1101.Eye test 'could spot Alzheimer's'(22 July 2006 http://news.bbc.co.uk)
1102.Blood test for Alzheimer's(Daily Mail 24th July 2006)
1103.The Genetic Secrets of Longevity(July 24, 2006 www.techreview.com)
1104.Slowing Alzheimer's disease by keeping mind and body active(24-Jul-2006 American Journal of Pathology)
1105.High Estrogen Levels Linked to Dementia in Elderly Men(July 24, 2006 www.medpagetoday.com)
1106.Alzheimer's robs young of futures(Jul. 24, 2006　　www.bradenton.com)
1107.New Tests to Measure Executive Function in the Neurologically Impaired24 July '06 http://pub.ucsf.edu)
1108.Implant slows symptoms of Alzheimer's(25th July 2006 www.dailymail.co.uk)
1109.Morningside House in the Bronx Implements Alzheimer Video Project with Surprising Results(BUSINESS WIRE July 24, 2006)
1110.Keeping tabs while keeping care(NBC News July 24, 2006)
1111.TorreyPines Therapeutics Completes Second Phase I Study For NGX267, A Selective M1 Agonist For The Treatment Of Alzheimer's Disease(25 Jul 2006 www.medicalnewstoday.com)
1112.Study suggests 'type 3 diabetes'(7 March, 2005 http://news.bbc.co.uk)
1113.Madrid: ICAD Conference Draws to a Close (www.alzforum.org 21 July 2006)
1114.Shape Matters: NC State Scientists Characterize Structure of Protein Involved in Preventing Alzheimer’s, Huntington’s Diseases(July 24, 2006　www.ncsu.edu)
1115.Glaxo says Avandia for Alzheimer's could be huge(Jul 26, 2006 Reuters)
1116.Keeping Mind And Body Active Slows Alzheimer's(26 Jul 2006 www.medicalnewstoday.com)
1117."Promising" Treatments Coming For Alzheimer's Disease(www.wusf.usf.edu 2006-07-26)
1118.BTG completes early Alzheimer's trial; says started yr in strong position(26th July 2006 www.lse.co.uk)
1119.Groundbreaking research highlights myriad health benefits of flavanol-rich cocoa(26-Jul-2006 Weber Shandwick Worldwide)
1120.Alzheimer's disease　Puzzling out the truth(Jul 27th 2006 The Economist)
1121.Double-barreled Weapon Against Alzheimer's as Near as the Bathroom Cabinet (press release)
(July 27, 2006 www.NewsTarget.com)
1122.Families Advocate for Alzheimer's Disease to Be National Priority(July 26, 2006 www.pbs.org)
1123.Is There Really a Connection Between Diabetes and Alzheimer's?(July 27, 2006 www.24-7pressrelease.com)
1124.ABC 7 Medical: Chinese Herb Offers Hope for Alzheimer's Patients(July 27, 2006 www.wjla.com)
1125.Drug Triggers Body's Mechanism To Reverse Aging Effect On Memory Process(University of California - Irvine
July 27, 2006)
1126.Alzheimer's drugs: Real benefits despite limitations(Jul 29, 2006　www.mayoclinic.com)
1127.In the Works: Contrast Agents for Alzheimer's(July 28, 2006 www.medgadget.com)
1128.Alzheimer's drugs fail to deliver(July 27, 2006 www.ocregister.com)
1129.Ageing and memory diseases: the Alzheimer’s story(31 July 2006　http://ec.europa.eu)
1130.New Study Provides Further Evidence that The MCI Screen Accurately Detects Mild Cognitive Impairment (2006-07-31 www.prweb.com)
1131.Penn Researchers Examine The Effects Of Meditation On Early Cognitive Impairment(University of Pennsylvania School of Medicine July 30, 2006)
1132.Alzheimer's Drug Therapy May Be Stopped Too Soon To Benefit Slow Responders(31 Jul 2006 www.medicalnewstoday.com)
1133.Bipartisan Resolution Encourages Those With Memory Loss to Seek Evaluation and Diagnosis(July 31, 2006 PRNewswire)
1134.Drug Triggers Body's Mechanism To Reverse Aging Effect On Memory Process(31 Jul 2006 www.medicalnewstoday.com)
1135.FDA Provides Clearance to Initiate Phase I Clinical Trial with Alzheimer's Disease Drug Product AZD-103(Aug. 1 www.newswire.ca)
1136.Caregivers Struggle with Needs of Alzheimer's Patients (July 31, 2006 www.pbs.org)
1137.Desire to Fill Social Needs for Elderly Change Face of Respite Care(August 1, http://finance.yahoo.com)
1138.UMass Lowell research shows benefits of apple juice on neurotransmitter affecting memory(1-Aug-2006 www.eurekalert.org)
1139.Neuren Selects New Compound Targeted for the Oral Treatment of Parkinson's and Related Neurological Diseases( August 2, http://finance.yahoo.com)
1140.Strategies That Teach A Caregiver To Manage A Loved One’s Illness Also Helps In Coping With Death(8/1/2006 www.webwire.com)
1141.Lexicon gets OK to start test of Alzheimer's drug(Aug. 2, 2006 www.chron.com)
1142.Missing woman's death raises awareness about Alzheimer's(8/2/2006 www.kare11.com)
1143.NC Scientists learn more in preventing Alzheimer's & Huntington's Diseases(August 2, 2006 www.cherokeesentinel.com)
1144.The occasional curry 'could prevent Alzheimer's'(Daily Mail 2nd August 2006)
1145.Art boosts Alzheimer's patients' spirits(Aug 3, 2:57 http://news.yahoo.com)
1146.Cortex AMPAKINE Drugs Can Reverse Age Related Memory Decline in an Animal Model(www.engelpub.com ,Aug 2, 2006)
1147.Dementia risk predictor devised(2 August 2006 www.bbc.co.uk)
1148.Alzheimer's cruelly robs from the old and young(Aug. 03, 2006 www.macon.com)
1149.Nuns lead study in Alzheimer's(August 3, 2006 http://daily-journal.com)
1150.Brain imaging identifies best memorization strategies, details differing parts of brain used in each(http://news-info.wustl.edu Aug. 3, 2006)
1151.Triflusal Might Slow Dementia Progression in Patients With Mild Cognitive Impairment: Presented at ICAD(July 19, 2006 DGDispatch)
1152.Hurricane preparation tips for Alzheimer'S caregivers(08/04/06　 www.sun-herald.com)
1153.Alzheimer's disease, drinking not linked, study says(08/03/2006　www.stltoday.com)
1154.Good Question: Why Do Some Get Alzheimer's Young?(Aug 4, 2006 http://wcco.com)
1155.LV chosen as training ground for treating Alzheimer's (August 4 www.inbusinesslasvegas.com)
1156.Alzheimer's mobile clinic brings free services(Aug. 05, 2006　www.bradenton.com)
1157.Middle-Aged Women Care for Older Generation(04 August 2006 www.voanews.com)
1158.What to look for in dementia-care facilities(August 7, 2006 http://seattletimes.nwsource.com)
1159.Alzheimer's drugs offer modest improvements, equal effectiveness(08/08/2006 www.xagena.it)
1160.Eye Doctors May Someday Screen for Alzheimer's(August 07, 2006　www.webmd.com)　
1161.Write Your Care Plan Before You Need It(08/08/2006　www.saworship.com)
1162.Evotec's Alzheimer's drug OK in phase 1(Aug. 8 UPI)
1163.Multiple Newly Published U.S. and European Peer-Review Studies Support Statin Drug Potential Therapeutic Use in Alzheimer's Disease; Nymox Has Global Patent Rights for Statin Drugs for the Treatment and Prevention of Alzheimer's Disease(August 8 CNW)
1164.Professor explores Alzheimer's causes(August 8, 2006　MIT)
1165.Reduced brain volume may predict dementia in elderly people(08/09/2006　XagenaMedicine)
1166.Who should take the car keys away from Alzheimer's patients?(South Florida Sun-Sentinel August 9 2006)
1167.Too much weight ups your Alzheimer's risk(8/9/2006 www.toledofreepress.com)
1168.Alzheimer's disease: two forms of mild cognitive impairment identified(10/08/2006　XagenaMedicine)
1169.A “Leaky” Blood-Brain Barrier and Alzheimer’s(American Association of Naturopathic Physicians 09-Aug-2006)
1170.Tests may predict progression to Alzheimer's(Aug 10, 2006 Reuters Health)
1171.Scientists make discovery in Alzheimer's(August 10, 2006 http://seattlepi.nwsource.com)
1172.Books, blog help doctor cope with Alzheimer's(August 10, 2006 www.signonsandiego.com)
1173.Microglia, a natural defence mechanism for Alzheimer's disease(12/08/2006　XagenaMedicine)
1174.Calories and Alzheimer’s(08.11.06 www.sciencentral.com)
1175.Exercise Helps Sustain Mental Activity As We Age; And May Prevent Dementia-Like Illnesses(American Psychological Association 8/11/2006)
1176.New biomarkers could help doctors spot Alzheimer's and other neurodegenerative diseases(August 11, 2006 www.physorg.com)
1177.Scientists Discover Age-regulated Cellular Activities that Protect Against Protein Aggregation(www.bio.com 08/11/06)
1178.Aging Critical For Alzheimer's Disease(12 Aug 2006 www.medindia.net)
1179.THC Blocks Alzheimer's Plaque Formation(August 12, 2006 www.futurepundit.com)
1180.Few know about Alzheimer's(Aug. 14, 2006 www.azcentral.com)
1181.Study provides new insights into brain organisation(02.08.2006　www.innovations-report.com)
1182.Copper in high-fat diet risks mental decline(Aug 14, Reuters)
1183.Program nurtures Alzheimer's patients and their caregivers(August 15, 2006 www.islandpacket.com)
1184.Skin Test Could Detect Alzheimer's Disease Early(Aug. 14 HealthDay News)
1185.New biomarkers could help doctors spot Alzheimer's and other neurodegenerative diseases(Aug. 11, 2006 www.uwnews.org)
1186.Region of DNA strongly associated with Alzheimer's disease(08/17/2006　　XagenaMedicine)
1187.SLS makes breakthrough in pre-clinical study for MCI treatment(Aug. 16, 2006 www.indiadaily.com)
1188.Slowing Alzheimer's disease by keeping mind and body active(August 16, 2006 http://canucwhatic.blogspot.com)
1189.Wells County Law Enforcement Agencies Trained on Alzheimer's Related Procedures(August 17, 2006 www.news-banner.com)
1190.Enhancing Gene Delivery with Nanoparticles Could Ultimately Lead to a Cure for Alzheimer's (www.newswiretoday.com s, 08/18/2006)
1191.Allies aid memory loss fight Humor, medicine, community support help Candor man(August 18, 2006 ww.pressconnects.com)
1192.Sale or rental of house to finance parent's Alzheimer's care?(August 18, 2006 www.mcall.com)
1193.Solving Alzheimer’s riddle (17-Aug-2006 www.straight.com)
1194.A new tool against brain disease Snail toxin may spur new meds for Alzheimer's, Parkinson's, depressionPublic release date: 20-Aug-2006 The Brain Institute at the University of Utah University of Utah)
1195.Myriad Genetics Closes Enrollment In US Phase 3 Clinical Trial Of Flurizan For Alzheimer's Disease - Quick Facts( August 22, 2006 RTTNews)
1196.Alzheimer's Caregivers Report More Stress, Higher Costs And A Greater Commitment Of Time, According To New MetLife Mature Market Institute Study (22.08.2006 www.finanzen.net)
1197.Ablynx Completes ?40 Million (~US$50 Million) Series C Financing ? One of the Two Largest Private Placements in European Biotech This Year(www.engelpub.com Aug. 23, 2006)
1198.Even when the mind forgets, the heart always remembers(August 24, 2006 www.thevictoriaadvocate.com)
1199.Lessons in living　Montessori-based method eases symptoms of Alzheimer's(Aug. 24, 2006 www.dfw.com)
1200.SFU discovery could prevent Alzheimer's(www.canada.com August 24, 2006)

Last Updated: Saturday, 22 July 2006, 23:11 GMT 00:11 UK
http://news.bbc.co.uk/
1101.Eye test 'could spot Alzheimer's'

Early dementia could be detected with a simple eye test, similar to those used to test for high blood pressure and diabetes, US scientists believe.
The test, developed by a team led by Dr Lee Goldstein, of Brigham and Women's Hospital, Boston, uses a non-invasive laser to study the lens of the eye.

It checks for deposits of beta-amyloid - the protein found in the brains of those with Alzheimer's disease.

The procedure has worked in a trial in mice, a conference in Spain heard.

During the trial, a brief pulse of infrared light into the eyes of four mice with Alzheimer's and four without accurately identified which had the condition.

Dr Goldstein and his team envisage the test could be used to detect the disease at its earliest stages as well as to track disease progression and monitor how people respond to Alzheimer's treatments.

Currently there is no simple test to make a diagnosis of dementia and it can only be confirmed with certainty by looking at someone's brain in a post-mortem examination.

The scientists believe the technology, known as quasi-elastic light scattering, may detect the very earliest stages of amyloid deposits in the lens, even when they appear completely clear to the naked eye.

Early detection window

The amyloid deposits appear as unusual cataracts. These are different from common, age-related cataracts.

Dr Goldstein told the International Conference on Alzheimer's Disease and Related Disorders in Madrid: "Amyloid in the lens can be detected using extremely sensitive, non-invasive optical techniques.

"This makes the lens an ideal window for early detection and disease monitoring in Alzheimer's."

The scientists acknowledge that much more work is needed before such a test could be available to use in patients.

Professor Clive Ballard, of The Alzheimer's Society, said: "This exciting study uses a new imaging technique which has enormous potential as a relatively inexpensive and non-evasive way to chart the growth of amyloid, the protein at the core of the plaques which develop in the brain in a person with dementia.

"But we are long way from eye scans being regularly used to diagnosis someone with dementia.

"More research is needed to show exactly how the amount of protein in the eye relates to development of dementia."

1102.Blood test for Alzheimer's
Breakthrough offers hope of early treatment

By JENNY HOPE, Daily Mail

00:26am 24th July 2006

Reader comments (4)

A blood test to detect Alzheimer's has been developed by scientists. The breakthrough means doctors could be able to diagnose the disease before any symptoms appear, allowing earlier treatment.
The test, which is almost 90 per cent accurate, is expected to start trials by the end of the year.

Doctors rely on a patient complaining of a failing memory to detect Alzheimer's, sometimes confirmed with a brain scan.

But research using genetic analysis has found a signature - a cluster of proteins in the blood - linked to the disease. Scientists at the Norwegian biotechnology company DiaGenic ASA used this to develop a blood test to distinguish those with Alzheimer's from healthy patients and those with Parkinson's, which can have similar early symptoms.

The next step is to devise a test that can be used by doctors, probably after very early signs of the disease appear, allowing the treatment to slow its progression. High-risk patients could also be offered regular tests in later life.

Dementia, most commonly caused by Alzheimer's, affects more than 700,000 in Britain.

Rebecca Wood, of the Alzheimer's Research Trust, said: "An accurate blood test for Alzheimer's would be a major step forward - it would mean current and future treatments could be given before the brain is too damaged."

Charities, doctors and drug firms, backed by the Daily Mail, are appealing against a plan by the National Institute for Health and Clinical Excellence watchdog that would stop Alzheimer's patients with mild symptoms being prescribed the drugs Aricept, Exelon and Reminyl.

Add your comment | View all Reader comments (4)

4 people have commented on this story so far. Tell us what you think below.

Here's a sample of the latest comments published. You can click view all to read all comments that readers have sent in.

Everyone at risk should have access to the tests but more importantly, those who already have mild symptoms should - without delay- receive the drugs that are available to halt or slow the disease. Why is it impossible to make these drugs available to all who need them? There is so much money being wasted elsewhere- is ANYONE ever going to direct the NHS funds to where they are needed?

- Margaret Maclean, Bournemouth Dorset
This blood test will help save money in the long run by detecting this horrible illness earlier. My father was suffering from this illness & perhaps if it was known earlier his medication may have help him more as Alzheimer's effects the whole family.

- Patricia Young, Southampton
There is already a test which is available, definitely privately & maybe elsewhere, which can detect a person prone to Alzheimer's through abnormal amounts of a certain protein in their blood. A member of my family had it done as we have Alzheimer's in the family, & my relative is on tablets to reduce this protein's levels. I have had so much experience outside of the NHS that when I see things talked about as if "new" or for the "first time" it's frustrating. Because half these things if not similar things/tests/treatments which are closely related, already exist! Why do people not know about these things or have access to them? They shouldn't have to go privately. Not many have the luxury to do that. Nor spend the many years tracking down top research specialists in different areas in the way that my family has. So many people do not have these resources. It is just so wrong, not right & unfair. I might be able to get treatment, but what about everyone else who don't know it exists?
- Louise, County Down

Monday, July 24, 2006
http://www.techreview.com/index.aspx
1103.The Genetic Secrets of Longevity
A study of long-lived families will help isolate the genetic mysteries that allow some people to live disease-free into their nineties and beyond.

By Emily Singer

Thomas Perls has definitive proof that both mind and body can escape the decay of time. He's seen firsthand the brain of a deceased 100-year-old woman that showed no signs of the neurological wear-and-tear that usually accumulates in the aging brain. Not a hint, for example, of the plaques and tangles that accompany normal aging and are a hallmark of Alzheimer's disease. What's more, before her death, the donor had the cognitive abilities of a 60-year-old.

