided 135 people 65 and older who'd been diagnosed with mild to moderate dementia into two groups. One group received 10 home-based sessions with experienced occupational therapists over five weeks who taught the patients to use various techniques to cope with mental decline. The people looking after them were taught methods of coping as well.

Assessments six weeks and three months after the therapy found that 75 percent of the patients who had the training showed an improvement in motor skills, and 82 percent needed less assistance in day-to-day tasks. The same sort of improvement was seen in only 10 percent of those who did not get the training.

Nearly half the caretakers who received the training felt more competent to do their duties, compared to a quarter of those who did not.

"Because outcomes such as improvements in activities of daily living and sense of competence are associated with a decrease in need for assistance, we believe that in the long term, occupational therapy will result in less dependence on social and health-care resources and less need for institutionalization," the researchers wrote.

Mary Mittleman, director of the psychosocial research program at New York University's Silberman Aging and Dementia Research Center, said she knew of no previous controlled study on occupational therapy for dementia patients.

Mittleman herself just reported a long-term study showing that spouses of Alzheimer's patients are less likely to place their loved ones in a nursing home if the spouses receive enhanced counseling and caregiver support.

The study of 406 spouses/caregivers found that those who received sessions of individual and family counseling, access to telephone counseling and participation in a support group delayed placing a loved one in a nursing home by about 18 months, compared to those who did not.

As for occupational therapy, Cruz said that training families to use adaptive techniques using familiar objects such as clocks and calendars can help people in the early stages of dementia. "It makes Alzheimer's disease less of a death sentence," she said.

Families can consult their primary-care physician about a referral to a rehabilitation clinic that provides in-home services, Cruz said: "There is a huge home industry, and occupational therapy is very much a part of it. The rub is that if a patient has a diagnosis of dementia that makes it difficult to get coverage. The insurers want to cover only people who are going to get well again. This study may help to change that."

More information

A professional's look at occupational therapy for dementia patients is provided by the University of Texas Medical Branch at Galveston.


1388.Better Alzheimer's test developed
November 19, 2006

LONDON (BBC Health News) -- A new test may help researchers understand why a toxin builds up in the brains of Alzheimer's patients.

Amyloid beta protein accumulates in the brain in Alzheimer's disease but whether the body produces too much or cannot break it down is unclear.

But by labeling the protein with a carbon isotope, doctors can measure the rate of turnover, a report in Nature Medicine suggests.

Experts said the test could help improve diagnosis and treatment.

Doctors are already able to measure amounts of amyloid beta protein -- or abeta -- in the cerebrospinal fluid but that doesn't indicate why the build-up is occurring.

By working out whether the body is producing too much or is unable to break it down, researchers develop drugs too accurately target the right process.

Furthermore, the test may also prove useful in the diagnosis of Alzheimer's prior to the onset of clinical symptoms.

The team at the Washington School of Medicine gave eight healthy volunteers an intravenous infusion which contained an amino acid -- Leucine -- that had carbon molecules with one extra neutron.

They then took samples of cerebral spinal fluid -- the fluid that surrounds the brain -- over a period of 36 hours.

The body uses amino acids to form proteins so the researchers were able to measure how the carbon isotope was taken up in the production of amyloid beta protein and then how long it took to break the labeled proteins down.

Fast turnover

They found the production rate of the amyloid protein was 7.6% per hour and the clearance rate was 8.2% per hour -- much faster than anyone had predicted.

"Abeta has the second-fastest production rate of any protein whose production rate has been measured so far," said lead author Dr. Randall Bateman, assistant professor of neurology at Washington University Medical School. "In a time span of about six or seven hours, you make half the amyloid beta found in your central nervous system."

There are Alzheimer's drugs in development which either decrease or increase the clearance of the protein.

"This new test could let us directly monitor patients in clinical trials to see if the drug is really doing what we want it to," said Dr. Batemam. "If further study confirms the validity of our test, it could be very valuable for determining which drugs go forward in clinical trials and at what doses." He added: "We hope to study whether we can develop ways to identify potential Alzheimer's patients on the basis of a metabolic imbalance between Abeta synthesis and clearance rates."

Rebecca Wood, Chief Executive, Alzheimer's Research Trust, said: "The results so far suggest that both the production and clearance of amyloid from the brain is much faster than has previously been supposed. "It is very interesting and, if validated, the method could provide new avenues for scientists looking for better early diagnostic tests and improved ways of targeting and monitoring the effects of new drugs."

But she added: "The research used measurements of cerebral spinal fluid that surrounds the brain, but we need to assess what extent they reflect what it happening inside the brain itself. "More work is needed before we can say this is a valid and reliable method, but this research could bring us a step closer towards finding an answer to Alzheimer's disease."

Dr. Susanne Sorensen, Head of Research at the Alzheimer's Society said: "This test could be of real value in research into the processes that leads to Alzheimer's disease and in understanding what the drugs do. "However, it is not in its present format useful as a way to diagnoses Alzheimer’s routinely."


1389. Brain's Oxygen Supply Key to Alzheimer's Risk

By Ed Edelson
HealthDay Reporter
Monday, November 20, 2006; 12:00 AM

MONDAY, Nov. 20 (HealthDay News) -- Less oxygenated blood to the brain may mean a bigger build-up of the protein plaques that are so closely tied to Alzheimer's disease, new research shows.

The Canadian team says a specific gene may be key to this process

"If you have less oxygen, you turn up this gene and obviously generate more beta-amyloid [protein]. If you have a higher level of beta-amyloid, you form more plaque. If you have this plaque, then you will have dementia," explained lead researcher Weihong Song, a professor of psychiatry who holds a Canada Research Chair in Alzheimer's disease at the University of British Columbia in Vancouver.