As director of the New England Centenarian Study at Boston Medical Center, Perls has spent the last decade hunting for genetic and environmental clues to these ageless wonders. He hopes studies of very long-lived people will explain why some individuals succumb to diabetes, heart disease, or Alzheimer's at a relatively young age, while others live two decades beyond the average life expectancy and show remarkably few signs of the passage of time. (The extraordinary brain described above was donated by a participant in the study.)

Perls' study, made up of 800 centenarians, is the largest ever conducted of people who have lived to the age of 100 and beyond. Not only do these people live long, but many of them seem to escape the disability associated with diseases of aging or to compress that disability period into a short time span very late in life.

While researchers haven't yet found the source of centenarians' enviable passage into old age, they have published numerous studies showing that longevity runs in families.

Perls' team is now starting a new, larger study of long-lived families, which he hopes will bring better insight into the specific genetic and environmental factors that underlie longevity. His center will conduct one arm of the Long Life Family Study, funded by the National Institute on Aging, in which scientists at four different sites will recruit 1,000 families that show exceptional longevity. Eventually he hopes to be able to translate the findings from these families into broadly usable treatments for the diseases of aging.

Here Perls tells Technology Review what he's learned so far about aging -- and what he hopes to uncover.

Technology Review: What makes centenarians so interesting from a medical perspective?

Thomas Perls: These individuals have a remarkable potential for resilience. Forty percent of centenarians have diseases they've been living with 20 years, but they don't show disability from these diseases until their early-to-mid-nineties. What is this resilience that allows people to live with these diseases and not have problems until the relative end of their extremely long lives?

In addition, 13 percent of centenarians seem to escape the diseases of aging altogether. Some even do this despite some horrendous health habits. We want to figure out how to translate that into strategies for other people. Our goal is to get people to markedly delay or escape disability associated with aging. If we could do that, it would be a huge boon to the health system and our society.

TR: Has conducting these studies changed your own view on aging?

TP: Most people think, 'the older you get, the sicker you get.' But the reality is, the older you get, the healthier you've been. Living to 100 is an important marker of aging well and good health.

TR: What are the most important factors that influence aging?

TP: The keys to achieving extreme old age probably vary a great deal for different people. But we know from other studies what's needed to reach your eighties in good health. The best example is the Seventh-Day Adventist Health study. Seventh-Day Adventists have an average life expectancy of 88 years, the oldest life expectancy for any group in the United States -- ten years longer than the rest of the country. Because of their religious beliefs, they don't eat meat, smoke, or drink alcohol (though perhaps some alcohol is good for you). They set aside weekends for religious practice and family time, which may help them effectively manage stress. These habits are likely what it takes to get where most of us should be able to get to -- into our late eighties in good health.

TR: What about getting beyond that?

TP: We hope that our participation as a study center for the NIH's Long Life Family Study will help shed light on that. We will study families with at least several very old living siblings and look for factors that they have in common which might explain their abilities to achieve extreme old age. We go to the subjects' homes and collect some basic physical data -- height, weight, blood pressure, lung function and strength, as well as measures of cognitive function. We'll also draw blood for genetic and other tests.

TR: How does focusing the study on long-lived families help the search for genetic factors?

TP: With family members, we have a better chance of figuring out what these people have in common. It's more than just genetics; it's environmental factors like smoking, religion, obesity, the ability to handle stress.

We hope that collecting these environmental, medical, and behavioral data will ultimately help guide us in our choices of genes for further study. If you find everyone doesn't have diabetes, you might look at genes related to insulin signaling and fat metabolism.

Extremely old individuals will also probably lack certain genetic variations, such as those that increase the risk for early heart disease or cancer. And maybe they'll have genes that help them age slowly, have increased resilience, and escape or markedly delay age-related disease.

TR: What genes do you think will be most crucial for longevity?

TP: I think genes that modulate risk for heart disease will be very important. That's still the number-one killer, even among the very old. In addition, more and more scientific studies show that fat metabolism will play a big role.

These people must certainly lack genetic variations that lead to high cholesterol or early cancer. But there might also be something protective, so-called longevity-enabling genes, especially in very old people who show no signs of disease or who have terrible health habits and yet still survive to 100 years and older. This is a very controversial idea in the field, but they may have genes that play a role in the rate of aging. If you could translate that into drugs, it would be huge. [For an in-depth look at how scientists are using longevity studies in animals to develop drugs to treat the diseases of aging, see "The Fountain of Health," March/April 2006.]

TR: Have you identified any candidate genes?

TP: We previously found that centenarians were more likely to have a certain variant of the gene for microsomal transfer protein, which plays a role in packaging cholesterol. However, subsequent studies have had different results. One study confirmed the findings, while a few others did not. That shows how important it is to confirm results in different populations and suggests that the importance of various genetic longevity factors varies from one population to another.

TR: Previous studies in animals suggest that caloric restriction is one of the most effective ways to extend life. Is this a factor in your studies?

TP: Male centenarians are almost always lean. But there is no evidence that they had low calorie intakes compared to the average for their birth cohort, certainly not to the degree that would be analogous to calorie-restriction diets in primates and mice. Interestingly, many of the centenarian women can be stocky. Women may be able to get away with having more fat because they are much better able to deal with age- and fat-related diseases.

TR: What excites you most about starting the Long Life Family Study?

TP: It's been a while since I had the chance to go out and visit centenarians. They are historical treasures and tend to be very gregarious. They've been around for 100 years, so they have a lot to say and are terrific fun to be with.
For more information on the study, visit http://www.bumc.bu.edu/centenarian, or call 1.888.333.6327.
To calculate your own life expectancy, try Perls' life expectancy calculator.

Public release date: 24-Jul-2006

Contact: Audra Cox
acox@asip.org
301-634-7409
American Journal of Pathology

1104.Slowing Alzheimer's disease by keeping mind and body active
Muenster, Germany -- Researchers have uncovered the pathways behind the protection offered by environmental stimulation in Alzheimer's disease, further confirming that enhanced mental and physical activity slows neurological decline. The paper by Ambr馥 et al., "Reduction of amyloid angiopathy and Aβ plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways," appears in the August issue of The American Journal of Pathology.

Alzheimer's disease, the leading cause of senile dementia, presents with cognitive and behavioral deficiencies resulting in part from accumulation of ?-amyloid (A?) deposits within the brain (A? plaques) and its blood vessels (amyloid angiopathy). Although previous studies have shown that increased mental and physical activity can slow the progression of the disease, how such deceleration occurs has been unclear until now.

Dr. Kathy Keyvani's group at University Hospital Muenster examined the effects of environmental stimulation on the brain pathology of TgCRND8 mice. These mice, which express a mutant form of A? found in some Alzheimer's patients, develop Alzheimer-like features including A? plaques and cognitive deficits. To study the effects of enrichment, mice were housed in either standard cages or enriched cages, similar to the standard but with access to a stimulus cage containing permanent fixtures (rope and gnawing wood) as well as removable items (tunnels, balls, ladders, ramps, and exercise wheels) that were changed on a rotating basis.

Following five months of standard versus enriched housing, mouse brains were examined for signs of disease. Mice housed in the enriched environment had fewer A? plaques, smaller plaque size, and reduced amyloid angiopathy compared to mice housed in standard cages. Interestingly, there were no differences in the levels of soluble A? peptide or the transcriptional/translational expression levels of its precursor protein (APP) or the processing of APP between the two groups. So how did environmental stimulation prevent disease?

To answer this question, Ambr馥 et al. performed DNA microarray analysis to determine which genes were differentially regulated in mice housed in the enriched environment compared to standard cages. Enriched mice exhibited down-regulation of pro-inflammatory genes but up-regulation of genes related to anti-inflammatory processes, protein degradation and cholesterol binding. These results were confirmed by specifically analyzing gene expression for examples in each category. Together these data suggest that an enriched environment elicits protection via pathways that prevent A? accumulation and enhance its clearance.

The authors speculate that the altered expression of inflammatory genes may shift the immune response from one that is neurotoxic to one that is phagocytic, i.e., able to clear unwanted debris, such as A?. In accordance with this, a significant enhancement of microglial activity was found by Western blot and morphometric analyses of microglia, which often surround and infiltrate A? plaques. In addition, activating cellular protein degradation pathways provides another means of removing excess A?. Finally, changes in cholesterol homeostasis, elements of which have been shown to correlate with A? deposition, may exert beneficial effects by preventing plaque formation in the first place.

These data provide strong evidence that an environment rich in mental and physical stimulation slows the progression of Alzheimer-like brain pathology. Further investigation of the pathways and individual elements involved in such protection may provide novel treatment strategies for Alzheimer's disease. Until that time, keep your running shoes and crossword puzzles handy.

###

This work was supported by grants from Innovative Medical Research and German National Academic Foundation.

Work was directed by Dr. Kathy Keyvani of University Hospital Muenster and involved collaborators at University of Muenster.

Ambr馥 O, Leimer U, Herring A, G�rtz N, Sachser N, Heneka MT, Paulus W, Keyvani K. Reduction of amyloid angiopathy and Aβ plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways. Am J Pathol 2006 169:544-552

For press copies of the articles, please contact Dr. Audra Cox at 301-634-7409 or the Journal Editorial Office at 301-634-7959.

For more information on Dr. Keyvani, please contact Jutta Reising at University Hospital Muenster, Germany: +49 251 832 2115; jutta.reising@uni-muenster.de.

The American Journal of Pathology, the official journal of the American Society for Investigative Pathology (ASIP), seeks to publish high-quality original papers on the cellular and molecular mechanisms of disease. The editors accept manuscripts which report important findings on disease pathogenesis or basic biological mechanisms that relate to disease, without preference for a specific method of analysis. High priority is given to studies on human disease and relevant experimental models using cellular, molecular, biological, animal, chemical and immunological approaches in conjunction with morphology

1105.High Estrogen Levels Linked to Dementia in Elderly Men

By Judith Groch, MedPage Today Senior Writer
Reviewed by Robert Jasmer, MD; Assistant Professor of Medicine, University of California, San Francisco
July 24, 2006
http://www.medpagetoday.com/index.cfm

MedPage Today Action Points

Explain to interested patients that the increased levels of estradiol in these men in this study may be a consequence of an earlier marker for Alzheimer's rather than the cause of the disease.

Be aware that testosterone levels in elderly men did not affect cognitive decline or the risk of Alzheimer's disease.

Note that testosterone replacement therapy is not recommended for healthy older men.

Additional Alzheimer's Disease Coverage
Review
UTRECHT, The Netherlands, July 24 -- For men ages 70 to 91, Alzheimer's disease and other dementias have been associated with high levels of endogenous estrogen, but not high levels of testosterone, researchers here reported.

The retrospective analysis of the role of endogenous hormones in elderly men emerged from analysis of data in the prospective cohort of 2,974 Japanese-American men, ages 71 to 91, in the Honolulu-Asia Aging Study. The men were dementia-free at baseline in 1991 to 1993.

The investigators undertook the analysis in the light of contradictory evidence for the effect of testosterone on cognition in older men, and the unexpected results from the Women's Health Initiative Memory Study, which found that women receiving estrogen therapy had an increased risk for cognitive impairment and dementia. So wrote Mirjam Geerling, Ph.D., at the University Medical Center Utrecht here and colleagues in an online report in the August Annals of Neurology.

Blood samples were drawn at baseline and then three more times over an average of six years for evidence of cognitive decline or dementia, using the Cognitive Abilities Screening Instrument (CASI).

A quantitative competitive immunoassay was used to measure 17-beta estradiol, while total testosterone was measured by a chemiluminescent enzyme immunoassay.

A total of 134 men developed Alzheimer's, including 40 with contributing cerebrovascular disease, while 44 developed vascular dementia, the analysis said.

Adjusting for age and other covariates, the researchers found that testosterone was not associated with a risk for dementia (using Cox regression analyses) or cognitive decline (using random coefficient analyses).

On the other hand, higher levels of estradiol were associated with an increased risk for Alzheimer's disease. With each standard deviation increase in estradiol level, the risk for Alzheimer's went up 25% (hazard ratio per standard deviation increase, 1.25; 95% CI, 1.05-1.47), Dr. Geerlings and colleagues reported.

For each standard deviation increase in estradiol level, the risk for Alzheimer's with cerebrovascular disease rose almost 20% (HR, 1.19; CI 1.02-1.38), he added.

Furthermore, compared with the lowest tertile of estradiol, men in the middle and highest tertiles scored 0.24 and 0.28 points lower on the CASI test, respectively, for each year increase in age.

In the original dementia-free cohort, the mean total testosterone level was 16.8 nmol/L; the mean bioavailable testosterone and free levels were 8.3 and 0.3 nmol/L, respectively.

In these dementia-free participants, the mean total 17-beta Estradiol (E2) level was 94.9 pmol/L, and the mean bio-E2 and free-E2 levels were 62.7 and 2.2 pmol/L, respectively. With increasing testosterone levels, estradiol levels also increased, the researcher said.

The researchers hypothesized that the estradiol association with impaired cognition could be explained by increased aromatase activity in the brain, which might be associated with a neurodegenerative process.

Or, perhaps, it's the converse. Neurodegeneration as a result of early Alzheimer's could lead to increased aromatase expression and a consequent increase in estradiol production in the brain. If this hypothesis is correct, they wrote, the results of this study would suggest that relatively high levels of estradiol were a consequence of an early marker, rather than a cause of the disease. It is possible, Dr.Geerlings said, that "the disease itself disrupts hormone regulation."

According to the investigators, the strengths of the study included the large size of the cohort, that it was a prospective population-based study, and the fact that both hormones were examined in the same study.

Limitations included the loss to follow-up of 23% of the subjects, the inability to run the hormone assays in duplicate, and the fact that the levels of cognitive decline, though statistically significant, were based on group differences and could not be interpreted on an individual level.

Little consensus exists as to what constitutes a normal sex hormone profile for an aging man or what specific effect the male andropause has on cognitive function, Dr. Geerlings said. Future research, he said, should focus on defining a normal balance between these two hormones not only in the periphery, but also in the brain.

The finding of an increased risk for cognitive decline and Alzheimer's with higher levels of estradiol are similar to the recent finding in postmenopausal women, so that further studies are needed to examine the possible mechanisms for this risk.

However, Dr. Geerlings said, androgen replacement to increase testosterone levels in healthy men is not recommended.

Additional Alzheimer's Disease Coverage

Primary source: Annals of Neurology
Source reference:
Geerlings MI, et al, "Endogenous Sex Hormones, Cognitive Decline, and Future Dementia in Old Men," Annals of Neurology 2006; 60 (2) doi: 10.1002/ana.20918.

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Posted on Mon, Jul. 24, 2006　　http://www.bradenton.com/mld/bradenton/
1106.Alzheimer's robs young of futures
BONNIE MILLER RUBIN
Chicago Tribune
CHICAGO - Surrounded by friends, Jim Mueller is gregarious and quick with a quip - until he's asked the age of his three children.

The jokes stop. Silence hangs in the air while the burly sheet-metal worker discreetly peeks at a small notebook before coming up with the right answer.

That Mueller - just 37 years old - would need a cheat sheet for such a basic fact might raise eyebrows elsewhere, but not here, at the monthly meeting for people with early-onset Alzheimer's disease.

"I look healthy, I feel healthy . . . and it's just so frustrating because I can't be the man I once was," said Mueller, of Lombard, Ill.

Of the 4.5 million Americans with Alzheimer's disease, as many as half a million fall into the early-onset category, defined as younger than 65, according to a recent report by the Alzheimer's Association that was the first to focus on a younger generation.

This group is not yet well-understood - no figures are available on whether early-onset cases are increasing, for example, experts said. But the group deserves more attention because of its unique challenges, the report concluded.

"We're really just at the beginning of understanding this illness," said Dr. David Bennett, medical director of Chicago's Rush Alzheimer's Disease Center, which runs the meetings.

Alzheimer's is difficult at any age, but the early-onset strain is particularly cruel because it strikes in the prime of life, when people have children to raise and careers in full bloom. For the elderly, the brain disorder robs them of memories of the past; for this population, it also steals their hopes for the future.

Rush's support group, called Without Warning, draws people from throughout the Midwest. It is split into two parts; one for individuals, the other for friends and family. Members gather at a church, swapping tips on daily living tasks, comparing medicines and venting to the only people who truly understand.

"What's really frustrating is that people don't even believe that you have it," Mueller said as the others nodded their heads sympathetically. There's Marty Bahr, 57, formerly an executive at an insurance company; Harvey Newman, a 51-year-old postal worker; Jack Edling, 51, a vice president at a Fortune 100 firm, and Mike Gannon, 60, a construction manager who once could move complex projects from blueprints to reality.

Experts say a person diagnosed with the disease at age 40 is likely to live another 20 years, a daunting prospect for a condition that costs caregivers an average of $19,000 a year in out-of-pocket expenses. Many people also leave their jobs before diagnosis, making it harder to qualify for disability payments.

The report released last month by the Alzheimer's Association, presented to a congressional task force co-chaired by Sens. Hillary Clinton, D-N.Y., and Susan Collins, R-Maine, proposed a number of recommendations, including a program to increase awareness about younger people with the disease.

The forums at Rush started in 2004, when Bahr yearned to meet with others his age. Now about 70 names are on the mailing list, including about 17 regulars.

The disease sometimes progresses so mercilessly that patients can decline visibly from one monthly meeting to the next. When participants can no longer follow the conversation, they join another group, led by a music therapist, which delivers an hour of "connectedness."

To Michelle Mueller, the priority is spending as much time with her husband as possible - an urgency that seems incredible when referring to a gregarious 37-year-old wearing a Notre Dame cap at a jaunty angle.

Like most participants, he needs constant supervision. The next step will be finding some type of residential care.

For now, though, Mueller still lives with his family - even coaching his daughter's softball team.

Earlier in the season, some parents became miffed when Mueller called players by the wrong names. Eventually, his wife penned a note informing each family of the disease.

"The hardest part is to watch someone slip away," she said. "You know the end from the beginning. . . . It really is the long goodbye."

First Appeared Monday, 24 July '06
http://pub.ucsf.edu/today/cache/index.html
1107.New Tests to Measure Executive Function in the Neurologically Impaired

by Carol Hyman

When hearing the term “executive function,” we might conjure up an image of a CEO behind a big desk, doing her daily routine. These daily tasks ? or executive functions ? involved in her routine rely upon the cognitive abilities neurologists call executive function. Some of these functions include making decisions, multitasking and coming up with creative solutions to problems. While often taken for granted, these functions are necessary for carrying out our daily lives. However, people with certain illnesses and conditions, particularly those that involve neurological function, may have deficits in these areas.

Recognizing the need to have accurate, standard measurements for executive function (EF), the National Institutes of Health’s National Institute of Neurological Disorders and Stroke has awarded a five-year contract to UCSF’s Neurology department to help in this endeavor. The goal is to develop an innovative neuropsychological battery of tests that could be used by clinicians all over the country to help measure executive function in a wide variety of conditions. The group taking on this task is led by Memory and Aging Center neuropsychologist Joel Kramer, PsyD.

“Researchers who study aging have had a pretty good handle on measuring memory loss,” Kramer said. “But executive function is less well defined and may have more importance in our ability to carry out day-to-day activities.”

Kramer, along with other faculty, staff and an advisory panel that includes experts from around the country, has taken on the challenge to develop this battery that will not only benefit clinicians as they treat patients, but will also help researchers as they design clinical trials.

The tests will be standardized and used to measure executive function in patients with a variety of illnesses and conditions, including Alzheimer’s, multiple sclerosis, attention deficit hyperactivity disorder, Parkinson’s and dementia. The tests will be adaptable across a wide range of ages and disorders, and will be translated into Spanish.

“This will be an industry standard that will be available to any researcher,” Kramer said. And because of advances in technology, the tests may be computer-based, allowing for accurate measures of reaction times in attention and working-memory tasks. “Being able to more reliably diagnose EF deficits may greatly influence quality of life for both patients and their caregivers,” Kramer concluded.

1108.Implant slows symptoms of Alzheimer's
By PAT HAGAN, Daily Mail

09:30am 25th July 2006
http://www.dailymail.co.uk/
Reader comments (2)

An implant that looks like a tiny piece of spaghetti is the latest breakthrough in the treatment of Alzheimer's disease.

The inch-long device is injected under the skin on the abdomen and gradually releases medicine into the bloodstream. Once the drug travels to the brain, trial results suggest, it appears to halt the progression of the disease for up to a year.

Once-a-day pill hope in Alzheimer's fight

Each implant lasts up to six months, pumping out a constant supply of medicine to keep symptoms at bay. When empty, it simply dissolves into the bloodstream harmlessly.

Scientists behind the spaghetti implant say it will not only banish the need for daily or weekly drug injections, it will also reduce the peaks and troughs in symptoms that patients can experience with drugs which are swallowed or injected.

With a constant drug supply, symptoms are less likely to keep returning. But the biggest advantage could be that patients whose memories are deserting them need no longer worry about taking their drugs.

Each implant contains a medicine called leuprolide acetate, which has been used for over 20 years to treat prostate cancer. Now new research suggests it could dramatically slow the progress of Alzheimer's.

A study of women with mild-to-moderate brain disease compared those given the drug with women on a placebo.

After three months of treatment, both groups were tested with a range of memory-related tasks. The implant group performed significantly better. The results were presented at an Alzheimer's conference in Madrid.

'These findings mean that, for a sustained period of time, women treated with the drug were able to maintain their memory and their ability to do things like dress themselves,' said Dr Christopher Gregory, vice president of the drug firm behind the invention, Voyager Pharmaceutical Corporation of North Carolina.

Alzheimer's affects an estimated 750,000 people in the UK, robbing them of their memory and faculties.

Most sufferers die within ten years of being diagnosed and the cost of caring for victims is more than stroke, heart disease and cancer put together.

The disease destroys chemical messengers within the brain and starts with the build-up of deposits ? called plaques and tangles ? that can disrupt normal messaging systems by causing inflammation.

Memory loss

One of the main symptoms is loss of memory. Although sufferers may recall things that happened decades ago, they struggle to remember recent events. Other signs of the disease include lack of concentration, confusion and a tendency to wander aimlessly.

The main form of treatment in the UK is a group of drugs called acetylcholinesterase inhibitors, such as Aricept.

The Government's health watchdog, the National Institute for Health and Clinical Excellence, has ruled that patients with moderate Alzheimer's can have these drugs on the NHS.

But they can only stay on them if their condition improves or does not get worse in the first six months of treatment, while those in the early stages of the disease must wait until their symptoms worsen before they can have the drugs.

The drugs do not work for everyone and the brain eventually starts to deteriorate again.

The new treatment first attracted interest ten years ago when women whose husbands were taking leuprolide acetate for prostate cancer reported significant improvements in their partner's mental state, too.

Experts began investigating whether the drug was also acting on brain cells. It works by blocking the effects of a hormone produced by the pituitary gland at the base of the brain.

Called luteinising hormone, it plays a key role in human reproduction. But evidence suggests that, in excess, it also tries to stimulate nerve cells in the brain to divide.

Although our brain cells divide all the time in the early stages of life, by adulthood this process has stopped. If it starts again, it can disrupt all the brain's learning and memory circuits, leading to conditions such as Alzheimer's.

The theory is that an implant made with a drug that stops this cell division could halt Alzheimer's in its tracks. Bigger trials involving more than 500 patients are due to begin soon.

Men who have the implant fitted would also need to wear testosterone patches, since the treatment also suppresses the production of the male hormone.

A spokesman for the Alzheimer's Society said the new drug appeared safe and that early results were promising.

Susanne Sorenson, head of research at the organisation, added: 'Tests on mice have shown it is effective in reducing levels of a chemical strongly associated with Alzheimer's, and first tests on humans have indicated it could help slow the progression of the disease.

'But it's too early to tell if it will stop the disease developing.'


Add your comment Reader comments (2)

Here's what readers have had to say so far. Why not add your thoughts below?

This is a great breakthrough. We definitely need a drug that will slow or stop this dreaded disease. Thank you, Voyager, for doing the research to bring this drug to fruition. Hopefully, the FDA will fast track this drug and get it on the market for all Alzheimer's patients to use.

- Steve, Charleston, SC

July 24, 2006 12:31 PM US Eastern Timezone
1109.Morningside House in the Bronx Implements Alzheimer Video Project with Surprising Results
NEW YORK--(BUSINESS WIRE)--July 24, 2006--Morningside House, a nursing home in the Bronx, recently installed four flat screen video monitors in the hallway of their Alzheimer's unit. Dubbed the "A3 Hallway Media Project," the program has accomplished the original goal, to engage residents seated in the unit hallway in a meaningful pastime and introduce upcoming group activities, but it has also had surprising results. Staff on the unit report that the residents are calmer and more interactive with both staff and family members during the time the videos are played.

The monitors, purchased with a grant from Verizon, were not intended to play traditional television shows or substitute for human interaction, but rather to play videos and DVDs that would represent the upcoming activity in the group lounge. For example, prior to a spiritual service a video of religious hymns and songs is played, before a yoga class images of nature are presented and prior to a horticultural activity a video with gardening images is played. In addition, the monitors can be used to portray weather or daytime events such as snowfall on winter days, ocean scenes during the summer or even sunrises and sunsets.

The monitors have transformed the once noisy, curving section of the hallway into a peaceful environment helping both residents and staff cope with life on the unit. While formal results are still being compiled, success is apparent in the calmer demeanor of the nearly 50 residents and the feedback from the staff.

Morningside House is a 386-bed teaching nursing home located at 1000 Pelham Parkway in the Bronx. It is a subsidiary of Aging in America. Since 1852, Aging in America, and its four subsidiaries, has been caring for those in need with compassion and understanding. The programs of Aging in America are designed to promote independence for older individuals. Morningside House, fully accredited by the Joint Commission on Accreditation of Healthcare Organizations, is the only facility in the Bronx contracted with the NYU Hospitals Center to participate in the Rusk Institute Rehabilitation Network.

For more information call 718-409-8213.

1110.Keeping tabs while keeping care
How one assisted living facility helps loved ones monitor residents

By Jennifer London
Correspondent
NBC News
Updated: 7:27 p.m. ET July 24, 2006

PORTLAND, Ore. - It's lunchtime in downtown Portland, and Susan Sloan wants to check in on her 94-year-old mother, Florence Westerhausen. From her desk at work, she logs onto a secure Web site and gets real-time information about her mom.

"She's in her bedroom," says Sloan as she watches her computer screen.

Westerhausen lives 10 miles away, at an assisted living home called Oatfield Estates. No long hallways or institutional lighting here ? six homey houses make it feel like a community instead of a facility.
But what you can't see makes it even more unique. Nearly 1,000 hidden sensors are part of its high-tech approach to elderly care. The sensors work with a small black badge that residents cand choose to wear. It keeps track of where they are and what they're doing.

"It tells us exactly where she's at," says Oatfield Estates employee Misty Tedford as she tracks a resident named Dorothy. "She's in the doorway of her room."

At night, when the residents aren't wearing their badges, they can still be monitored. Sensors attached to the bed sound an alarm if they get up. It's fondly called the bed bug.

About two-thirds of the 80 residents have dementia or Alzheimer’s, and without the technology, many might have to be locked in their rooms. But not at Oatfield.

"That's really our dream," says Lydia Lundberg, the owner of Oatfield Estates. "The technology will help us manage the facilities but also give residents freedoms that they might not otherwise have."

Lundberg says members ? anywhere in the world ? can stay connected, simply by logging online.

"We have one family member in New Zealand," she says. "We have some in Arizona, Wisconsin."

And for the residents, like Florence Westerhausen, it can be a life-saver. When she took a nasty fall, her badge alerted the staff instantly.

"I think it saved my life, I really do," she says.

"The way they approach their care and the independence they give them is so critically important," says Susan Sloan.

Important, because for these seniors it's not about a place to live until the end of their lives, it's about the freedom to live life to the end.

? 2006 MSNBC Interactive

1111.TorreyPines Therapeutics Completes Second Phase I Study For NGX267, A Selective M1 Agonist For The Treatment Of Alzheimer's Disease
Main Category: Alzheimer's News
Article Date: 25 Jul 2006 - 0:00am (PDT)
http://www.medicalnewstoday.com/

TorreyPines Therapeutics, Inc. today announced completion of its second Phase I study with NGX267 in clinical development for the treatment of Alzheimer's disease. This study evaluated the safety of NGX267 in healthy elderly volunteers. In a previous Phase I study, NGX267, administered as single doses, was shown to be well-tolerated in healthy, younger adult males. NGX267, a selective cholinergic muscarinic, or M1, receptor agonist, has demonstrated potential in providing both symptomatic improvement and disease modification in animal models of Alzheimer's disease.

This second Phase I study was a double-blind, placebo-controlled, single ascending dose study that evaluated the safety, tolerability and pharmacokinetics of NGX267 in healthy males and females between the ages of 65 and 80, reflecting the age of the primary Alzheimer's disease population. The trial enrolled 26 volunteers at one center in the U.S. Clinical data showed that NGX267 was well tolerated at single doses up to and including 15 mg and that evidence of cholinergic activation was detected at these doses. Additionally, exposure levels of NGX267 in elderly men and women at doses of 15 mg or lower may be comparable to those levels tested in a transgenic mouse study, published in the journal Neuron (Vol 49, 671-682) in March of this year. In that animal study, NGX267 improved behavioral symptoms and lowered brain AB42, a toxic peptide that is the major component of amyloid plaques. These plaques are considered a primary histopathological hallmark of Alzheimer's disease.

"These favorable safety data in a population at highest risk of developing Alzheimer's disease support development of NGX267 as a potential therapy for Alzheimer's disease," said Neil Kurtz, M.D., President and Chief Executive Officer of TorreyPines. "This compound may potentially provide patients and caregivers with a meaningful advance in the treatment of this disease by addressing both the symptoms and the progression of Alzheimer's disease."

About TorreyPines Therapeutics

TorreyPines Therapeutics, Inc. is a biopharmaceutical company that discovers and develops small molecule drugs to treat diseases and disorders of the central nervous system. Led by an accomplished management team, TorreyPines is leveraging novel drug targets and technologies to deliver new therapies for migraine, chronic pain, including neuropathic pain, and Alzheimer's disease. Its therapies are intended to offer advantages over current therapies. On June 8, 2006, TorreyPines announced that it had entered into a definitive merger agreement with Axonyx Inc. (Nasdaq: AXYX). The resulting company will be named TorreyPines Therapeutics, Inc. and be headquartered in San Diego. Further information is available at http://www.torreypinestherapeutics.com.

Additional Information about the Merger and Where to Find It In connection with the proposed merger, Axonyx and TorreyPines Therapeutics intend to file relevant materials with the Securities and Exchange Commission (SEC), including a registration statement on Form S-4 that will contain a prospectus and a joint proxy statement. Investors and security holders of Axonyx and TorreyPines Therapeutics are urged to read these materials when they become available because they will contain important information about Axonyx, TorreyPines Therapeutics and the merger. The proxy statement, prospectus and other relevant materials (when they become available), and any other documents filed by Axonyx with the SEC, may be obtained free of charge at the SEC's web site at http://www.sec.gov.

In addition, investors and security holders may obtain free copies of the documents filed with the SEC by Axonyx by directing a written request to: Axonyx, 500 Seventh Avenue, 10th Floor, New York, NY 10018, Attention: Investor Relations. Investors and security holders are urged to read the proxy statement, prospectus and the other relevant materials when they become available before making any voting or investment decision with respect to the merger.

This communication shall not constitute an offer to sell or the solicitation of an offer to sell or the solicitation of an offer to buy any securities, nor shall there be any sale of securities in any jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such jurisdiction. No offering of securities shall be made except by means of a prospectus meeting the requirements of Section 10 of the Securities Act of 1933, as amended.

Participants in the Solicitation

Axonyx and its directors and executive officers and TorreyPines Therapeutics and its directors and executive officers may be deemed to be participants in the solicitation of proxies from the stockholders of Axonyx in connection with the proposed transaction. Information regarding the special interests of these directors and executive officers in the merger transaction will be included in the proxy statement/prospectus referred to above. Additional information regarding the directors and executive officers of Axonyx is also included in Axonyx's Annual Report on Form 10-K for the year ended December 31, 2005, which was filed with the SEC on March 16, 2006. This document is available free of charge at the SEC's web site (http://www.sec.gov) and from Investor Relations at Axonyx at the address described above.

This press release contains and the presentation made at the conference may contain forward-looking statements or predictions, including statements regarding the potential closing of the proposed merger between Axonyx and TorreyPines Therapeutics and the combined company resulting from the merger.

Actual results may differ materially from the above forward-looking statements due to a number of important factors, including the possibility that the proposed merger may not ultimately close for any of a number of reasons, including, but not limited to, Axonyx not obtaining shareholder approval of the issuance of shares and warrants in the merger, the change in control resulting from the merger or the reverse split of Axonyx common stock; TorreyPines Therapeutics not obtaining shareholder approval of the merger, the possibility that NASDAQ will not approve the listing of the combined company's shares for trading on the NASDAQ Stock Market or that the combined company will not be able to meet the continued listing requirements after the closing of the merger; that Axonyx and TorreyPines Therapeutics will forego business opportunities while the merger is pending; that prior to the closing of the proposed transaction, the businesses of the companies, including the retention of key employees, may suffer due to uncertainty; and even in the event the transaction is completed, that combining Axonyx and TorreyPines Therapeutics may not result in a stronger company, that the technologies and clinical programs of the two companies may not be compatible and that the parties may be unable to successfully execute their integration strategies or realize the expected benefits of the merger.

Risks and uncertainties that could materially affect Axonyx are described in the documents Axonyx files from time to time with the SEC, including Axonyx's annual report on Form 10-K. Statements with regard to product candidates of either Axonyx or TorreyPines Therapeutics are subject to risks and uncertainties relating to development, regulatory approval and commercialization, including whether any preclinical studies or clinical trials, either ongoing or conducted in the future, will prove successful, and if successful, whether the results can be replicated; whether safety and efficacy profiles of any of its drug candidates will be established, or if established, will remain the same, be better or worse in future clinical trials, if any; whether pre-clinical results will be substantiated by ongoing or future clinical trials, if any, or whether any of its drug candidates will be able to improve the signs or symptoms of their respective clinical indication; whether any of its drug candidates will support an NDA filing, will be approved by the FDA or its equivalent, or if approved, will prove competitive in the market; or whether the necessary financing to support its drug development programs will be available. Neither Axonyx nor TorreyPines Therapeutics undertakes any obligation to publicly release the result of any revisions to such forward-looking statements that may be made to reflect events or circumstances after the date hereof or to reflect the occurrence of unanticipated events.

TorreyPines Therapeutics, Inc.
http://www.torreypinestherapeutics.com

Last Updated: Monday, 7 March, 2005, 23:19 GMT
http://news.bbc.co.uk/
1112.Study suggests 'type 3 diabetes'

Scientists say they may have discovered a previously unknown form of diabetes, after finding the brain produces insulin as well as the pancreas.
Unlike other types of diabetes, the form - dubbed type 3 by the US Brown Medical School team - is not thought to affect blood sugar.