His team described the findings in this week's issue of theProceedings of the National Academy of Sciences.

Experts have long known that lowered brain-oxygen levels, caused by reduced blood flow, increase the risk of Alzheimer's disease. For example, Song said, "If you have a stroke, you have a two or three times increased risk of dementia."

The link between low oxygen and plaque formation may be a gene called BACE 1, he added. This gene encodes a protein that converts the precursor amyloid molecule to the more dangerous beta-amyloid form.

In their studies with mice, Song's group found that lower oxygen levels increased the activity of the gene.

But its not quite that simple, added Dr. Ralph A Nixon, professor of psychiatry and cell biology at New York University and a spokesman for the Alzheimer's Association.

To start with, there is an ongoing debate about whether the amyloid plaques cause the loss of mental function seen in Alzheimer's disease, Nixon said.

"What this paper does is add to a hypothesis that relates to amyloid overproduction and accumulation in the brain," he said. "Whether it establishes an association is the issue."

Hypoxia -- low blood-oxygen levels -- "does a lot of things to the brain," Nixon said. "It has a lot of effects on brain function other than what is being described here. There should be at least some consideration of the broader context -- that hypoxia itself is a cause of impairment."

Nevertheless, Nixon said, the report "is an interesting additional link that has not been appreciated before between hypoxia and this metabolic pathway."

Nixon and Song did agree on one point.

"The study reinforces another message that has emerged in recent years -- that the health of the cardiovascular system is very important for the health of the brain," Nixon said. "The things one does to promote the health of the cardiovascular system are going to help the brain when it is challenged in Alzheimer's disease. Lifestyle factors such as diet and exercise are also an edge against hypoxia."

Song concurred. "If we can improve blood flow to the brain, maybe we can help slow Alzheimer's progression. This report provides the mechanics for that. Increasing blood flow for the heart also helps slow Alzheimer's disease," he said.

More information

Find out much more on Alzheimer's disease at the Alzheimer's Association.

SOURCES: Weihong Song, Ph.D., professor, psychiatry, University of British Columbia, Vancouver, Canada; Ralph A. Nixon, M.D., Ph.D., professor, psychiatry and cell biology, New York University, and spokesman, Alzheimer's Association; Nov. 20-24, 2006,Proceedings of the National Academy of Sciences


1390.More insight into Alzheimer's disease with Stanford discovery of possible cause
The finding, published in the November issue of the Journal of Clinical Investigation, offers researchers an insight into how humans may develop Alzheimer's, said the study's senior author Tony Wyss-Coray, PhD, associate professor of neurology and a researcher at the Veterans Affairs Palo Alto Health Care System.

2006-11-21.

(PressZoom) - STANFORD, Calif. - A peacekeeper in the body's defenses against infection may hold the key to understanding - and eventually treating - Alzheimer's disease. Researchers at the Stanford University School of Medicine discovered that when a molecule responsible for dialing down the immune system malfunctions in the brain cells of mice, the rodents develop symptoms of the degenerative brain disease.

The finding, published in the November issue of the Journal of Clinical Investigation, offers researchers an insight into how humans may develop Alzheimer's, said the study's senior author Tony Wyss-Coray, PhD, associate professor of neurology and a researcher at the Veterans Affairs Palo Alto Health Care System.

Alzheimer's disease is characterized by an excessive buildup of proteins into plaques and tangles of cellular gunk that are likely to cause brain cells to die and lose their connections to other neurons. But for the most part, scientists do not understand the underlying biological problems behind Alzheimer's, making it difficult for doctors to treat, let alone cure.

"We don't have a treatment that alters the course of the disease," said Wyss-Coray.

Wyss-Coray and Ina Tesseur, PhD, an instructor in the Department of Neurology, examined thin slices of the brains of Alzheimer's patients who had died, and discovered abnormally low levels of a molecule involved in controlling the body's response to infection. That molecule allows the brain to detect and respond to TGF-beta, or transforming growth factor, a protein teeming through our bodies, involved in fighting infection, stopping cancer and perhaps keeping brain cells alive.

No other researchers had seen this change before, so Tesseur and Wyss-Coray set out to investigate whether it had some connection to Alzheimer's disease. They hypothesized that by protecting neurons, TGF-beta may help prevent Alzheimer's disease. If the TGF-beta pathway is turned off, the brain becomes more susceptible to a toxic buildup of proteins.

"We tried to see what happens if we block neurons from getting this beneficial signal," said Wyss-Coray.

To investigate that hypothesis, the researchers genetically engineered mice with a defect similar to the one they found in the brains of Alzheimer's patients: These mice had brain cells that could no longer respond to TGF-beta's salutary signal.

The mutation did not directly affect the TGF-beta protein, which is found throughout the body. Instead, it blocked brain cells' ability to detect and respond to the molecule. This way, the TGF-beta pathway was active everywhere else besides the neurons of the mice.

Unable to receive the beneficial TGF-beta signal, the rodents with the broken pathway showed signs of Alzheimer's disease. Brain cells died as the mice grew older, and the cells failed to make connections to other brain cells, a defining trait of the cells.

The results were even more striking when the researchers blocked the TGF-beta pathway in mice that were already susceptible to an Alzheimer's-like disease. These mice had a rare version of a human gene that causes people to develop Alzheimer's in their 40s and 50s, said Wyss-Coray. Blocking TGF-beta in these mice caused the animals to display signs of Alzheimer's disease that researchers had until then failed to recreate. The brains of the mice had more dead cells and a protein buildup characteristic of the disease in humans.

"Our study offers the possibility that if you have a reduction in this pathway, then you can accelerate the pathology," said Wyss-Coray. The flip side is that activating the TGF-beta pathway may offer a treatment for Alzheimer's, he said.