Type 3 affects brain insulin levels, and appears to be linked with Alzheimer's disease.

The team's research appears in the Journal of Alzheimer's Disease.

Type 1 and type 2 diabetes occur when the body is unable to produce or use insulin from the pancreas.

The so-called 'type 3' diabetes refers to lower than normal levels of newly discovered brain insulin, which appears to be associated with Alzheimer's disease in some way.

Scientists have known for some time that people with diabetes have an increased risk of Alzheimer's disease - by up to 65%.

They have also discovered that many type 2 diabetics have deposits of a protein in their pancreas which is similar to the protein deposits found in the brain tissue of people with Alzheimer's disease.

Research has been going on to find out what links the two conditions.

Dr Suzanne de la Monte and colleagues now believe it is down to what they are calling type 3 diabetes.

By looking at rodents and post-mortem brain tissue from people with Alzheimer's disease they have found that insulin and its related proteins are actually produced in the brain, and that reduced levels of both are linked to Alzheimer's disease.

'Brain' insulin

They say this insulin and its related growth factors and receptors in the brain are vital for the survival of brain cells.

If they are not produced at normal levels, the cells die.

In the case of Alzheimer's, the cells that die are located in the part of the brain involved with memory, called the hippocampus.

Dr de la Monte, who is a neuropathologist at Rhode Island Hospital, said: "What we found is that insulin is not just produced in the pancreas, but also in the brain.

"These abnormalities do not correspond to type 1 or type 2 diabetes, but reflect a different and more complex disease process that originates in the central nervous system."

Not only does this opens the way for targeted treatment to the brain and changes the way we view Alzheimer's disease, "it raises the possibility of a type 3 diabetes", she said.

"The implication is that treating type 1 or type 2 diabetes may have no impact on Alzheimer's disease. We believe that therapeutic agents need to be designed that specifically influence the actions of insulin in the brain," she said.

Cathy Moulton, care advisor at Diabetes UK, said: "So far studies on a potential link between Alzheimer's and diabetes have come up with inconclusive results.

'More research'

"There is some evidence to suggest that poorly controlled diabetes also affects the functioning of the brain.

"However, far more research on a link between Alzheimer's and diabetes is needed before we can draw any firm conclusions."

A spokeswoman from the Alzheimer's Research Trust said: "Researchers have believed for some time that the role of insulin and its growth factors are very important in Alzheimer's disease.

"Scientists have suggested that the link could be down to molecular changes affected by insulin.

"Work funded by the Alzheimer's Research Trust is currently investigating the way insulin acts on the brain and should improve our understanding of Alzheimer's and hopefully lead to way to new treatments.

Professor Greg Cole, from the University of California Los Angeles' Alzheimer's Disease Research Center, said: "This is a new finding. It is interesting that the brain makes very low levels of insulin.

"But its significance is unclear. The levels are so low that they have not been detected with less sensitive methods. I don't think we can say they are high enough to matter.

"I suspect that the brain insulin itself is not very significant and neither is its deficit in Alzheimer's disease and, therefore, I wouldn't call it type 3 diabetes."

But he said there was evidence that diabetes and Alzheimer's are linked in some way.

1113.Madrid: ICAD Conference Draws to a Close

http://www.alzforum.org/
21 July 2006. The 10th International Conference on Alzheimer’s Disease and Related Disorders, ICAD for short, ended yesterday just outside the palatial capital of Spain. The conference attracted not only a record number of attendees?just above 5,000 from 50 countries?but also a visit by Queen Sofia, whose philanthropy supports AD care and research in her country. (The first ICAD conference, held 1988 in Las Vegas, hosted around 300 attendees.)
In several dozen informal interviews in hallways, ballrooms, on escalators and shuttle buses, attendees applauded that many scientists presented unpublished data in their talks and posters. Presentations included major new developments, such as the discovery that the progranulin gene causes a form of frontotemporal dementia (see ARF related news story) as well as the discovery of a physiological function for the enzyme BACE (see ARF related news story) Smaller nuggets of news solidified emerging trends or opened up new research directions. Some scientists grumbled about feeling crammed into a crowded poster area while the neighboring company exhibits enjoyed all the space and air that’s necessary for animated conversation. Others viewed the commercial presence, together with the large number of presentations on a variety of experimental therapies, as a positive sign of the field’s needed movement toward translational science as patient numbers grow inexorably.

Even a casual flick through the conference program makes clear that a large fraction of the presentations focused on a panoply of different early detection and diagnostic efforts. Research in this area has exploded compared even to as recently as 5 years ago. It included attempts to detect telltale fingerprints of preclinical AD in body fluids, such as innovative work on leukocyte gene expression profiles or more advanced attempts to validate known biomarkers in the cerebrospinal fluid. Efforts ranged from imaging methods and more refined neuropsychological tests to proxy markers derived from epidemiological research on risk factors in the cardiovascular and metabolic fields. On the imaging front, news included updates on the amyloid imaging agent PIB and its use in presymptomatic carriers of familial AD mutations, as well as talks on promising new approaches such as diffusion tensor imaging and perfusion MRI to measure the degradation of the brain’s white matter that is thought to precede overt AD.

This early detection work reflects an emerging consensus among scientists that Alzheimer disease develops for a decade, perhaps even longer, before clinical signs become apparent. In fact, researchers increasingly compare the phase of diagnosed AD as we know it to terminal, metastatic cancer?the end stage of a disease that ideally should be treated years before the patient shows up at the neurologist’s door. The need for early detection is pressing, and many scientists wonder whether some drugs fail partly because they are tested too late in the disease.

The lack of validated, consensus biomarkers notwithstanding, this year’s ICAD program indicates that therapeutic approaches appear to grow exponentially at the present stage of AD research. The majority of them dig into some aspect of the amyloid hypothesis, but not all. Outliers that buck this overwhelming trend include intranasal insulin, growth factor gene therapy, gonadotropal hormones, tau immunotherapy, and dietary supplements. Immunotherapy approaches appear to have mushroomed, but many scientists remain as wary of their potential side effects as they are hopeful about their ability to remove forms of Aβ or amyloid. Finally, if γ-secretase inhibitors could speak, they might borrow a quote from Mark Twain and declare that the reports of their death have been greatly exaggerated. β-secretase inhibitors, still largely guarded behind the doors of pharmaceutical companies, are beginning to show their face, as well.

What works? To date, some trials remain ongoing and blinded, other approaches look promising in pilot trials only to fail in larger ones, and yet others appear to be limping along with rather small effect sizes. Piecing together the shards of the shattered AN1792 trial, scientists appear to be finding hints that the patients might yet have benefited a whit from the prototype vaccine after all. That said, the croupier is still taking bets on which of the current approaches will survive the minefield of cost, trial design headaches, patient recruitment and dropout woes, side effects, bad press, and struggle with the FDA that together characterize today’s drug development environment.

Some issues were notable for their absence. For example, there were fewer discussions than at prior conferences about whether Aβ oligomers, fibrils, or plaques were the toxic species in AD. Researchers appeared to have adopted the stance that all of these are damaging when present in excess over a long period of time (though more are also coming around to think that, at the proper levels, Aβ may indeed have a physiological role to do with synaptic activity). Broadly speaking, oligomers are suspected of triggering acute cognitive deficits, whereas plaques are thought to damage the structure and transmission capability of the brain and to fuel chronic inflammatory states. Likewise, investigators no longer debated whether Aβ or tau are detrimental factors in AD. Most view both proteins as critical, and Aβ as upstream of tau. At the Alzforum symposium, Bart de Strooper referred to the “Amyloid Tau Hypothesis” as a framework for AD research. What’s more, some scientists suggested that tau pathology appears to occur downstream of many amyloids, not just amyloid-β but also prion amyloid and synuclein deposits, for example. Yet another shift appears to occur around the notion that, increasingly, basic scientists no longer focus as relentlessly on Aβ or tau as they tended to do before, but view them as but two players in a broader drama of oxidative, synaptic, and proteasomal stress, confounded by systemic changes such as high blood pressure, insulin resistance, and other components of what is collectively called metabolic syndrome. Consequently, future treatments will likely have to include combinations of drugs directed against Aβ, against tau, as well as neuroprotective, cardiovascular, and other agents.

Details from roughly 340 talks and 400+ posters in six days can make the most capacious brain overflow. More than 300 conventioneers took advantage of a break offered by the Alzforum and joined our 10th anniversary symposium. Called “Mapping the Next Decade of Alzheimer Research,” it took a crack at integrating major ideas and trends in AD research. Admission was possible only for those who passed a spatial learning paradigm called the Madrid Paper Maze. Probants had to navigate a trail of signs to find the hidden platform?that is, a location changed at the last minute to a different quadrant of the convention center. We will post coverage of this event, as well as a stream of news stories from the ICAD conference, over the next two weeks. As always, contributions from our readers are warmly invited.?Gabrielle Strobel.

July 24, 2006　　http://www.ncsu.edu/

1114.Shape Matters: NC State Scientists Characterize Structure of Protein Involved in Preventing Alzheimer’s, Huntington’s Diseases

Scientists at North Carolina State University have effectively lifted the veil from an important protein that is linked to the prevention of neurodegenerative diseases like Alzheimer’s and Huntington’s.

Dr. John Cavanagh, professor of molecular and structural biochemistry, teamed with colleagues from the Mayo Clinic and Duke University to describe the shape of the protein, calbindin-D28K. Understanding a protein’s structure allows researchers to learn more about how it functions and interacts with other proteins, which, in this case, may provide clues to developing drugs to halt the diseases.

The research appears in the July 2006 edition of Nature Structural and Molecular Biology.

Calbindin-D28K is a protein that either grabs calcium from areas that have too much or serves as an on/off switch for further chemical reactions. It is known for its flexibility; it is found in the kidneys, pancreas, ocular nerve and in abundant quantities in the brain. Recent studies show, Cavanagh says, that it acts as a bodyguard in the brain, binding to and inhibiting caspase-3, a protein that stimulates plaque formation and tangle formation, which are hallmark characteristics of neurodegenerative disease. Until now, however, the structure of calbindin-D28K remained a mystery.

“If you don’t know the shape of the protein, you can’t figure out how it works,” Cavanagh says. “It took a long time ? about five years ? but we’ve characterized the structure of this protein and found where it binds caspase-3. Insight into how it binds to caspase-3 might lead to a way of exploiting those interactions to develop therapeutics.”

It took a long time to characterize calbindin-D28K, Cavanagh says, because it was initially a challenge to force cells to make enough protein in order to do the requisite studies. Additionally, many parts of the protein are very similar and so are extremely difficult to distinguish from each other.

The research team used nuclear magnetic resonance to get a high-resolution picture of what the protein looks like. In this painstaking technique ? occurring inside machines that have magnetic fields several hundred times greater than the Earth’s magnetic pull ? radio waves are bounced off the approximately 5,000 nuclei in the protein.

“When you hit a nucleus with a radiofrequency pulse, it resonates, sort of making its own little noise, like a tuning fork,” Cavanagh says. “The frequency at which the nuclei resonate after being hit with a pulse is very specific to their specific position in the protein. So after we hit all of them with a pulse, it’s like hitting all the keys of a piano at the same time and it’s just an awful mess. And remember, we’re doing this for 5,000 separate keys. Yet, we’re able to untangle this mess to find the specific frequency of each nucleus and relate that to where it lies in the protein.”

Cavanagh isn’t satisfied with this knowledge, however. He says the shape-shifting protein sometimes contains no calcium. When it grabs calcium, it changes its shape.

“This could be why the protein plays so many different roles,” Cavanagh says. “Proteins that change shape usually serve as on/off switches, but this protein also grabs calcium and takes it elsewhere. Now we’re working to determine the structure of this protein when it has no calcium.”

The National Institutes of Health, the American Foundation for Aging Research and the Kenan Institute for Engineering, Technology & Science supported the research.

- kulikowski -

1115.Glaxo says Avandia for Alzheimer's could be huge
Wed Jul 26, 2006 9:24am ET

LONDON, July 26 (Reuters) - Using diabetes drug Avandia as a treatment for Alzheimer's disease could be a huge opportunity for GlaxSmithKline Plc (GSK.L: Quote, Profile, Research), its chief executive said on Wednesday.

"If this succeeds, Avandia XR could be the most important asset in our pipeline," Jean-Pierre Garnier told analysts in a conference call.

Europe's biggest drugmaker has started a Phase III clinical trials programme involving more than 2,500 patients to assess the use of an extended release version of its diabetes medicine in Alzheimer's.

The study follows a growing body of scientific evidence that drugs which help regulate blood sugar may help patients with dementia as well.

Causes of Alzheimer's are poorly understood, but researchers told the International Conference on Alzheimer's Disease and Related Disorders in Madrid this month they had found clear links with diabetes

1116.Keeping Mind And Body Active Slows Alzheimer's
Main Category: Alzheimer's News
Article Date: 26 Jul 2006 - 9:00am (PDT)
http://www.medicalnewstoday.com/
Researchers have uncovered the pathways behind the protection offered by environmental stimulation in Alzheimer's disease, further confirming that enhanced mental and physical activity slows neurological decline. The paper by Ambr-e et al., "Reduction of amyloid angiopathy and A?? plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways," appears in the August issue of The American Journal of Pathology.

Alzheimer's disease, the leading cause of senile dementia, presents with cognitive and behavioral deficiencies resulting in part from accumulation of ???-amyloid (A???) deposits within the brain (A??? plaques) and its blood vessels (amyloid angiopathy). Although previous studies have shown that increased mental and physical activity can slow the progression of the disease, how such deceleration occurs has been unclear until now.

Dr. Kathy Keyvani's group at University Hospital Muenster examined the effects of environmental stimulation on the brain pathology of TgCRND8 mice. These mice, which express a mutant form of A??? found in some Alzheimer's patients, develop Alzheimer-like features including A??? plaques and cognitive deficits. To study the effects of enrichment, mice were housed in either standard cages or enriched cages, similar to the standard but with access to a stimulus cage containing permanent fixtures (rope and gnawing wood) as well as removable items (tunnels, balls, ladders, ramps, and exercise wheels) that were changed on a rotating basis.

Following five months of standard versus enriched housing, mouse brains were examined for signs of disease. Mice housed in the enriched environment had fewer A??? plaques, smaller plaque size, and reduced amyloid angiopathy compared to mice housed in standard cages. Interestingly, there were no differences in the levels of soluble A??? peptide or the transcriptional/translational expression levels of its precursor protein (APP) or the processing of APP between the two groups. So how did environmental stimulation prevent disease?

To answer this question, Ambr-e et al. performed DNA microarray analysis to determine which genes were differentially regulated in mice housed in the enriched environment compared to standard cages. Enriched mice exhibited down-regulation of pro-inflammatory genes but up-regulation of genes related to anti-inflammatory processes, protein degradation and cholesterol binding. These results were confirmed by specifically analyzing gene expression for examples in each category. Together these data suggest that an enriched environment elicits protection via pathways that prevent A??? accumulation and enhance its clearance.

The authors speculate that the altered expression of inflammatory genes may shift the immune response from one that is neurotoxic to one that is phagocytic, i.e., able to clear unwanted debris, such as A???. In accordance with this, a significant enhancement of microglial activity was found by Western blot and morphometric analyses of microglia, which often surround and infiltrate A??? plaques. In addition, activating cellular protein degradation pathways provides another means of removing excess A???. Finally, changes in cholesterol homeostasis, elements of which have been shown to correlate with A??? deposition, may exert beneficial effects by preventing plaque formation in the first place.

These data provide strong evidence that an environment rich in mental and physical stimulation slows the progression of Alzheimer-like brain pathology. Further investigation of the pathways and individual elements involved in such protection may provide novel treatment strategies for Alzheimer's disease. Until that time, keep your running shoes and crossword puzzles handy.

###

This work was supported by grants from Innovative Medical Research and German National Academic Foundation.

Work was directed by Dr. Kathy Keyvani of University Hospital Muenster and involved collaborators at University of Muenster.

Ambr-e O, Leimer U, Herring A, Gertz N, Sachser N, Heneka MT, Paulus W, Keyvani K. Reduction of amyloid angiopathy and A?? plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways. Am J Pathol 2006 169:544-552

For more information on Dr. Keyvani, please contact Jutta Reising at University Hospital Muenster, Germany: jutta.reising@uni-muenster.de.

The American Journal of Pathology, the official journal of the American Society for Investigative Pathology (ASIP), seeks to publish high-quality original papers on the cellular and molecular mechanisms of disease. The editors accept manuscripts which report important findings on disease pathogenesis or basic biological mechanisms that relate to disease, without preference for a specific method of analysis. High priority is given to studies on human disease and relevant experimental models using cellular, molecular, biological, animal, chemical and immunological approaches in conjunction with morphology.

Contact: Audra Cox
American Journal of Pathology

1117."Promising" Treatments Coming For Alzheimer's Disease
By STEVE NEWBORN

http://www.wusf.usf.edu/NewLogo_History.cfm
TAMPA (2006-07-26) A skin patch containing the drug Exelon may get approval from federal regulators by the end of the year. It's one of the most promising treatment for Alzheimer's, which currently affects nearly five million Americans.

In Tampa, a different kind of treatment is being devised at the Johnnie Byrd Alzheimer's Center. Dr. Huntington Potter is its CEO and research director.

POTTER: The best approach is to first try the drugs in mice that have Alzheimer's Disease, and see if they get better. We have such a drug, called Rolipram - it's actually an old drug developed for depression. But it essentially cures the memory problems of the Alzheimer's Disease in the mice.

Potter says Rolipram has been tried in humans, but has been found to cause nausea. He says the instutite paroposed several months ago to put the drug into a skin patch. It would be easier to take, and could last longer, which would be beneficial to Alzheimer's patients who sometimes forget to take their medication.

? Copyright 2006, WUSF

Wednesday, 26th July 2006 07:38　　http://www.lse.co.uk/index.asp

1118.BTG completes early Alzheimer's trial; says started yr in strong position

LONDON (AFX) - Medical innovations group BTG PLC said it has successfully completed a phase I trial of BGC20-1259, a treatment for Alzheimer's, and that a follow on trial will start once regulatory approval is granted.

Full results are anticipated by the end of the year.

In a statement released ahead of its annual shareholder meeting, the company said reduced costs, increasing royalty revenues and the commercialisation of non-core assets has enabled it to start the new financial year in a strong position.

More than a dozen potential drug programme acquisition targets are being reviewed, BTG said.

And the first patient should be treated in early 2007 in the key Phase II safety study in the US for its varicose vein treatment Varisolve.

Meanwhile, results from the phase I/II trial of Plevitrexed in patients with advanced and/or metastatic gastric cancer are expected at the end of 2006.

BTG shares closed Tuesday at 121.75, valuing the company at 183 mln stg.

amy.brown@afxnews.com

ab/abr

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Public release date: 26-Jul-2006
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Contact: Leah Farrasso
lfarrasso@webershandwick.com
312-988-6617
Weber Shandwick Worldwide

1119.Groundbreaking research highlights myriad health benefits of flavanol-rich cocoa
Mars, incorporated scientists and researchers around the world find link between cocoa flavanols and brain, cardiovascular improvements
HACKETTSTOWN, NJ ? July 25, 2006 ? Research has demonstrated that consumption of naturally occurring compounds in cocoa can lead to a range of circulatory health benefits including the first observed brain and cardiovascular blood flow improvements, according to research published in the latest issue of the Journal of Cardiovascular Pharmacology, in a supplement that focuses on the potential health benefits of flavanol-rich cocoa.
Previous studies have demonstrated that the consumption of flavanol-rich cocoa can improve blood vessel function and may even reduce the formation of damaging clots. This new, published research extends these findings by showing that the regular consumption of flavanol-rich cocoa can lead to improved blood flow in menopausal women with elevated cholesterol, as well as reporting for the first time that the increase in blood flow following flavanol-rich cocoa consumption can also be observed in the brain.

"The totality of this research is impressive and gives us new insights into how cocoa flavanols may improve health in a variety of ways not previously known," said Harold Schmitz, PhD, Chief Science Officer of Mars, Incorporated, which has conducted and supported a majority of the research on cocoa flavanols and health for more than 15 years. "This publication, resulting from the science presented at an international meeting convened last year in Lucerne, Switzerland, is exciting as it adds to the growing body of scientific research demonstrating that the consumption of flavanol-rich cocoa can potentially lead to a range of physiological benefits resulting from improved blood flow."

Researchers studied the effects of cocoa flavanols in vitro (test tube) and in human subjects, on various age groups, on women and men in order to better understand the potential benefits of these natural food compounds. Among the new studies, the highlights include:

Brain blood flow in the elderly and young adults: Two independent studies, one in a healthy elderly population and another in young healthy women, demonstrate that the consumption of flavanol-rich cocoa can increase blood flow to the brain. This work, the first of its kind with cocoa, suggests that this cocoa may have promising effects on cognitive performance ? particularly promising because decreased brain blood flow is associated with dementia and deterioration in brain function.
Blood flow in postmenopausal women: Scientists found that the regular consumption of flavanol-rich cocoa resulted in a significant increase in blood flow in hypercholesterolemic postmenopausal women, suggesting that this cocoa may improve vascular function in this population with higher cardiovascular risk.
Different flavanols have different functions: Flavanol-rich cocoa has previously been shown to decrease the potential for formation of blood clots. In this new investigation, researchers coupled studies of platelet function in humans with in vitro studies with highly purified flavanols from cocoa. The results of these studies support that cocoa flavanols may have beneficial effects on platelets, and report for the first time that certain flavanols and flavanol-rich cocoa itself may also reduce the cascade of events that can lead to vascular damage.
Benefits for a high cocoa flavanol consuming population: Previous research has identified the island dwelling Kuna Indians of Panama as a population with an unusual absence of age-related hypertension and cardiovascular disease, despite a level of salt intake comparable to that in Western societies. The investigators conducted a comprehensive dietary survey to see if specific dietary factors may be responsible. Most notable was the finding the Kuna consumed high levels of cocoa, confirmed by analysis to be rich in flavanols, suggesting that there may be a link between the habitual intake of flavanol-rich cocoa and their low incidence of vascular disease.
"We are excited by this research as it provides promising evidence that cocoa flavanols may have an important role not only in treating, but also possibly preventing a range of health issues related to blood flow problems," said Schmitz. "This new science sets the stage for the potential development of cocoa flavanol based products useful for a wide variety of important public health issues impacted by decreased blood flow, ranging from, cardiovascular health to dementia."


###
Mars Leadership in Cocoa Flavanol Research Working in collaboration with top research institutions throughout the world, Mars has led research on nutritional and medical potential of cocoa flavanols, with more than 100 peer-reviewed research articles and more than 80 patents held by Mars scientists. The Journal of the American College of Cardiology named a recent study of cocoa flavanols and blood vessel function by a collaborative group of researchers in Germany, the University of California, Davis and Mars to be one of the major advancements in cardiovascular research in 2005. (DeMaria AN et al. Highlights of the Year in JACC 2005. Journal of the American College of Cardiology. 2006; 47(1):184-202.)

Scientists at Mars, Incorporated developed a patented process called Cocoapro? that helps retain consistent level of cocoa flavanols that occur naturally in cocoa beans. Mars products that are made with the Cocoapro process include Dove? Dark Chocolate and CocoaVia?, a new line of heart healthy snacks that are guaranteed to contain at least 100 mg of cocoa flavanols per serving. Cocoapro cocoa is the most studied cocoa in the world in terms of health impact.

For more information on the many research studies on cocoa flavanols, visit www.cocoapro.com. For additional information on the individual studies, contact Leah Farrasso at 312-988-6617 or via email at lfarrasso@webershandwick.com.

Mars, Incorporated is one of the world's top producers of chocolate, and has a strong commitment to health research. With well over 15 years of research into the health benefits of cocoa flavanols, and decades of research invested into improving the cocoa plant and farming techniques, Mars, Incorporated has become the global leader in cocoa science. Mars uses patented and proprietary methods of processing cocoa beans to retain much of the naturally occurring flavanols, marking these products with the Cocoapro? seal, a hand holding a cocoa bean to signify the careful handling.

Source:

Journal of Cardiovascular Pharmacology 2006; 47: S99-S225.

1120.Alzheimer's disease　Puzzling out the truth
Jul 27th 2006 | MADRID
From The Economist print edition

A century after its characterisation by Alois Alzheimer, senile dementia remains almost untreatable. But there is hope

Alamy
BETA or tau? That is the question. On it hang both the health of many of the baby-boomer generation as they reluctantly stare old age in the face and the financial health of rich countries' medical and social-security systems. For, as the 10th International Conference on Alzheimer's Disease and Related Disorders, held recently in Madrid, heard, the relentless growth in the number of people with Alzheimer's threatens health-care provision in the developed world.

Medical advance means that other diseases are failing to cull the population before Alzheimer's destroys people's minds. And Alzheimer's is both expensive and lingering. In America, the average cost of looking after someone with the disease between diagnosis and death is at least $174,000.

At the moment, 4.5m Americans have Alzheimer's. By 2050, if nothing changes, that number will have trebled. But if a treatment that delayed the disease's onset by seven years were to be available by the end of the decade, the number of sufferers would decline by 40% by the middle of the century. Hence the importance of understanding how Alzheimer's works, the better to devise a treatment.

Beta (in the form of beta-amyloid plaques) and tau (in the form of tau tangles) are the physical manifestations of Alzheimer's. The plaques are globs of rogue protein in the spaces between nerve cells. The tangles are made of a different rogue protein, and form inside nerve cells.

The smart money says that plaque formation triggers the disease, and that the tangles are a secondary effect. This is known as the amyloid-cascade hypothesis, and most searches for treatment are based on it. But there are dissenters who reckon that this is the wrong conclusion. Some think that the role of the tangles is being underplayed, others that something altogether different has gone wrong.

It's all Greek
Amyloid plaques form when a molecule called amyloid precursor protein (APP) is chopped up by two enzymes known as beta-secretase and gamma-secretase. One of the products, with the long-winded name amyloid beta-peptide 42, has the unfortunate property that its molecules like to stick to each other. The resulting plaques, reckon supporters of the cascade theory, trigger the brain damage that manifests itself as memory loss, behavioural and personality changes, and general and irreversible cognitive decline. So, stop the plaques forming?or get rid of them once they have formed?and you should be able to control the disease.

One way to do so might be to develop a vaccine that stimulates antibodies against amyloid beta-peptide 42. That is the path being pursued by Elan Pharmaceuticals and Wyeth Research. In 2000, these two firms began a clinical trial of such a vaccine. Unfortunately, they had to halt it when 18 of the 300 patients involved developed severe inflammation of the brain. In the time that the trial had run, however, the researchers noticed that those patients who had reacted to the vaccine, but whose brains had not swollen up, showed a marked slowing of cognitive decline. This suggested they were on the right track, and the companies are now testing what they hope is a less toxic vaccine.

An alternative to vaccination is to make the antibodies in a factory, and then inject them. This is called passive immunisation. Preliminary trials suggest it is safe, and a study carried out by Wyeth showed that treatment with a single dose of antibody produced significant cognitive improvements over the course of four months. In other words, the drug does not just slow the disease, it reverses it.

Nor is the immunological approach the only one under investigation. For the past decade there has been a lot of work on drugs called secretase inhibitors, which alter the activity of the enzymes that create amyloid beta-peptide 42.

Researchers have known for some time that the long-term use of aspirin and ibuprofen, which belong to a group of drugs called non-steroidal anti-inflammatories, roughly halves a person's risk of developing Alzheimer's. This has nothing to do with their anti-inflammatory properties, though. It is because they also act on gamma-secretase. They alter the way it cleaves amyloid precursor protein. Instead of producing amyloid beta-peptide 42 (so called because it has 42 of the amino-acid units of which proteins are composed), they make peptides 37 or 38 amino acids long. These do not stick to one another.

Kenton Zavitz and his colleagues at Myriad Genetics presented the firm's latest findings on a non-steroidal anti-inflammatory derivative called R-flurbiprofen. Like many other molecules, flurbiprofen has a left-handed and a right-handed form. Normally, when the drug is synthesised, these are made in equal numbers. But it is possible to separate them.

Right-handed flurbiprofen lacks the anti-inflammatory effects of the left-handed version. This means it is less likely to cause the gastrointestinal problems associated with non-steroidal anti-inflammatories, so it is safe for long-term use. It still retains its APP-cleaving properties, though. The results of a trial with 200 Alzheimer's patients are encouraging. Patients with a mild version of the disease who took a high dose of the drug had a slower rate of decline than those who did not.

Hedging bets
Not everybody believes that focusing on amyloid is the right way to go, however. That is because there is, in fact, no clear correlation between the deposition of the plaques and the development of cognitive problems. Some dissenters think that tau tangles play a more central role than the cascaders have been willing to admit. There are also those, like Larry Goldstein, a professor of cellular and molecular medicine at the University of California, San Diego, who believe the triggering event is unrelated to either beta or tau, and is, in fact, a defect in the way that materials are transported through the filamentary protrusions, known as axons, that connect nerve cells to each other in the brain and to other cells a long way away in the body.

For tau, at least one drug is being tried out. Memantine has been prescribed for more than 20 years for various brain disorders, including dementia, because it is believed to protect against high levels of a neurotransmitter called glutamate. But there is evidence from several animal studies that it also prevents the modification of tau protein that leads to the formation of intracellular tangles. Work by Malin Gunnarsson and her colleagues at Uppsala University in Sweden recently confirmed that this is true in people, too.

Such bet-hedging is sensible. Alois Alzheimer's original paper, identifying both plaques and tangles, was presented in November 1906. A century later, the disease that bears his name is still a mystery?as is the question of how to treat it.

1121.Double-barreled Weapon Against Alzheimer's as Near as the Bathroom Cabinet (press release)
Posted Thursday, July 27, 2006 by NewsTarget, Key concepts: melatonin, Alzheimer's and antioxidant.
Printable article Permalink: http://www.NewsTarget.com/019794.html
http://www.newstarget.com/index.html
Researchers in China, Japan, Spain, Greece, the Netherlands, the US, and Turkey have recently zeroed in on a common supplement that has doubled-barreled benefits in the fight against Alzheimer’s disease. Well-known by travelers as an aid to cope with jet lag, melatonin may help prevent Alzheimer’s disease through its potent antioxidant properties. It can also ease sleep-disruption and sundowning in Alzheimer’s victims, according to recently published studies.
Sundowning, a typical symptom of Alzheimer’s disease, gets its name because it usually occurs around sundown. Alzheimer’s victims often display increased agitation and disorientation during the late afternoon or early evening.

“I’ve always kept a supply of melatonin,” says Dr. Phyllis Staff, a psychologist whose father had Alzheimer’s disease. “I’ve used it to combat jet lag for many years, but I didn’t realize it could help my father.”

“For years, at dusk, Dad would put on his cap and jacket and head out the door to ‘go home.’ A couple of times he made it out to the street unnoticed. My mother and I are grateful to a compassionate police force that picked him up, but it would have been such a blessing to have something to help him stop sundowning.”

Melatonin, a hormone produced by the pineal gland in the brain, regulates sleep and wakefulness in humans. Largely ignored by pharmaceutical companies because they cannot patent natural substances, melatonin is inexpensive and readily available over-the-counter in drugstores.

Melatonin’s benefits extend to dementia prevention. Able to pass through the blood/brain barrier, it exhibits powerful antioxidant effects in the brain. Researchers have found that melatonin combats oxidative stress and reduces the tangles and plaques typical of Alzheimer’s disease.

Originally Aired: July 26, 2006
http://www.pbs.org/newshour/
1122.Families Advocate for Alzheimer's Disease to Be National Priority

An estimated 4.5 million Americans have Alzheimer's, and the number is expected to triple within 10 years. Families of patients are making efforts to push the private and public sectors toward finding better treatments.

MERYL COMER, Has Husband with Alzheimer's Disease: It's going to be good. Eat it for Harvey. Good job.

SUSAN DENTZER, NewsHour Health Correspondent: This is Harvey Gralnick, age 70, 12 years into the ravages of Alzheimer's.

This was Harvey Gralnick at his prime. His diplomas and awards speak to his distinction as a longtime physician and research scientist at the National Institutes of Health. Gralnick was 58 at the peak of his NIH career when he was diagnosed with early-onset Alzheimer's.

MERYL COMER: OK, good job.

SUSAN DENTZER: His wife, former television journalist Meryl Comer, describes how this main form of dementia sapped his intellect and destroyed his personhood.

MERYL COMER: Somebody once described it as a house where you see one light go off at a time, or watching somebody in slow motion die, lose their mind in front of your eyes, literally lose their mind in front of your eyes. Very painful to watch, especially knowing what he was.


Raising urgency to fight disease
SUSAN DENTZER: Comer, who's 62, now works with a team of nursing aides to care for her husband at home. She says her and her husband's story is a harbinger of things to come for her generation, the baby boom.

MERYL COMER: I want people to understand this disease, because it's going to be part of our future. It has the potential to be an epidemic in our generation, in the baby boom generation.

SUSAN DENTZER: So she's joined forces with a new group called ACT-AD, for Alzheimer's disease, to dramatically raise the sense of urgency to fight the condition. She spoke at a recent news conference.

MERYL COMER: I've come with another agenda that is shared in principle by everyone signing on to ACT-AD: the urgent need to change the conversation about this disease; accelerate the delivery of promising drugs to patients; improve the plight of families; and make this disease a national priority.

SUSAN DENTZER: An estimated 4.5 million Americans have Alzheimer's today, and the number is expected to triple within 10 years. The disease mainly strikes people in their 60s and beyond. By age 85, a stunning one-half of people have it.

MERYL COMER: Harv, can you see me? Harvey?

SUSAN DENTZER: But Gralnick's early-onset form mainly affects those in their 50s. Steve McConnell oversees policy and advocacy for the Alzheimer's Association.

STEPHEN MCCONNELL, Alzheimer's Association: We have found that as many as 600,000, somewhere between 200,000 and 600,000 baby boomers, people under age 65, have Alzheimer's disease, and that is truly terrifying.

SUSAN DENTZER: Early-onset Alzheimer's is traceable to genetic mutations passed down through families, but its symptoms are virtually identical to the form that hits other people later in life. Comer describes the first signs she saw in her husband.

MERYL COMER: His mood changed. The papers that were orderly in his mind became chaos. Frustration levels soared, couldn't find things, highly frustrated, agitated.

You OK? Feeling better?


Mystery behind the disease
SUSAN DENTZER: Comer says that, as she grew more concerned, she persuaded him to see a neurologist, who declared nothing amiss. Gralnick was later hospitalized for two months while doctors struggled to figure out what was wrong. Only later, as his symptoms worsened, did one venture the tentative diagnosis of Alzheimer's.

Dr. Sam Gandy is a leading neuroscientist at Thomas Jefferson University and chief scientific adviser to the Alzheimer's Association. He says scientists still don't fully understand what causes Alzheimer's disease and have several competing theories. Perhaps the leading one links the condition to changes in a common body protein, called amyloid.