In the past, researchers have tried using molecules that work like TGF-beta to provide protection against Alzheimer's, but they had trouble getting them into the brain, said Wyss-Coray. Those proteins, or the cells used to carry them, are too large to enter the brain through the bloodstream.

To sidestep that problem, Wyss-Coray is working with chemists to identify small molecules - drugs - that can boost the TGF-beta pathway in neurons. Because of TGF-beta's many roles in the body, Wyss-Coray will also be searching for molecules that act only on brain cells. He will test whether these drugs can ameliorate the Alzheimer's-like disease he created in mice.

Wyss-Coray said that for now the strategy is "wishful thinking," but based on the results of this study, it's worth trying.

###
Co-authors of the study included Kun Zou, PhD; Elisabeth Berber, PhD; Judith Van Can, and Amy Lin, PhD, who all were involved in the research while at the medical school's Department of Neurology. The John Douglas French Alzheimer's Foundation, the Alzheimer's Association and the National Institutes of Health funded the research.

Stanford University Medical Center integrates research, medical education and patient care at its three institutions - Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children's Hospital at Stanford. For more information, please visit the Web site of the medical center's Office of Communication & Public Affairs at http://mednews.stanford.edu.

Rosanne Spector
manishma@stanford.edu
650-725-5374


1391.Hormone Replacement Therapy May Improve Visual Memory Of Postmenopausal Women
Main Category: Women's Health / OBGYN News
Article Date: 22 Nov 2006 - 1:00am (PST)

Many women experience declines in their memory during and after menopause, a change thought to be due, in part, to the rapid hormonal changes they weather during that time.

Now, research from the University of Michigan Health System suggests that hormone therapy might help women retain certain memory functions. In a study in the new issue of The Journal of Clinical Endocrinology & Metabolism, they report that a group of postmenopausal women showed more brain activity during a visual memory test than did women who were not taking the hormone therapy.

The 10 postmenopausal women in the study, ages 50-60, were given hormone therapy or a placebo for four weeks, followed by a month with no medications, and then four weeks of the other treatment. Their brain activation was measured as they were shown a complex grid of 81 squares, with 40 of them darkened to form a pattern.

Participants were asked to find the matching image from a choice of two, with the new set of images presented after varying time periods (one to four seconds). During the time that the two images were shown, participants were asked to choose the one that matched the initial grid by pressing one of two buttons on an MRI (magnetic resonance imaging)-compatible response pad.

Those who were taking combined estrogen-progestin hormone therapy showed significantly increased activity in the prefrontal cortex, a region of the brain that is critical in memory tasks, compared with those on placebo (a pill with no medicinal value). The researchers used images from functional MRI, or fMRI, to compare the participants' brain activity.

"Our findings suggest that even relatively short periods of hormone therapy have effects on the memory systems that may be of benefit to some women during the perimenopausal transition or early postmenopause," says lead author Yolanda R. Smith, M.D., associate professor in the Department of Obstetrics and Gynecology at the U-M Medical School.

"Other studies have indicated that long-term hormone therapy is not beneficial for the prevention of chronic illnesses," Smith says. "But our study indicates that the effects of short-term hormone therapy on brain circuitry and function warrant further study."

The role of estrogen in maintaining brain function is of great significance as the population ages and the incidence of dementia increases, says senior author Jon-Kar Zubieta, M.D., Ph.D., associate professor of psychiatry and radiology at the U-M Medical School and associate research scientist at U-M's Molecular & Behavioral Neuroscience Institute (MBNI).

Zubieta notes that working memory - that is, a limited-capacity storage system that allows the brain to actively maintain and manipulate information that is critical for conducting many daily activities over short time periods - has been demonstrated to be less efficient in older adults. This decline has been linked with changes in the prefrontal cortex.

"Our finding of increased activation in the prefrontal cortex in older women using hormone therapy is important and suggestive of potential therapies that need to be explored further," he says. "Eventually, this could lead to new options for women as they enter a time when memory problems typically develop."

The researchers also point out that there have been shown to be risks with hormone replacement therapy. Information is available at http://www.nhlbi.nih.gov/health/women/pht_facts.pdf.

###

In addition to Smith and Zubieta, other authors were Tiffany Love, B.S., of the U-M Department of Psychiatry and MBNI; Carol C. Persad, Ph.D., of the Department of Psychiatry; Anne Tkaczyk, M.S., of the Department of Obstetrics and Gynecology; and Thomas E. Nichols, Ph.D., of the Department of Biostatistics at the U-M School of Public Health.

The research was supported in part by a grant from the National Center for Research Resources and an investigator-initiated grant from Pfizer Pharmaceuticals Group. Smith received an investigator-initiated grant from Pfizer Pharmaceuticals, Nichols has consulted for GlaxoSmithKline Inc., and Zubieta has received lecture fees from GlaxoSmith Kline Inc., Eli Lilly and Co., and Forest Laboratories.

Citation: The Journal of Clinical Endocrinology & Metabolism, "Impact of Combined Estradiol and Norethindrone Therapy on Visuospatial Working Memory Assessed by Functional Magnetic Resonance Imaging," first published ahead of print Aug. 15, 2006.

Contact: Katie Gazella
University of Michigan Health System


1392.Playing catch-up in Alzheimer's labs
SHARON BEGLEY
November 24, 2006 6:59 AM

The Wall Street Journal

In hockey, as in life, what you want is lots of shots on goal. After years in which most of the scientific firepower in Alzheimer's research was focused on the notorious ''amyloid plaques'' that gum up brain neurons like a wad of Wrigley's, this field is finally shaking off the amyloid dogma.

Thank goodness. ''If everything (now in the drug pipeline) crashes and burns,'' says Rudolph Tanzi of Harvard Medical School, who is leading a project in which 437 families with Alzheimer's are undergoing genetic screening, ''at least we'll have many more potential targets'' for Alzheimer's therapies.

As I described last week, the belief that amyloid plaques are the chief cause of this disease so dominated Alzheimer's research that it became ''orthodoxy,'' says Zaven Khachaturian, who oversaw Alzheimer's funding at the National Institute on Aging from 1977 to 1995. ''Having one view prevail is harmful; it becomes a belief system, not science.''

Orthodoxy also stifles research on other culprits. ''Where the field made its mistake was in trying to make everything fit one common (amyloid) pathway,'' says Robert Mahley, president of the J. David Gladstone Institutes, San Francisco. ''We've got to realize there are multiple ways you can wind up with (Alzheimer's).''

With that realization setting in, the search for ways to prevent, slow or treat Alzheimer's is entering what you might call its ''let 1,000 flowers bloom'' period.

How likely is Dr. Tanzi's crash-and-burn nightmare? Several treatments now in development focus on enzymes that, by snipping a particular protein, produce the sticky brain plaques. Solution: knock out the evil enzymes. But one enzyme, BACE1, also is important for myelination, the process that coats neurons with the insulation they need to work, scientists will report in December in Nature Neuroscience. Poor myelination underlies multiple sclerosis. Targeting BACE1, therefore, sounds like a good way to give Alzheimer's patients MS-like symptoms. The challenge will be to dial down BACE1 enough to prevent or reverse Alzheimer's without hurting myelination.

Another evil enzyme, gamma secretase, turns out to be used in gastrointestinal and lymphoid tissue. Disabling it to strangle production of amyloid may, therefore, produce serious side effects unless scientists can spare its healthy functions. The verdict is out on that, but Dale Schenk, chief scientific officer of Elan Pharmaceuticals, South San Francisco, says he's ''optimistic.''

A number of companies are pursuing immune approaches. If you sic antibodies on amyloid, perhaps with a vaccine, you should be able to eliminate amyloid and thus prevent plaques and Alzheimer's. But because amyloid is important for normal neuron function, eliminating it might not be a good idea.

If we have wasted decades and hundreds of millions of dollars on a bankrupt theory, that is a tragedy for the 4.5 million Alzheimer's patients in the U.S. today and the nine million expected by 2020. But all is not lost. With recognition that the sticky plaques that mark Alzheimer's are tombstones and not killers, researchers are resurrecting leads long overshadowed by the amyloid dogma.

In 1993, Allen Roses at Duke University discovered that a gene called apoE4 increases the risk of Alzheimer's. About all he got for his trouble was loss of funding and skepticism - even though apoE4 turns out to be behind 50 percent to 70 percent of Alzheimer's cases. (If you inherited two copies of apoE4, one from mom's egg and one from dad's sperm, your risk of developing AD is 50 percent to 90 percent; with zero copies, the risk is 20 percent.)

ApoE4 research hung on by its fingernails, and this month drug giant Merck and Gladstone announced a research collaboration, with a $3.25 million up-front payment, to develop Alzheimer's therapies based on apoE4.

One approach Gladstone scientists are working on is to turn the protein that apoE4 makes into its healthy cousin, apoE3. ''We've identified a dozen molecules that do this,'' says Dr. Mahley. Another is to block an enzyme that snips the apoE4 protein into fragments. These snippets enter neurons, attack their vital energy-making mitochondria, form toxic tangles and thus kill them. If you prevent the snippets from forming, maybe neurons would never face these killers.

In a recent paper, Dr. Roses, now at GlaxoSmithKline, expressed guarded optimism about a molecule called rosiglitazone. In a Phase II trial of 511 patients, it produced ''significant clinical improvement'' in some patients, GSK reported in January. Rosi seems to increase the number of mitochondria in neurons. Since fragments of the apoE4 protein attack mitochondria, a drug that keeps making new ones would keep neurons alive despite the attacks, like a battalion that remains at full strength, despite casualties, with new recruits.

Anti-inflammatory drugs and statins may protect brain neurons from Alzheimer's. So might blocking an enzyme that changes harmless proteins into the toxic tangles that kill neurons, or compounds that increase synapses as fast as Alzheimer's destroys them, or ...

Yes, the approaches are eclectic. This disease won't be felled by a single magic bullet. Researchers must scramble to make up for time lost on overemphasizing one approach.

AP-WS-11-24-06 0956EST


Posted on Sat, Nov. 25, 2006 thishttp://www.bradenton.com/mld/bradenton/
1393.When love blossoms in the nursing home
KAREN UHLENHUTH
McClatchy Newspapers
KANSAS CITY, Mo. - Jayne Porter and Raymond Brooks think they met in their retirement home breakfast room about three weeks ago. Sparks flew.

What was it exactly? Was it the way Brooks, 91, pushed Porter, 92, in her wheelchair?

"We don't know why," Brooks admitted. What he does know is this: These two residents of a long-term care unit at John Knox Village connected "right off the bat."

Intimacy happens, even at long-term care facilities. And when it does, what a tangled web it can weave. Care-center employees haven't always looked kindly on elderly people having romantic feelings - and acting on them. Family members who have the same reservations also have the power to short-circuit nursing-home romances, and have been known to do so.

Then there are the logistics. Double rooms, the standard in long-term care facilities, pose the same issues they do in college dormitories. And sometimes, nursing-home residents need help just getting in and out of bed.

Because of those factors and more, intimacy "has always been a touchy issue that tends to get swept under the carpet," said Marynell Hendricks, director of family education at Garden Terrace at Overland Park, Kan.