DR. SAM GANDY, Thomas Jefferson University: Amyloid is actually normally made by all cells in the body all throughout life. In Alzheimer's disease, this protein changes its shape, becoming extremely sticky, forming clumps, and building up in between and outside of nerve cells.

SUSAN DENTZER: The amyloid proteins in Harvey Gralnick's brain had probably begun to change at least a decade before his symptoms became apparent. Gandy demonstrated how with a piece of wire.

DR. SAM GANDY: The process that begins Alzheimer's disease is what we call protein folding, and literally the amyloid protein folds back on itself like a big bobby-pin. And this then is a sticky form, and many of these bobby pin-like sticky structures aggregate together, clump together.

SUSAN DENTZER: Those sticky clumps of proteins are called amyloid plaques. For unknown reasons, they form only in certain parts of the brain rather than a whole body. Then they kill the vital neurons, or nerve cells, through which the brain does its primary work.

DR. SAM GANDY: Scientists sometimes describe these as resembling Brillo pads. You could see them building up outside nerve cells and in between nerve cells. These then would be supplying the poison that would kill this nerve cell.

SUSAN DENTZER: As the nerve cells die, their inner skeletons collapse, forming what are called tangles. Many scientists also think this process plays a pivotal role in Alzheimer's.

Using a plastic brain model, Gandy then showed us how all this damage starts in the brain's hippocampus region, which is responsible for memory and thought. That helps to explain a classic early Alzheimer's symptom: the loss of short-term memory, even as memories from long ago can somehow remain intact.

DR. SAM GANDY: As the disease progresses, it's on a malignant process. It destroys not only the nerve cells in the hippocampus responsible for memory, but many of the cells throughout the top of the brain, called the cortex. This is the master circuitry of the brain.

As the disease progresses, people become withdrawn from their environment, ultimately take to bed, and lose all ability to communicate with their environment or interact at all.


Developing new drugs
SUSAN DENTZER: In perhaps the disease's final insult, the part of the brain responsible for regulating basic body functions, like breathing, are not affected.

DR. SAM GANDY: This region here is called the brain stem.

SUSAN DENTZER: So even after having lost the ability to interact, patients like Gralnick can live a long time until an unrelated infection, like pneumonia, kills them.

Gandy says an effective treatment for Alzheimer's would block, reverse or at least slow down the formation of plaques and tangles. But current drugs on the market for treating Alzheimer's -- with names like Aricept, Exelon and Reminyl -- fall far short of that.

DR. SAM GANDY: They help the brain to compensate for a chemical deficiency that's present early in the disease. But as the disease progresses, their effect wears off and they become totally ineffective.

SUSAN DENTZER: So one goal now is to develop combinations of drugs that would work in various ways to attack the fundamental disease process.

That's the hope now of global pharmaceutical companies, which are exploring as many as 140 different compounds for that purpose. If successful, several could one day be used much like AIDS cocktails to hold Alzheimer's in check, or at least turn it from an inevitable slide downward into a more slowly progressing, chronic disease.

STEPHEN MCCONNELL: If science can produce a breakthrough that simply slows the progression of this disease and delays its onset just by a couple of years, it will save $50 billion a year in the Medicare program, a savings of $13 for every dollar spent on research.

SUSAN DENTZER: One pharmaceutical company working especially hard toward that goal is Wyeth, where Bob Essner is chairman and CEO. He says watching several friends and relatives suffer from the disease has made him impassioned on the subject.

ROBERT ESSNER, Chairman and CEO, Wyeth: What we're trying to do is to kind of put Alzheimer's disease now into the same priority that we've seen in the past with HIV-AIDS, with cancer, treatments for cancer, and most recently with avian flu.

SUSAN DENTZER: At the urging of Wyeth scientists, Essner agreed several years ago to plunge the company into a high-stakes, high-cost partnership with an Irish firm, Elan Pharmaceuticals.

Elan was working on a vaccine aimed at stimulating the body's immune system to make antibodies to destroy the amyloid plaques. Although the vaccine has been shown to work in mice, so far the human brain has proved far more complicated. In 2002, a clinical trial of the vaccine in patients with Alzheimer's was halted when it produced dangerous side effects.

Menelas Pangalos heads up neuroscience research at Wyeth.

MENELAS PANGALOS, Vice President for Neuroscience Research, Wyeth: There was basically an inflammation in the brains of these patients, and so the trial had to be stopped. But what was very exciting was that there were some hints that this drug was doing what it did in mice, in people.


A safer vaccine
SUSAN DENTZER: Wyeth is now helping Elan develop a potentially safer vaccine approach, as well as working on several other Alzheimer's-fighting drugs. And the company seems every bit as determined as Meryl Comer to raise awareness about the disease.

As a result, it provided seed money to form that organization she joined, ACT-AD. Essner says part of the goal is to persuade the U.S. Food and Drug Administration to find new ways to bring Alzheimer's therapies to patients as quickly as possible.

ROBERT ESSNER: If the FDA were to engage as a partner and give the same kind of priority they give to cancer drugs or HIV drugs, that they could move the process of development along faster and potentially get a cure available faster than they otherwise might.

SUSAN DENTZER: FDA officials told us the agency shares ACT-AD's goal of moving ahead as fast as possible on Alzheimer's. In a statement, the agency said, it is, quote, "actively working with manufacturers, medical researchers, and the Alzheimer's patient community to facilitate development of new and better products for patients."

The agency said a key priority is developing new ways to test the effectiveness of Alzheimer's drugs by using imaging devices, such as this one, to monitor subtle changes in the brains of patients.

Meanwhile, an even harder task for Alzheimer's advocates may be working to reverse cuts in the research budget for the disease at the National Institutes of Health. Congress cut the NIH's overall budget this year for the first time in 36 years, and President Bush has proposed no further increase for fiscal 2007; that would translate into $6 million less next year for Alzheimer's research.

DR. SAM GANDY: The outlook is incredibly grim. It's difficult now to encourage new, young investigators to enter this enterprise. And so, as the NIH budget goes down, these scientists, these professors, cannot be employed, and they go elsewhere.

SUSAN DENTZER: The NIH's Dr. Norka Ruiz Bravo told us the proposed cuts were unfortunate, but unless Congress reverses them, they're inevitable at a time when the NIH budget is being squeezed to meet other government priorities.

DR. NORKA RUIZ BRAVO, Deputy Director for Extramural Research, NIH: There's no question that Alzheimer's is a devastating disease. I think we can all recognize that. It is, however, a very tough budget environment for NIH. The tough budget environment is going to affect all diseases, and Alzheimer's is one of many that it's going to affect.

SUSAN DENTZER: Comer says that's intolerable at a time that progress is so essential.

MERYL COMER: We need it fast, sooner rather than later, because I am terrified just by the notion that our generation will end up looking like my husband.

SUSAN DENTZER: Meanwhile, Comer knows that, for millions like her husband, it's already too late.

GWEN IFILL: In her next report, Susan will look at the impact Alzheimer's has on families and caregivers.

View press releases for July 27, 2006 Press Release Contact Information:
Joel Binder
Med America Research
PR
Whitestone, New York
E-Mail: medamerica1@cs.com
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1123.Is There Really a Connection Between Diabetes and Alzheimer's?
Asks Physician Lawrence Broxmeyer, MD
Summary; Shock waves from the recent Madrid Alzheimer's meeting sent scientists scurrying for an explanation for how a Seattle VA study showed that diabetes could lead to a nearly 70% increase in Alzheimer's disease. One scientist not caught off-guard was internist/researcher Lawrence Broxmeyer MD.

/24-7PressRelease/ - WHITESTONE, NY, July 27, 2006 - Lawrence Broxmeyer MD had long ago as much as predicted, through his peer reviewed publications, that Diabetes and Alzheimer's diseases were related through their root cause, a destructive protein called amyloid, which was the by-product of what to Broxmeyer was a common chronic infectious disease.

While some speculated that diabetic's insulin deficient or resistant cells led to a cut-off of vital blood sugar to brain neurons, disabling their ability to remove clumps of incapacitating Alzheimer's amyloid - others thought it was a one-two punch: Alzheimer's tendency to attack cell's mitochondria or energy factories, leading to a neuronal death facilitated by diabetes's own attack on the brain's neurons.

Broxmeyer was neither convinced nor impressed by either view.

"Over 3 decades ago", said Lawrence Broxmeyer MD, "pathologist and lead researcher, Dr. Phillip Schwartz, in a 50 year autopsy-driven study for a State facility in Warren Pennsylvania, published a report of 331 autopsied cases of amyloid, ages ranging from 16 to 87, with the finding that with regard to both diabetes and Alzheimer's there were not only tuberculous lesions somewhere in the body in practically all cases, usually from childhood infection, but more specifically amyloidosis of the pancreas in 224 out of the 331 from previous tuberculosis infection."

Furthermore, Schwartz found similar amyloid from similar cause and effect with regards to Alzheimer's.

"Moreover", continued researcher Lawrence Broxmeyer MD, "in the case of diabetes, most of those diagnosed as diabetic prior to death showed intense islet cell amyloidosis and Schwartz hypothesized that once amyloidosis of the pancreatic islet cells hit a critical mass, the result was diabetes mellitus. Thus, according to Schwartz, most cases of pancreatic amyloidosis, as well as the inflammatory infiltrate of the islet cells characteristic of Juvenile diabetes, and Alzheimer's, ought to be considered an immunopathy induced by tuberculosis and the mycobacteria. Diabetes was easy enough to pick up with routine laboratory tests, TB was not, its main weapon being its insidious nature, often taking decades to discover, if then."

Although stressing that it is still highly experimental, Lawrence Broxmeyer MD mentioned that The Puget Sound Seattle VA study showed subtle improvement in Alzheimer's patients placed on insulin mist. As a result researchers have now begun to reemphasize that diabetes not only attacks the body but the mind. "There are even those who, as a result of recent studies, now consider Diabetes a precursor for Alzheimer's," said Lawrence Broxmeyer MD.

"One thing is certain, as blood sugar control in diabetes worsens, Alzheimer's risk climbed," said Lawrence Broxmeyer MD, " in one study by 70%, in another by 83%."

Why this poses a particularly challenging problem is the present explosion of diabetes with approximately 20 million in the US already having the disease and 40 million prediabetics with faulty blood sugar-insulin response, close to joining their ranks. These pools could just increase the current 4.5 million American Alzheimer's sufferers.

Lawrence Broxmeyer MD, lead author in an October, 2002 study published in the prestigious Journal of Infectious Diseases and many other Medline publications, thinks the diabetes-Alzheimer link is important and certain to stimulate still other meaningful studies.

For a more complete picture of how these diseases originate, download and read Lawrence Broxmeyer MD's articles on the common cause of Diabetes and Alzheimer's please visit http://medamericaresearch.org.

Distribrution: Lawrence Broxmeyer MD, Lawrence Broxmeyer, Diabetes mellitus, Alzheimers

1124.ABC 7 Medical: Chinese Herb Offers Hope for Alzheimer's Patients
Thursday July 27, 2006 5:20pm
http://www.wjla.com/index1.html
Anchor:
EXCITING NEWS ABOUT A CHINESE HERB THAT SOME DOCTORS FEEL MIGHT DO MORE TO HELP ALZHEIMER'S PATIENTS THEN ANY DRUG CURRENTLY ON THE MARKET.
AS MEDICAL REPORTER KATHY FOWLER EXPLAINS, LOCAL DOCTORS ARE RECRUITING PATIENTS TO STUDY THIS HERB FOR THE FIRST TIME.

Kathy Fowler:
THIS HERB IS CALLED HUPERZINE A... IT'S AN EXTRACT FROM MOSS THAT GROWS IN CHINA. CHINESE DOCTORS USE IT TO TREAT ALZHEIMER'S PATIENTS AND NOW LOCAL DOCTORS ARE TESTING IT TO SEE JUST HOW GOOD IT IS.

Story Script:
"What'd you do Thursday?"

LAVOIE OLSEN HAS ALZHEIMER'S DISEASE, HER DAUGHTER JUDY WILL NEVER FORGET THE DAY LAVOIE HERSELF REALIZED SHE WAS FORGETTING THINGS.

Judy Olsen Ortega, Daughter: " 'She said, Don can't your dad help you with that,' and he told her Lavoy my father died and that just really broke her because she didn't remember that he already died."

LAVOIE ENROLLED IN A CLINICAL TRIAL AT GEORGETOWN UNIVERSITY MEDICAL CENTER, WHERE DOCTORS ARE TESTING AN OLD CHINESE HERB CALLED HUPERZINE A, THAT EXPERTS SAY MIGHT END UP BETTER FOR ALZHEIMER'S THAN ANY PHARMACEUTICAL CURRENTLY ON THE MARKET.

Dr. Paul Aisen - Georgetown university: "It is being used in China now, and there have been studies in China that suggest that it's a good treatment."

THERE HAVE BEEN LABORATORY STUDIES IN THE U.S. TOO THAT SHOW THE HERB HELP RESTORE MEMORY AND ALSO PROTECT THE BRAIN AGAINST FURTHER DAMAGE, WITH FEW OF THE SIDE AFFECTS AS OTHER DRUGS ON THE MARKET.

Dr. Paul Aisen: "We've done some phase one clinical studies in this country that also confirm that this drug has properties that should improve memory in people with Alzheimer's disease and in fact it will also slow the progression of Alzheimer's disease."

THE CLINICAL TRIAL IS DOUBLE BLINDED, SO LAVOIE'S FAMILY HAD NO IDEA IF SHE WAS TAKING THE HERB OR A PLACEBO.

Judy Olsen Ortega: "I think we noticed some improvements at first and it didn't cause any side affects."

Kathy Fowler:
"HUPERZINE A" CAN BE FOUND IN OVER THE COUNTER SUPPLEMENTS BUT DOCTORS SAY THE DOSE IN THOSE SUPPLEMENTS IS SO LOW. THEY DON'T THINK IT WOULD PROVIDE MUCH BENEFIT.

DOCTORS AT GEORGETOWN UNIVERSITY ARE RECRUITING MORE PATIENTS TO TAKE "HUPERZINE A" FOR THEIR STUDY. FOR MORE INFORMATION - LOG ONTO OUR WEB SITE AT WJLA.COM. JUST CLICK ON MEDICAL REPORTS.

For More Information: Memory Disorders Program at Georgetown

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

? Questions or Comments? Click Here To Email ABC 7

Source: University of California - Irvine

Posted: July 27, 2006

1125.Drug Triggers Body's Mechanism To Reverse Aging Effect On Memory Process
A drug made to enhance memory appears to trigger a natural mechanism in the brain that fully reverses age-related memory loss, even after the drug itself has left the body, according to researchers at UC Irvine.

Professors Christine Gall and Gary Lynch, along with Associate Researcher Julie Lauterborn, were among a group of scientists who conducted studies on rats with a class of drugs known as ampakines. Ampakines were developed in the early 1990s by UC researchers, including Lynch, to treat age-related memory impairment and may be useful for treating a number of central nervous system disorders, such as Alzheimer’s disease and schizophrenia. In this study, the researchers showed that ampakine drugs continue to reverse the effects of aging on a brain mechanism thought to underlie learning and memory even after they are no longer in the body. They do so by boosting the production of a naturally occurring protein in the brain necessary for long-term memory formation.

The study appears in the August issue of the Journal of Neurophysiology.

“This is a significant discovery,” said Gall, professor of anatomy and neurobiology. “Our results indicate the exciting possibility that ampakines could be used to treat learning and memory loss associated with normal aging.”

The researchers treated two groups of middle-aged rats twice a day for four days with either a solution that contained ampakines or one that did not. They then studied the hippocampus region of the rats’ brains, an area critical for memory and learning. They found that in the ampakine-treated rats, there was a significant increase in the production of brain-derived neurotrophic factor (BDNF), a protein known to play a key role in memory formation. They also found an increase in long-term potentiation (LTP), the process by which the connection between the brain cells is enhanced and memory is encoded. This enhancement is responsible for long-term cognitive function, higher learning and the ability to reason. With age, deficits in LTP emerge, and learning and memory loss occurs.

Significantly, restoration of LTP was found in the middle-aged rats’ brains even after the ampakines had been cleared from the animals’ bodies. The drug used in the injections has a half-life of only 15 minutes; the increase in LTP was seen in the rats’ brains more than 18 hours later. According to the researchers, this study suggests that pharmaceutical products based on ampakines can be developed that do not need to be in the system at all times in order to be effective. Most drugs used to deal with central nervous system disorders, such as Parkinson’s disease, are only effective when they are in the body. Further studies will be needed to determine exactly how long the effect on LTP will be maintained after the ampakines leave the system.

The lingering presence of LTP also appears to contribute to BDNF remaining in the body, researchers said. “Ampakines work in two important ways to improve learning and memory,” Lauterborn said. “They directly stimulate the connection between nerve cells, which has an immediate effect of boosting LTP. But they also increase the presence of this important protein, BDNF, that can stay in the body and keep boosting memory after the drug has worn off.”

Collaborators on the study were Christopher Rex, Ching-Yi Lin, Eniko A. Kramar and Gary Rogers of Cortex Pharmaceuticals.

The study was funded by grants from the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, and from National Institute of Mental Health. The ampakine drug was provided by Cortex.

Jul 29, 2006　http://www.mayoclinic.com/

1126.Alzheimer's drugs: Real benefits despite limitations
Alzheimer's still has no cure, but two different types of drugs have been found to slow the progression of the disease.
Medication can improve the quality of life for people with Alzheimer's and their caregivers. It may even delay placement in a nursing home.