The complications are such that the Kansas City-based Center for Practical Bioethics, at the urging of some local long-term care facilities, convened a panel a year ago to debate the issues. From that came a set of voluntary guidelines, recently issued, emphasizing the need for care centers to establish a written policy, to train staff, and to protect vulnerable residents, particularly those with dementia.

But perhaps the most fundamental point in the report is that the desire for physical intimacy is perfectly normal among people until the day they die, and should be respected.

Although many people seem to consider sexuality and other forms of physical intimacy the exclusive prerogative of the young - and possibly those in midlife - Carol Scott said, "No matter what our age, sexual expression is a part of being human." She's Missouri's long-term care ombudsman and was a member of the bioethics center's panel.

In fact, a survey of 250 residents in 15 Texas nursing homes found that 8 percent of them said they'd had sexual intercourse in the preceding month, and 17 percent more were wishing they had. In a separate study cited in the journal Clinical Geriatrics, 90 percent of 63 physically dependent nursing-home residents said they'd had sexual thoughts, fantasies and dreams.

When those thoughts turn to action in the fishbowl environment of a long-term care facility, the results can be more intriguing than reality television.

Hendricks related the amorous adventures of a single man living in a facility she once managed. He had a "lady friend" living outside the facility whose daughter ferried her to the facility for regular visits. At the same time, the nursing-home staff noticed the man sitting and holding hands with a woman who lived in the same facility.

"It became an issue for our staff who felt they needed to say to him, 'What about this other person?'" Hendricks said. "They lost sight of the fact that this was an adult male who was able to make choices."

The morals and values of nursing-home personnel can bear heavily on such scenarios - but shouldn't, said John Carney, vice president of aging and end-of-life issues for the bioethics center. When romances start to blossom between residents, disapproving nursing-home employees have been known to separate couples by moving one person to a different floor or unit, or by moving wheelchairs apart in common areas.

"We need to get over that," said Carney, one of the authors of the bioethics center guidelines. "One of our purposes was to elevate this to a matter of respect as opposed to, 'Oh my God, why would they do that!'"

Compounding issues of morality is the possibility of litigation. Nursing homes are obligated to both respect the privacy and dignity of their residents, and, at the same time, to protect them. And what if someone is injured in the course of an intimate encounter?

Although nursing homes tend to act out of fear of lawsuits or sanctions from regulatory agencies, they needn't, said Daniel Reingold, president and chief operating officer of the Hebrew Home in New York. At his urging, his staff has taken an innovative approach to the matter. Facilities can protect themselves by making a written policy, training their staff, communicating with residents' families, and ensuring the safety of vulnerable residents, he said.

Where romance and intimacy are concerned, Reingold sees his role mostly as one of enabler.

"We lose so many things as we age," he said. "Vision, the sense of smell, mobility. Intimacy and touching are the last pleasurable things an elderly person gives up. What made us look into it was the notion that we need to preserve that pleasure.

"To see a 90-year-old woman acting like a teenager in love," he said. "How cool is that?"

When it comes to elder intimacy, the Hebrew Home in New York is acutely sensitive and "out there," says Daniel Reingold, its president and chief operating officer.

When the staff there learns of a coupling in the works, they don't wait for residents to ask for a private room. They make a point to relocate one of the partners to a private room if both partners are in shared rooms.

Reingold said that at the 1,000-resident facility, he currently knows of half a dozen, perhaps a dozen, people who are "exhibiting outward sexual behavior." To Reingold, it's not disconcerting - it's thrilling.

A decade ago, he and his staff began to seriously ponder the issue and how they might best serve their residents. He decided it required some attention when "a staff member came to me and said, 'Mr. So-and-so and Mrs. So-and-so are having sex. What should I do?'"

Reingold's response: "Tiptoe out and close the door."

Five or six years ago, policies were instituted. Training began.

Reingold remembers the staff being "incredibly appreciative. They said, 'Now we know what to do.'"

Very often, that's nothing at all. The policy at Hebrew Home is grounded "in the understanding that this is a resident right," Reingold said. "Anything that people might do at home, they're allowed to do here."


1394.Acumen, Merck amend Alzheimer's agreement
29th November 2006@http://www.pharmaceutical-business-review.com/home.asp
By Victoria Harrison
Acumen Pharmaceuticals has amended its existing license agreement with Merck & Co to grant a license to develop products using Acumen's technology for Alzheimer's disease.

The two companies signed a license agreement in 2004 to research and develop disease-modifying therapeutic drugs for Alzheimer's disease and other memory-related disorders utilizing Acumen's amyloid-derived diffusible ligand products (ADDL) technology.

AdvertisementUnder the terms of that original agreement, Merck obtained an exclusive license to research and develop monoclonal antibody products, an option to develop vaccine products, and the non-exclusive rights to develop diagnostic products. The amendment to the agreement grants Merck exclusive rights to develop and commercialize diagnostic products directed to ADDLs.

ADDLs are small protein assemblies that are widely believed to be the cause of Alzheimer's disease. They bind to synapses and initiate aberrant signaling, destroying the brain's capability to store and retrieve information. In collaboration with Merck, Acumen is developing an ADDL antibody program designed to prevent ADDLs from causing brain damage.

"There is strong synergy between Acumen's discovery capabilities and ADDL-related know-how, and Merck's discovery and development capabilities," said David Summa, president and CEO of Acumen.


1395.Alzheimerfs Disease:a 21st century challenge - Part 2: Whofs at risk?
http://www.tenerifenews.com/cms/front_content.php@29/11/2006
So, just what are my chances of falling victim to Alzheimerfs? Without a doubt, the greatest risk factor is increasing age. At 65 years of age there is just a 3% chance of becoming an Alzheimerfs patient, but this doubles with every 5 years, to roughly 48% by 85 years of age.

Causes of the disease are probably a combination of genetic and environmental factors.
A variant of the gene that enables the body to make a protein for development and maintenance of the brain, has been identified as significant, but not necessarily the cause of Alzheimerfs.
Given that similar gene structure will be found within families, one would expect Alzheimerfs to run in families and, to some extent this is the case. If you had two parents affected, your risk of having the disease at 80 years of age would be five times greater than if neither parent was affected.
Studies of twins, who have the same gene pattern, have been inconclusive. If one twin develops Alzheimerfs, the other twin has a high risk of developing the disease , but not necessarily at the same time. Does this suggest a genetic factor, or have twins had similar environmental experiences? Even racial groups who have a gene construct identified as a contributory factor in developing Alzheimerfs, have different risk factors in different environments. One study suggests that Cherokee Indians have a resistance to the disease!
There does seem to be a heart and head connection. Diseases that damage blood vessels, and in turn blood cells, greatly increase the risk of dementias in general. Strokes, high blood-pressure and diabetes damage blood-vessels. It must be stressed, however, that sufferers from these conditions do not automatically develop Alzheimerfs.
Similarly, head injuries, if sufficiently frequent, as in the case of boxers perhaps, may provoke a slightly increased risk, but lifefs average knocks are not considered a factor. Neither is mental stress, although a traumatic life experience may cause family and close friends to recognise an early stage of dementia that had not previously been apparent.
There have been several studies that suggest a high-fat, low-fibre diet increases the risk of Alzheimerfs, as well as all the other conditions of which we have been warned. Dietary fat apparently causes oxygen molecules to leap around and upset bodily functions. It seems this can affect brain tissues and contribute to the degenerative condition of Alzheimerfs. Countries where more fish is eaten had a correspondingly lower incidence of the disease.
While it is difficult to quantify, doctors generally agree that those who are mentally and socially INactive, seem to be at a greater risk of developing Alzheimerfs.
I do feel some concern that many of my grandchildrenfs generation seem to restrict mental and social interaction to pressing buttons, either to send messages to friends, or to negotiate cartoon characters through flashing lights.
We will be offering advice about gpreventionh in a later article.
In the meantime, I will eat plenty of fish, high in omega-3, do the daily Sudoku, meet friends daily, and look for a Cherokee Indian to share his secrets with me. by Linda Fullegar


1396.Ink paintings on sale to assist Alzheimer's patients
29 Nov 2006
Regina Lee
http://www.nst.com.my/

KUALA LUMPUR: gThe Long Goodbyeh is not the name of a tear jerker romance. It is what Alzheimerfs patients and their families live day by day, sometimes for many years.

The patientfs memory begins to fail, the personality changes and eventually someonefs husband or wife, father or mother is unrecognisable, and no longer knows their loved ones.

It is estimated that a staggering one in 20 Malaysians over 65 years old have Alzheimerfs disease. And most go undiagnosed because their families think it is part of the normal ageing process.

Living with and caring for an Alzheimerfs patient is often said to feel like a 36-hour day. But there is help. The Alzheimerfs Disease Foundation Malaysia (ADFM) was set up in 1997 to educate people about the disease and provide support to families and caregivers of Alzheimerfs patients.

They run a day care centre in Taman Seputeh, which is now running at full capacity with 16 patients. On the drawing board is a 420 square metre facility in Petaling Jaya, which ADFM hopes to move into by 2008.

gWefre also looking into purchasing the land next to our plot to expand the centre so we can care for more patients. Petaling Jaya is a good area as it is easily accessible by public transportation,h said ADFM Board of Trustees president Jeffrey Ng.

He was speaking at a Press conference for a month-long charity art exhibition at the Maybank Art Gallery, beginning Dec 13.

Forty-six works donated by 25 of the top local ink-painting artists, including Dr Foo Yong Kong, will be up for sale. The proceeds will go to ADFMfs building fund. The foundation hopes to raise RM2 million.


Nov. 29, 2006
Copyright ? Las Vegas Review-Journal

1397.Company to start human trials on Alzheimer's drug

Medication has proven effective in clearing plaque in brains of animals

By ANNETTE WELLS
REVIEW-JOURNAL
A Las Vegas pharmaceutical company expects to begin human trials early next year of a drug it believes has the potential to delay or stop the progression of Alzheimer's.

The drug, known as caprospinol, has proven effective in clearing plaque, known as beta-amyloid, in the brains of animals, said Janet Greeson, chief executive officer of Samaritan Pharmaceuticals, which is located along Convention Center Drive.

Beta-amyloid is viewed by many scientists as the cause of degeneration and dementia in people with Alzheimer's, Greeson said.

"It's the same as when we were looking for heart medication that cleared plaque out of the heart,'' she said of caprospinol's potential.

"This is the real deal. It completely clears beta-amyloid in animals, and there is a good indication that it will do it in humans.''

Samaritan Pharmaceuticals, which has been in Nevada since 1994 and has a lab at Georgetown University, submitted an Investigational New Drug application to the FDA for caprospinol on Oct. 29, Greeson said.

Tom Lang, chief drug development officer for Samaritan Pharmaceuticals, said Tuesday that the U.S. Food and Drug Administration had 30 days to question the company about the drug, and the company has answered all of the agency's questions so far.

The 30-day period ends today, so barring any eleventh-hour questions, Samaritan Pharmaceuticals should be cleared to begin human trials as of Thursday, Lang said.

"We don't think there are going to be any major hold-ups,'' he said. "We have had answers to all of their questions.''

Dr. Charles Bernick, professor of medicine at the University of Nevada's School of Medicine, said first phase clinical trials of caprospinol could begin as early next year.