Unfortunately, Alzheimer's medications don't work for everyone. Some of the most commonly used drugs work in less than half the people tested. For those who are helped, the drugs' effects often are modest and temporary. Scientists continue to search for more effective drugs or perhaps even a vaccine that might someday prevent Alzheimer's.

Of the two main types of drugs currently approved by the Food and Drug Administration (FDA) for use in Alzheimer's, one variety seems to work best in the earlier stages of the disease while the other is reserved for treatment of the later stages.

Early-stage Alzheimer's treatments
Alzheimer's disease changes the brain in many ways. One of the changes results in a decrease in the levels of acetylcholine, a chemical messenger that is believed to be important for memory, thought and judgment.

Cholinesterase (ko-lin-ES-tur-ase) inhibitors are a type of drug that improves the effectiveness of acetylcholine either by increasing the amount of it in the brain or by strengthening the way nerve cells respond to it. These drugs appear to work best in the early to middle stages of Alzheimer's.

Types of cholinesterase inhibitors
The top three cholinesterase inhibitors seem to have similar rates of effectiveness and similar side effects ? nausea, vomiting or diarrhea.

Donepezil (Aricept). Perhaps the most popular cholinesterase inhibitor, donepezil offers a convenient once-a-day dosing not available in similar medications. This drug also appears to temporarily postpone the development of Alzheimer's in people with mild cognitive impairment (MCI), a separate memory-related condition that may precede Alzheimer's. In a recent study, magnetic resonance images show less brain shrinkage among people with MCI treated with donepezil than among people with MCI treated with a placebo. Donepezil had this effect only in people who carry a gene associated with higher risk of Alzheimer’s, however.
Galantamine (Razadyne). Approved by the FDA in 2001, galantamine is the newest cholinesterase inhibitor on the market.
Rivastigmine (Exelon). Rivastigmine may cause more severe gastrointestinal problems than other cholinesterase inhibitors do. Doctors typically prescribe a low dose of the drug initially and slowly increase the dosage as the body becomes accustomed to it.

Tacrine (Cognex). Tacrine has been on the market since 1993. However, it's rarely prescribed because of serious side effects, including possible liver damage.

MORE ON THIS TOPIC
Donepezil (Systemic)
Galantamine (Systemic)
Rivastigmine (Systemic)

Later stage treatment
Memantine (Namenda) is the first drug to be approved by the FDA for treatment of moderate to severe Alzheimer's disease. It works by regulating the activity of glutamate, a messenger chemical involved in learning and memory. Its most common side effect is dizziness.


MORE ON THIS TOPIC
Memantine (Systemic)

No cure yet
Until researchers find a cure ? or can halt the progression of Alzheimer's ? slowing the downward spiral remains the only benefit drugs can offer. But even temporary improvements in memory or thinking ability can help prolong the amount of quality time a person with Alzheimer's has with his or her family.

July 28, 2006 http://www.medgadget.com/

1127.In the Works: Contrast Agents for Alzheimer's

The press release by Schering AG of Germany and Avid Radiopharmaceuticals Inc. of Philadelphia, PA talks about the joint collaboration by these companies "to develop novel diagnostic imaging agents for Alzheimer's disease." The future contrast agents will be based on proprietary technology from Avid:

The compounds made by Avid directly bind to the amyloid plaques in the brain thought to cause Alzheimer's disease. They can be used with a variety of common, non-invasive imaging technologies such as positron emission tomography (PET) scanning. The potential of this compound class to accumulate preferentially in brain structures of Alzheimer's patients with high amyloid beta load has already been demonstrated in pilot human studies.
From Avid technology page (see pictures above and below):

Avid's Alzheimer's disease program is based on the hypothesis that in vivo detection of amyloid plaques by positron emission computed tomography (PET) or single photon emission computed tomography (SPECT) imaging would provide useful biomarkers for monitoring and diagnosis of Alzheimer's disease. To test this hypothesis, we have developed novel radiolabeled compounds that specifically and sensitively bind A b (the chief constituent of amyloid plaques), and are testing these compounds as molecular imaging agents in preclinical and clinical trials.

Thursday, July 27, 2006 http://www.ocregister.com/
1128.Alzheimer's drugs fail to deliver
Though research shows promise, current drugs offer modest benefits at an annual cost of $2.16 billion.

By ANGELA ZIMM and MICHELLE FAY CORTEZ
Bloomberg News

Thomas Finucane, a geriatric specialist, tells his Alzheimer's patients and their relatives not to get their hopes up when he prescribes Pfizer Inc.'s Aricept and similar drugs.
“In 10 years we are going to be embarrassed that we were sending billions of dollars to the drug companies for a pill that patients can't distinguish from a placebo,” said Finucane, a professor of medicine at Johns Hopkins University School of Medicine in Baltimore.

Alzheimer's medicines generated $2.16 billion last year, according to IMS Health Inc. Approved in 1996, Aricept became the world's top-selling drug for the disease even amid doubts about its effectiveness and that of similar pills. Today, in one of the largest reviews of clinical data on Alzheimer's drugs, researchers found that all medications in the same class as Aricept, known as cholinesterase inhibitors, offered the same small improvement in mental functioning.

The study by the U.K.-based Cochrane Collaboration analyzed data from 18 clinical trials involving 9,200 patients. Patients taking Alzheimer's drugs showed an average 2.5-point improvement on a 70-point scale measuring cognitive function and activities of daily living compared with those taking a placebo.

The analysis found that 29 percent of patients dropped out of the trials because of side effects, such as nausea, vomiting and diarrhea.

'Don't Expect Miracles'

“The average benefit is very small. It might escape notice,” said lead researcher Jacqueline Birks, a medical statistician for Cochrane's dementia and cognitive impairment group at University of Oxford. “Don't expect miracles.”

Doctors have long debated whether the drugs, which also include Novartis AG's Exelon and Johnson & Johnson's Razadyne, offer any benefit at all.

Finucane says his Alzheimer's patients and their relatives can't tell whether there is improvement after taking the pills. John Morris, a professor of neurology at Washington University School of Medicine, says the treatments do help patients. Both say there's dire need for new medicines.

“All the current drugs only treat the symptoms, they don't get at the underlying disease process,” Morris said.

Previous clinical trials have shown that more than half of patients show no improvement, and for those that do, the degree of benefit is small, according to the Alzheimer's Association. Findings presented today at the International Conference on Alzheimer's Disease and Related Disorders in Madrid will do little to sway opinion on either side of the debate.

'Not ultimately Satisfying'

“It's not ultimately satisfying to anyone, and I think the manufacturers would agree with that,” said William Thies, vice president of medical and scientific relations for the Chicago-based Alzheimer's Association. “If you put all these studies together you do get a consistent effect. It's modest.”

About 4.5 million Americans have Alzheimer's, which often begins with memory lapses and progresses into severe degeneration of brain cells that leaves the patients unable to care for themselves.

There are five FDA-approved Alzheimer's drugs, none of which stop the inevitable decline of people with the disease. Four of the five are cholinesterase inhibitors. Forest Laboratories Inc.'s Namenda, approved in 2003, works by a different mechanism and is approved for moderate-to-severe Alzheimer's disease.

The marginal efficacy of Alzheimer's drugs also raises the debate about cost effectiveness. A month's supply of Aricept pills costs about $150, according to Drugstore.com. Razadyne costs about $160 per month, and Exelon costs about $170.

Last year, the U.K.'s National Institute for Clinical Excellence, which evaluates a drug's cost against its benefits for the country's National Health Service, recommended against prescribing the drugs, saying they weren't worth the expense.

'No Clear Evidence'

“The reason there is such a dispute is that there is no clear evidence that they have an important clinical benefit or that they make a difference in the lives of patients,” Sidney Wolfe, director of the Washington-based Public Citizen's health research group, said in an interview.

Public Citizen has kept Aricept on its list of “worst pills” since 1999. Exelon and Razadyne are also on Public Citizen's list of medications to be avoided. The group accuses drug makers of playing on the “hope, fear and guilt” of Alzheimer's patients and their caregivers through advertising.

“Everyone recognizes that what we need are much better drugs,” said Washington University's Morris.

Morris is most excited about two new avenues of research designed to control the accumulation of beta amyloid and proteins that choke nerve cells in patients' brains. The protein buildup is a hallmark of the disease and is used to definitively diagnose it, typically during an autopsy.

Eli Lilly & Co., based in Indianapolis, is developing drugs to both block the secretion of amyloid and improve the body's ability to clear it out of the brain. Dublin-based Elan Corp. and Wyeth, based in Madison, New Jersey, are developing a similar treatment to remove amyloid deposits, while Switzerland's Novartis is refining a vaccine that would prompt the body's own immune system to destroy the plaque.

“While existing treatments are useful and effective in many people, the fact is they are dissatisfying because people continue to get worse,” Thies said. “The question of how long we'll wait to see these disease modifying drugs is always an impossible one to answer.”

31 July 2006　http://ec.europa.eu/

1129.Ageing and memory diseases: the Alzheimer’s story
To round off this week focused on health and ageing, Headlines draws on a recent commentary published in the July Nature Medicine which examines the EU’s research and policy footprint on the most debilitating of brain diseases ? Alzheimer’s.

Sometimes referred to as the ‘memory disease’, Alzheimer’s is the major contributor to dementia ? a condition affecting some 5 million people in the EU alone. On top of the pain and suffering it inflicts on the individuals and their families, the disease takes a sizeable toll on health care systems ? and growing as Europeans live longer and retire earlier.

The European Commission is well aware of the burden and challenges this field presents the scientific community and society as a whole. From its Fifth to its Sixth Framework Programme (FP5 and FP6) for research, it negotiated a doubling of funding ? from ?20 to ?40 million ? to be made available to Alzheimer’s researchers. It stressed the need for critical mass and collaboration among the actors to address this cruel disease and cut the amount of duplicated effort across the Union.

Although these amounts may appear small compared to the scale of the problem, note the authors Philippe Cupers, J?rgen Sautter and Alain Vanvossel, “it should be kept in mind that the budget for research and development, managed by the EU Framework Programmes, represents only approximately 5% of the total amount of public money spent on research in Europe”.

As FP6 draws to a close (it ran from 2002-2006), the Commission has managed to assemble a strong stable of Integrated Projects, Networks of Excellence, Specific Targeted Research Projects (STREPS) and ERA-NET projects helping to strengthen the foundations of the European Research Area in this field and beyond. And Europe needs every one of them to tackle Alzheimer’s and other neurodegenerative diseases.

Ageing disease
Brain diseases currently contribute to 35% of the total burden of all diseases in Europe, according to sources quoted in the commentary. Alzheimer’s and other forms of dementia take up 3% of that total, making them the second-leading cause of brain conditions behind unipolar depressive disorders. Between 5.9% and 9.4% of European citizens older than 65 suffer from dementia, the bulk of cases being Alzheimer’s. And it increases with age, affecting 28.5% of the population over 90.

“Increasing lifespan, however, will boost this number dramatically in the forthcoming years,” note the authors, “with potentially more than 10 million people affected by dementia in the year 2050.”

EU-funded projects, such as APOPIS, ADIT and InnoMed-AddNeuroMed, are on the task, providing a translational approach to the study of Alzheimer’s, from basic molecular and cellular mechanisms of the disease to identification and validation of new surrogate markers and therapeutic drug targets. Emphasis is also on the mechanisms and role of protein aggregation, a common feature of many neurodegenerative diseases, the commentary explains.

Large networks, like the NeuroNE, are putting the collective knowledge of 22 leading academic research groups and five SMEs towards an integrated and multidisciplinary research programme of functional genomics, proteomics, physiology, chemistry and clinical studies.

In FP7, the Commission is keen to continue its work in this important medical research, especially collaborative efforts focused on “the brain and related diseases, human development and ageing”. It is also proposing to launch new funding schemes, reinforce many of the current ones, and introduce measures to simplify and strengthen EU-funded research. “[In] addition to the proposed budget increase for European research in FP7, compared to FP6, it is expected that FP7 will offer a broad range of possibilities to address Alzheimer’s disease research at the EU level,” the authors conclude.

1130.New Study Provides Further Evidence that The MCI Screen Accurately Detects Mild Cognitive Impairment

2006-07-31
http://www.prweb.com/

Medical Care Corporation’s MCI Screen marks significant advancement in the early diagnosis for Alzheimer's patients. The MCI Screen is 97.3% accurate in distinguishing between normal aging and mild cognitive impairment, the first clinical stage of Alzheimer’s. The results of a recent study presented at the 0th International Conference on Alzheimer’s disease and Related Disorders provides further evidence that the MCI Screen detects mild cognitive impairment and memory loss very accurately.

Irvine, CA (PRWEB) July 30, 2006 -- A recent study, the Hancock County Aging Study, found 23% of patients in a primary care population had cognitive impairment. However, two-thirds of those who were diagnosed as impaired had no outward symptoms or functional decline. The MCI Screen enabled the diagnosis of pre-symptomatic patients and identified impaired patients much more accurately than assessments that have historically been used by clinicians. This high level of accuracy is in line with the findings of a peer-review study published in the Proceedings of National Academy of Sciences (Shankle, W. R. et al, (2005), PNAS, 102(13), 4919-4924) verifying that the MCI Screen is 97.3% accurate in distinguishing between Mild Cognitive Impairment (MCI) and normal aging. The recent findings were presented on July 17, 2006 at the 10th International Conference on Alzheimer’s disease and Related Disorders, presented by the National Alzheimer’s Association held in Madrid, Spain.

Mild Cognitive Impairment is the first clinical stage of Alzheimer’s disease and often lasts approximately seven years before progressing to mild Alzheimer’s. Currently, up to 95% of Alzheimer’s patients are diagnosed when the disease has progressed to the moderate stage. Diagnosing and treating Alzheimer’s disease in the mild cognitive impairment stage will have a tremendous impact on patients, caregivers and the health system. “In Alzheimer’s disease, the most common cause of memory impairment, the longest clinical studies have shown a delay in disease progression greater than 50% when treatment is initiated early” says Dr. William Shankle, Chief Medical Officer of Medical Care Corporation. “This delay often means that a patient spends their last years living more independently at home as opposed to confined to a care facility. Likewise, a delay in loss of independence and function reduces caregiver burden and healthcare costs.”

Dr. Douglas Trenkle, D.O., a board certified internist in Hancock County, Maine, assessed the memory of 240 patients aged 65 and older as part of their annual physical exam. Of the 240 patients, 183 were evaluated further as follows: each patient was assessed with the MCI Screen and two other widely used tests, the Mini Mental State Exam (MMSE), and the Clock Drawing Test (CDT). Additionally, the Functional Assessment Test (FAST) was used to establish the degree of functional capability in each person, from normal function to mild dementia. Patients with at least one abnormal result on any of the three assessments were further evaluated in accordance with published diagnostic guidelines which include blood and imaging tests.

Post assessment and diagnosis, 22.4% of patients were determined to be impaired and had structural evidence of cerebrovascular disease, global or hippocampal atrophy, hydrocephalus or tumor, and had a history or laboratory findings supporting MRI findings. 63.4% of patients identified as impaired had no or minimal subjective symptomatology.

Applying a complex scoring mechanism, the MCI Screen was able to accurately detect 96% of the impaired patients even though the majority did not manifest functional impairment.

In comparison, the MMSE detected 72% of the cases and the CDT detected 57%. The MCI Screen also properly classified 99% of the cases of the unimpaired patients as normal. The MMSE classified 68% and the CDT classified 70% of those without impairments as normal. Accuracy for the MMSE was 76% and for the CDT 69%. The MCI Screen? performed much better showing accuracy of 97%.

About Medical Care Corporation
Medical Care Corporation specializes in the development of medical technologies that enable healthcare providers to deliver improved levels of care in the field of dementia. Medical Care Corporation’s electronic dementia care system gathers, organizes, and synthesizes patient and treatment information so that healthcare providers are equipped to provide care at the highest possible level. www.mccare.com

About the Hancock County Aging Project
The Hancock County Aging Project, a non-profit organization, conducts research and aims to uncover methods of preventing, managing and delaying diseases in the elderly population in order to increase quality of life. Hancock County Aging Study was the first study conducted by the organization. Currently 300 individuals are enrolled in this study.

Source: University of Pennsylvania School of Medicine

Posted: July 30, 2006

1131.Penn Researchers Examine The Effects Of Meditation On Early Cognitive Impairment
Researchers at the University of Pennsylvania School of Medicine are examining the effectiveness of meditation on early cognitive impairment. Once this new study is completed, the results could help answer lingering questions over whether or not stress-reducing techniques and mind exercises can lessen or even prevent cognitive decline.

This is the first study at Penn's new "Center for Spirituality and the Mind," which evolved from work initiated in Penn's Department of Radiology to embrace and encourage researchers from the fields of medicine, pastoral care, religious studies, social work, nursing, and bioethics to expand our knowledge of how spirituality may affect the human brain.

"We'll be looking at patients with mild cognitive impairment or symptoms of early Alzheimer's disease," explains Andrew Newberg, MD, Associate Professor of Radiology, Psychiatry, and Religious Studies, who also directs the Center's investigations and is Principal Investigator of this pilot study. "We'll combine their meditation with brain imaging over a period of time to see if meditation improves cognitive function and is associated with actual change in the brain's activity levels. Specifically, we'll be looking for decreased activity in specific areas of the brain."

The dementia process causes a decreased function of neurons in the brain and can result in problems with memory, visual-spatial tasks, and handling emotional issues. As it worsens in a patient, it can also eventually lead to the need for round-the-clock care.

In this study, investigators want to look at the early symptoms of dementia. Study participants will learn a particular kind of meditation, called Kirtan Kriya, identified as one of the most fundamental types of meditation practice. It's a repeated chanting of sounds and finger movements designed to help the mind focus and become sharper. Study participants will perform this meditation program every day for eight weeks to see if this relaxation technique can change the brain's response to different tasks.