Bernick, who is involved in other Alzheimer's studies and in the development of the Lou Ruvo Brain Institute in Las Vegas, was approached by Samaritan Pharmaceuticals a few months ago about participating in the human trials.

"There are a lot of different strategies being looked at with respect to Alzheimer's treatment, and now the approach is looking for agents that will affect the disease's projectory,'' Bernick said.

"Most other drugs don't change the disease's progression, whereas this drug and other agents target the disease process itself. It has the potential to delay and slow the progression, which would be huge.''

Alzheimer's is a degenerative brain disease. It usually begins with a gradual forgetfulness about recent events or familiar tasks.

In later stages, the person has difficulty communicating, often struggling to find words, finish their thoughts or follow directions.

According to federal statistics an estimated 4.5 million Americans have Alzheimer's.

The direct and indirect costs of caring for individuals with the disease is estimated at $100 billion annual.

By 2030, when the baby boom generation is over 65, it is estimated that the number of people with Alzheimer's will soar to levels exceeding the country's ability to treat them or absorb those costs.

"If you can delay Alzheimer's for five years you can reduce in half the number of people with it,'' Bernick said. "You don't even have to cure it. You just have to have something that can stop its progression.''

Samaritan Pharmaceuticals' lab is in Maryland, but its Las Vegas office handles patents and licensing of drugs developed by the company, Greeson said.

Samaritan develops drugs for the treatment of AIDS, Alzheimer's, cancer and heart disease, Greeson said.

In terms of what this means for Nevadans, Bernick said it fits into the general strategic plan of health sciences development in the state.

"With the Nevada Cancer Institute and the Lou Ruvo Institute and the academic health sciences center that is being pitched, all these things are kind of jelling now,'' he said.

"And, I think with Samaritan being here, it shows that Las Vegas and Nevada are becoming more than just a town for hospitality and gaming. There is science going on and because of that, people are going to receive top care.''


1398.Training for Missing Alzheimer's Persons Could Save Lives

Megan Heidlberg
WNEG NewsCHANNEL 32
Tuesday, November 28, 2006

In Georgia, 161,000 people are diagnosed with Alzheimers Disease. 67% of them are at risk of wandering off and getting lost. The rest are usually in someone's full time care or in the early stages of the disease. Dealing with a missing Alzheimer's patient is more difficult than a typical missing persons case. So emergency workers in Jackson County are receiving special training on how to do just that.

Therion Boyd is among the group of Jackson County Sheriff's Deputies participating in some specialized training Tuesday.

"I think it's very beneficial," says Boyd.

Throughout the year deputies have to undergo hours of training. Tuesday's class wasn't mandatory, but rather crucial when it comes to finding missing persons, especially if they have Alzheimers.

"Sure is," says Boyd. "It's harder to communicate with them. Sometimes they don't respond when you call their name."

Instructor Alice Hoffmann says when they go missing a lot of times they don't know who they are or where they are.

"They get very confused and disorientated," says Return Safe Manager Alice Hoffmann. "They're stuck back in their long term memory which for some can be the 1940's or 1950's."

And that makes finding them and caring for them very difficult. Hoffmann works for a program called Safe Return. It's part of the Alzheimer's Association. She teaches Law Enforcement Officers how to respond and handle missing Alzheimer's alerts. She told the group the most important thing is to make them feel safe.

During Tuesday's three hour class, deputies and supervisors learned new ways to get the word out to the public.

"Every place that sells Lotto tickets has a scroll. They can put the alert on the machine," explains Boyd.

A lot of times the missing person is half a mile from where they were last seen. Since it's crucial to find the missing person in 24 hours or less, every resource available to officers could bring your loved one home safe.

Earlier this year Mattie's Call went into affect. It is similar to the Amber Alert or Levi's Call where the media and public is immediately notified if a person with Alzheimer's or Dementia goes missing. Mattie's Call was named after Mattie Moore of Atlanta. She went missing in the Summer of 2004. Her remains were found on Christmas Eve of that year just 500 yards from her home.


November 29, 2006 09:00 AM Eastern Time
1399.Research Collaboration between the University of Pittsburgh and GE Healthcare Reaches Significant Milestone in Development of F-18 PiB for Brain Amyloid Imaging

CHICAGO--(BUSINESS WIRE)--A key milestone in the imaging of Alzheimer's Disease (AD) has been reached through a close collaboration between radiochemists from the University of Pittsburgh and GE Healthcare. The University of Pittsburgh has started a study aimed at obtaining preliminary information on the performance of flourine-18 labelled Pittsburgh Compound B (F-18 PiB) to identify amyloid deposits in subjects with a diagnosis of AD. Chet Mathis, Professor Of Radiology, University of Pittsburgh School of Medicine and director of the PET Facility at UPMC reports, "early results are encouraging and we look forward to the larger multi-site trials that GE Healthcare will perform with F-18 PiB in early 2007."

The imaging of brain amyloid by carbon-11 PiB has been judged by Nature Medicine (Vol 12: 7, p767, 2006) to be one of the most significant advances in the field of AD in recent years. Multiple sites have now replicated the landmark studies reported by Klunk et al in Annals of Neurology in 2004. More recently the U.S.-based Alzheimer's Association and GEHC have funded a C-11 PIB add-on study to the Alzheimer's Disease Neuroimaging Initiative, a $60M study to determine the value of brain imaging.

Although C-11 PiB can be used for academic studies, the 20-minute half-life of C-11 and limited manufacturing access means the molecule is not suitable for widespread use as a routine diagnostic agent. F-18, with a half-life of 110 minutes, offers a much better opportunity for manufacturing and distribution.

In 2003, GE Healthcare licensed a number of compounds from the University of Pittsburgh. Proof of concept studies have already been performed in collaboration with GE Healthcare's IMANET organization, leading to the selection of the lead candidate for further research. Subsequent work has focused on producing the F-18 PiB material to the quality standards necessary for clinical trial use. Don Black, Head of R&D, Medical Diagnostics commented, "good progress is being made with the set up of the PET centres for the forthcoming trial. Recent news from the University of Pittsburgh about the first subjects injected with F-18 PIB is cause for optimism in the potential use of this agent as a future tool for both diagnosis and therapy monitoring."

Kim Gallagher, the newly appointed Head of External Affairs, R&D, Medical Diagnostics also remarked, "these are exciting times in the field of Alzheimer's Disease. The advent of amyloid imaging agents and the wealth of pharma programs in the area of amyloid targeted therapies, have given real hope that significant progress, in the notoriously slow field of dementia, can be made in the next decade."

About GE Healthcare

GE Healthcare provides transformational medical technologies that are shaping a new age of patient care. Our expertise in medical imaging and information technologies, medical diagnostics, patient monitoring systems, drug discovery, and biopharmaceutical manufacturing technologies is helping clinicians around the world re-imagine new ways to predict, diagnose, inform and treat disease, so their patients can live their lives to the fullest.

GE Healthcare's broad range of products and services enable healthcare providers to better diagnose and treat cancer, heart disease, neurological diseases, and other conditions earlier. Our vision for the future is to enable a new "early health" model of care focused on earlier diagnosis, pre-symptomatic disease detection and disease prevention. Headquartered in the United Kingdom, GE Healthcare is a $15 billion unit of General Electric Company (NYSE:GE). Worldwide, GE Healthcare employs more than 43,000 people committed to serving healthcare professionals and their patients in more than 100 countries. For more information about GE Healthcare, visit our website at www.gehealthcare.com.


1400.Senior Citizens Concerned About Memory but Reluctant to Tell Anyone

Study finds many do not even share with their doctor
http://www.seniorjournal.com/index.html
November 29, 2006 - Senior citizens, even those most concerned about possible memory loss, are not sharing this concern with their doctors. Among those who voluntarily attended free memory screening during National Memory Screening Day, 73 percent said they have concerns about their memory but 30 percent said they had not shared this concern with anyone.

Of those who did share their concerns, most confided in their spouse, according to the MetLife Mature Market Institute study

While 84% of those who completed a survey, while attending a the Alzheimer's Foundation of America screening, said they had visited their doctor within the previous six months, only 24% of those concerned about their memory shared their unease with their physician.

A large discrepancy existed between the genders, as more women (74%) than men (29%) said they had concerns about their memory.

Better than 36% of respondents said the memory screening was their first health screening of any type, with the top motivating factors being forgetfulness (50%), a desire to obtain a baseline score (56%) and having a relative with Alzheimer's disease (21%).

An estimated 4.5 million Americans now have Alzheimer's disease with that number predicted to grow to between 11.3 and 16 million by the year 2050. A MetLife Foundation Alzheimer's survey conducted in early 2006 showed that outside of cancer, Americans fear Alzheimer's more than heart disease, stroke and diabetes.

gWith the high incidence of Alzheimer's disease and the aging of the population, individuals are more much aware that certain changes in memory are not part of normal aging. While memory screening is relatively new, it will likely grow in usage as one way for individuals to begin to assess concerns about such memory changes," said Sandra Timmermann, Ed.D., director of the MetLife Mature Market Institute.

Memory Screening: Who Attends and Why was conducted on AFA's National Memory Screening Day in November 2005 by AFA, the MetLife Mature Market Institute and The Center for Productive Aging at Towson University. Seven hundred sites in 49 states participated, screening nearly 20,000 people.

A total of 2,562 (13%) of those screened completed the survey, which examined the reasons for participation, prior experience with health screenings, contact with physicians, memory concerns and the demographic characteristics of respondents.

The average age of those who responded to the survey was 69.9 years. Men in the survey were slightly older (71.3 on average) than women (69.3). Seventy-two percent were retired.

gThe findings of the study suggest that while individuals may be concerned about their memory, many may be reluctant to share their worry," said Eric J. Hall, chief executive officer of AFA. "There is a need to raise awareness and provide education about memory issues and the importance of evaluation to determine whether one may or may not have a problem that requires intervention. The earlier the intervention, the better one's quality of life can be."

National Memory Screening Day is an annual event at which qualified healthcare professionals provide free, confidential memory screening as a first step toward proper diagnosis and treatment. These screenings are not a diagnosis of any illness, but can indicate whether further evaluation is required. Now in its fifth year, National Memory Screening Day will be held on November 14, 2006.

Editor's Notes:

The MetLife Mature Market Institute is MetLife's information and policy resource center on issues related to aging, retirement, long-term care and the mature market. Staffed by gerontologists, the Institute provides research, training and education, consultation and information to support MetLife, its corporate customers and business partners. MetLife is a subsidiary of MetLife, Inc. (NYSE: MET), a leading provider of insurance and financial services with operations throughout the U.S. and the Latin America, Europe and Asia Pacific regions.

The Alzheimer's Foundation of America (AFA) is a national nonprofit organization focused on providing optimal care to individuals with Alzheimer's disease and related illnesses, and their families. It unites hundreds of member organizations nationwide that provide hands-on care to meet the educational, emotional, practical and financial needs of families affected by dementia. www.alzfdn.org

The Center for Productive Aging at Towson University provides a focal point for aging-related academic research and community outreach programs of the University. Academic programs at Towson include an undergraduate degree in Gerontology, a graduate certificate and Master's Degree in Applied Gerontology. Center faculty are involved in applied research related to the aging workforce, family caregiving and aging in the community.

The entire report, Memory Screening: Who Attends and Why, can be found at www.maturemarketinstitute.com under "What's New."