"This is a form of exercise for the brain which enables the brain to strengthen itself and battle the unknown processes working to weaken it. We want to keep the mind sharp and work that muscle," Newberg adds. "We might see improvements in baseline activity levels in the brain and these patients might be able to activate their brain in a more robust way in particular. So if this kind of meditation is successful in helping patients with neurological problems, it could then someday become a low-cost additional treatment to current therapy."

Newberg will use SPECT (Single Photon Emission Computed Tomography) imaging to capture the baseline image of the brain as well as the brain's activity during meditation. Images will be taken at the beginning of the study and then after the eight-week program.

This study, which is now enrolling patients, is funded by a research grant from the Alzheimer's Research and Prevention Foundation. ARPF President, Dharma Singh Khalsa, MD, is known for his expertise in the area of meditation and brain function.

1132.Alzheimer's Drug Therapy May Be Stopped Too Soon To Benefit Slow Responders
Main Category: Alzheimer's News
Article Date: 31 Jul 2006 - 8:00am (PDT)　 http://www.medicalnewstoday.com/

It is exactly one hundred years since Dr Alois Alzheimer first described the disease that still bears his name, a condition involving placques and nerve tangles in the brain resulting in severe memory problems. There is no cure for the disease but in the last decade drug treatments have become available that can slow the progression of disease and preserve the ability to function normally for longer. The first of these, and the one most commonly prescribed worldwide, is the cholinesterase inhibitor Aricept (donepezil).

Some people suffering from Alzheimer's Disease may be missing out on benefits from drug treatment, however, because their doctors erroneously decide therapy isn't working and should be stopped or changed. A physician survey released at the International Conference on Alzheimer's Disease and Related Disorders held in Madrid, July 2006, reveals many doctors who treat Alzheimer's are uncertain about the criteria for stopping or continuing drug therapy. As a result 85 per cent say there is an urgent need for clear and consistent guidelines.

A recent study, AWARE, shows about a third of patients do not show a definite response to treatment with Aricept for over six months but that nine out of 10 will go on to derive benefit in cognitive functioning and other symptoms over a further 12 weeks if they continue on treatment (1).

The physician survey, however, shows three out of four of the 376 participating doctors said they would decide whether or not treatment is working within three months with only one in 12 waiting six months or longer. If patients are thought to be declining or to be stable but not improving, over a third of doctors would alter treatment - either stop drug therapy altogether, add a further drug or choose an alternative.

Bengt Winbllad, Professor of Geriatric Medicine at the Karolinska Institute, Stockholm, Sweden commented: “Stabilisation of symptoms or a slowing of decline over time should be considered as treatment benefits when managing a progressive neurodegenerative disease such as Alzheimer's. It is important that physicians take this into account when carrying out initial treatment evaluations.”

The survey findings echo sentiments expressed by authors of the AWARE study, where a randomised double-blind phase showed patients who derived uncertain clinical benefit from Aricept initially, improved if given a further three months treatment whilst patients given a placebo did not. The study authors claim a 3 to 6-month timeframe is insufficient to fully assess treatment benefits and add that assessment should consider cognitive, functional (daily living activity performance) and behavioural symptoms. They warn: “Standard evaluations might miss the changes that are considered important and significant to patients and caregivers.” Clinicians in the study were very clearly biased towards cognitive scores on the standard mental functioning assessment tool, the Mini-Mental State Examination (MMSE) but patients and caregivers relied less on cognition and were more likely to recognise treatment benefits in all domains. The clinical reality in many countries is that treatment for Alzheimer's is often discontinued if patients decline by a single point on the MMSE, claim the authors.
Professor Winblad remarked: “The survey results, when analysed in light of the findings from AWARE, highlight the importance of continuous treatment and multi-domain assessment. Even in the absence of significant cognitive response to Alzheimer's Disease treatment, benefits in behaviour and function may be seen in patients over the long term which could significantly improve their quality of life.” Clear and consistent guidelines for diagnosing and managing Alzheimer's are necessary to standardise treatment and evaluation practices, he stressed.
Aricept is one of three cholinesterase inhibitors available for treatment of Alzheimer's Disease; others include rivastigmine and galantamine. These drugs suppress activity of the enzyme acetylcholinesterase which breaks down acetylcholine, a chemical playing an important role in memory and mental functioning. In Alzheimer's Disease certain neurons containing acetycholine degenerate so brain activity and memory are impaired. Increasing levels of acetychloline should enhance memory capacity.

Treatment with cholinesterase inhibitors such as Aricept has been shown to improve cognitive performance which includes memory, attention, reasoning, language, orientation and carrying out tasks when compared against placebo in double-blind, randomised, controlled trials. Treatment is well tolerated but some people experience side effects which are usually mild and diminish with time.

Guidelines for management and treatment of Alzheimer's Disease exist but differ from contry to country so there is currently no global standard for patient treatment.
By Olwen Glynn Owen
olwen@macline.co.uk

1133.Bipartisan Resolution Encourages Those With Memory Loss to Seek Evaluation and Diagnosis

NEW YORK, July 31, 2006 /PRNewswire/ -- A resolution originally proposed by the Alzheimer's Foundation of America (AFA) that recognizes the serious toll of Alzheimer's disease and encourages Americans with memory loss to seek an evaluation and diagnosis was introduced Friday by the leaders of the Congressional Task Force on Alzheimer's Disease.

The bipartisan resolution (H Res 964) was jointly introduced in the U.S. House of Representatives by Congressmen Christopher H. Smith (R-NJ) and Edward J. Markey (D-MA).

"We applaud the congressmen for their leadership and dedication," said Eric J. Hall, AFA's chief executive officer. "This is a huge step forward in our efforts to improve quality of care for millions of Americans. The eyes of the nation must focus on the enormity of this disease and its heartbreaking implications for families."

The resolution highlights "the seriousness of Alzheimer's disease and the toll it takes on individuals living with the disease, their caregivers, and other family members."

Among its key provisions, the resolution encourages all Americans who may be experiencing memory impairment to contact their physician or other qualified health professional to seek an evaluation and diagnosis. It emphasizes that early detection and diagnosis of the disease can help individuals pursue available treatments, address related medical problems and plan for their care, and enable these individuals and their families to embrace support services in their communities and at a national level.

Further, the resolution supports the goals of National Alzheimer's Disease Awareness Month, held each November, including efforts to raise public awareness about Alzheimer's disease; promote early evaluation, diagnosis, planning and treatment; and encourage progress toward a national health policy to raise awareness about Alzheimer's disease and to ensure that people with dementia receive a diagnosis and proper care.

AFA pressed for the resolution as part of its national initiative to bring attention to Alzheimer's disease and to encourage early detection, proper diagnosis and treatment.

Each November, for example, AFA sponsors National Memory Screening Day, in which hundreds of sites across the nation offer free, face-to-face memory screenings to those concerned about memory problems. The screenings are not a diagnosis; those whose scores are below normal are encouraged to pursue further evaluation and a full-scale medical examination. This year, AFA will hold National Memory Screening Day on November 14.

Alzheimer's disease currently affects an estimated five million Americans; the incidence is expected to triple by 2050. Symptoms include memory loss, confusion, behavioral changes, and loss of verbal skills and other intellectual function.

However, a recent AFA survey found that fear of stigma, denial, lack of knowledge and concern about health care costs can significantly delay a diagnosis.

"We hope that this resolution will give Americans that extra push to take action if they notice signs of dementia," Hall said. "Proper treatment and support can make a world of difference."

The New York-based Alzheimer's Foundation of America is a national non-profit organization that focuses on care for individuals with Alzheimer's disease and related illnesses, and their families. Its services include a toll-free hotline, counseling by licensed social workers, bilingual educational materials, a free caregiver magazine, and training for healthcare professionals. For more information, call toll-free 866-AFA-8484 or visit http://www.alzfdn.org.

CONTACT: Carol Steinberg, 1-866-AFA-8484, cell: +1-516-236-7101, afapr@aol.com

Web site: http://www.alzfdn.org/

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1134.Drug Triggers Body's Mechanism To Reverse Aging Effect On Memory Process
Main Category: Seniors / Aging News
Article Date: 31 Jul 2006 - 6:00am (PDT)
http://www.medicalnewstoday.com/
A drug made to enhance memory appears to trigger a natural mechanism in the brain that fully reverses age-related memory loss, even after the drug itself has left the body, according to researchers at UC Irvine.

Professors Christine Gall and Gary Lynch, along with Associate Researcher Julie Lauterborn, were among a group of scientists who conducted studies on rats with a class of drugs known as ampakines. Ampakines were developed in the early 1990s by UC researchers, including Lynch, to treat age-related memory impairment and may be useful for treating a number of central nervous system disorders, such as Alzheimer's disease and schizophrenia. In this study, the researchers showed that ampakine drugs continue to reverse the effects of aging on a brain mechanism thought to underlie learning and memory even after they are no longer in the body. They do so by boosting the production of a naturally occurring protein in the brain necessary for long-term memory formation.

The study appears in the August issue of the Journal of Neurophysiology.

"This is a significant discovery," said Gall, professor of anatomy and neurobiology. "Our results indicate the exciting possibility that ampakines could be used to treat learning and memory loss associated with normal aging."

The researchers treated two groups of middle-aged rats twice a day for four days with either a solution that contained ampakines or one that did not. They then studied the hippocampus region of the rats' brains, an area critical for memory and learning. They found that in the ampakine-treated rats, there was a significant increase in the production of brain-derived neurotrophic factor (BDNF), a protein known to play a key role in memory formation. They also found an increase in long-term potentiation (LTP), the process by which the connection between the brain cells is enhanced and memory is encoded. This enhancement is responsible for long-term cognitive function, higher learning and the ability to reason. With age, deficits in LTP emerge, and learning and memory loss occurs.

Significantly, restoration of LTP was found in the middle-aged rats' brains even after the ampakines had been cleared from the animals' bodies. The drug used in the injections has a half-life of only 15 minutes; the increase in LTP was seen in the rats' brains more than 18 hours later. According to the researchers, this study suggests that pharmaceutical products based on ampakines can be developed that do not need to be in the system at all times in order to be effective. Most drugs used to deal with central nervous system disorders, such as Parkinson's disease, are only effective when they are in the body. Further studies will be needed to determine exactly how long the effect on LTP will be maintained after the ampakines leave the system.

The lingering presence of LTP also appears to contribute to BDNF remaining in the body, researchers said. "Ampakines work in two important ways to improve learning and memory," Lauterborn said. "They directly stimulate the connection between nerve cells, which has an immediate effect of boosting LTP. But they also increase the presence of this important protein, BDNF, that can stay in the body and keep boosting memory after the drug has worn off."

###

Collaborators on the study were Christopher Rex, Ching-Yi Lin, Eniko A. Kramar and Gary Rogers of Cortex Pharmaceuticals.

The study was funded by grants from the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, and from National Institute of Mental Health. The ampakine drug was provided by Cortex.

About the University of California, Irvine: The University of California, Irvine is a top-ranked university dedicated to research, scholarship and community service. Founded in 1965, UCI is among the fastest-growing University of California campuses, with more than 24,000 undergraduate and graduate students and about 1,400 faculty members. The second-largest employer in dynamic Orange County, UCI contributes an annual economic impact of $3.3 billion. For more UCI news, visit http://www.today.uci.edu/

Contact: Farnaz Khadem
University of California - Irvine

http://www.newswire.ca/en/
1135.FDA Provides Clearance to Initiate Phase I Clinical Trial with Alzheimer's Disease Drug Product AZD-103
TORONTO, Aug. 1 /CNW/ - Transition Therapeutics Inc. ("Transition")
(TSX: TTH), announced today that they have received clearance from the United
States Food and Drug Administration ("FDA") to initiate a Phase I clinical
trial for its lead Alzheimer's drug product, AZD-103. The AZD-103 compound is
a possible disease-modifying therapeutic drug candidate for the treatment of
Alzheimer's disease. This unique class of drug candidates may provide
significant advantages over the current therapies on the market.
The Phase I trial is a single blind, randomized, placebo controlled study
in which healthy volunteers will receive placebo or an escalating acute dose
of AZD-103. The primary objectives of the trial are to evaluate the safety,
tolerability and pharmacokinetics of AZD-103. Enrolment for this trial is
expected to begin September 2006.
"The AZD-103 phase I clinical trial announced April 27, 2006 has
completed enrolment and Transition will release data from this study in the
near future."

About the AZD-103 Drug

The lead compound AZD-103 (scyllo-cyclohexanehexol) is part of an
emerging class of disease-modifying drugs that have the potential to both
reduce disease progression and improve symptoms such as cognitive function. As
reported recently in a Nature Medicine publication, oral treatment of AZD-103
reduces accumulation of amyloid beta and amyloid beta plaques in the brain, as
well as reduces or eliminates learning deficits in a leading transgenic mouse
model of Alzheimer's disease. In addition, AZD-103 is well positioned as a
potential Alzheimer's therapy as it can be taken orally, crosses the blood
brain barrier and has a favorable safety profile.

About Alzheimer's disease

Alzheimer's disease is a progressive brain disorder that gradually
destroys a person's memory and ability to learn, reason, make judgments,
communicate and carry out daily activities. The disease affects more than
4 million Americans, and with an aging population is expected to double over
the next 20 years unless an effective therapy is developed. Currently approved
Alzheimer's therapies primarily treat disease symptoms but do not reverse or
slow down disease progression. These products have annual sales of
US$3.1 billion; however, the Alzheimer's pharmaceutical market is expected to
grow significantly with the arrival of products that alter disease
progression.

About Transition

Transition is a product-focused biopharmaceutical company, developing
novel therapeutics for disease indications with large markets. Transition's
lead products include regenerative therapies E1-I.N.T.(TM) and GLP1-I.N.T.(TM)
for the treatment of diabetes, AZD-103 for the treatment of Alzheimer's
disease, MS-I.E.T. for the treatment of multiple sclerosis and HCV-I.E.T. for
the treatment of hepatitis C. Transition has completed target enrolment for
exploratory Phase IIa clinical trials of its lead regenerative product,
E1-I.N.T.(TM) in type I and type II diabetes patients. The Company is
currently enrolling subjects for a Phase I/II clinical trial for HCV-I.E.T. in
patients with hepatitis C, and a Phase II clinical trial for MS-I.E.T. in
patients with multiple sclerosis. Transition's shares are listed on the
Toronto Stock Exchange under the symbol "TTH".

Notice to Readers: Information contained in our press releases should be
considered accurate only as of the date of the release and may be superseded
by more recent information we have disclosed in later press releases, filings
with the OSC or otherwise. Press releases may contain forward-looking
statements based on the expectations of our management as of the date of the
release. Actual results may materially differ based on many factors, including
those described in the press releases.

%SEDAR: 00015806E

For further information: on Transition, visit
www.transitiontherapeutics.com or contact: Dr. Tony Cruz, Chief Executive
Officer, Transition Therapeutics Inc., Phone: (416) 260-7770, x.223,
tcruz@transitiontherapeutics.com; Mr. Elie Farah, CFO and VP, Corporate
Development, Transition Therapeutics Inc., Phone: (416) 260-7770, x.203,

Originally Aired: July 31, 2006
http://www.pbs.org/

1136.Caregivers Struggle with Needs of Alzheimer's Patients

As the number of patients stricken with Alzheimer's disease continues to grow, so does the community of families and caregivers who have pledged to look after loved ones, often risking emotional, physical and financial burdens


GWEN IFILL: Now, the battle against Alzheimer's, part two. Last week, the NewsHour's health correspondent, Susan Dentzer, looked at efforts to better understand how the disease affects the brains of its victims. Tonight, she considers its impact on the caregivers and families of the afflicted. Our Health Unit is a partnership with the Robert Wood Johnson Foundation.

SUSAN DENTZER, NewsHour Health Correspondent: This is how Meryl Comer begins each day: crouching, in the dim morning light, to empty her husband's urine bag.

MERYL COMER, Wife of Alzheimer's Patient: Just a minute, love. I'm coming.

SUSAN DENTZER: That accomplished, she removes his catheter and helps him out of bed.

MERYL COMER: OK, I'm going to swing your legs around, Harv?

SUSAN DENTZER: In a moment, she'll get one of the occasional fleeting acknowledgments that he knows she's there. He's probably not aware she's his wife; more likely, she's a familiar presence.

MERYL COMER: Hi.

HARVEY GRALNICK, Alzheimer's Patient: Good morning.

MERYL COMER: Good morning. Good morning. You OK?

SUSAN DENTZER: Harvey Gralnick, Comer's 70 year-old husband, is in his 12th year of Alzheimer's disease. He's entering the final phases, when most normal human interaction ceases and patients completely withdraw.

MERYL COMER: Let me check your eyes, huh? Honey, you're having some problems with your eyes.

SUSAN DENTZER: As devoted as she is to caring for him, Comer told us she's now in her 12th year of something like hell.

MERYL COMER: I call myself a POA. I'm a prisoner of Alzheimer's. I'm an extension of his disease.

SUSAN DENTZER: And Comer says she's madder than hell about inadequate support for the nation's caregivers, including proposed cuts in federal programs aimed at Alzheimer's care.

MERYL COMER: I feel compelled to speak out for both victims, because they have no voice, and for caregivers, who are worn out.

More than a one woman job

SUSAN DENTZER: Aside from those dramatic episodes, even routine care-giving tasks are taxing, especially on the staggered four hours of sleep Comer says she gets most nights. Determined to help his life stay as ordered as possible, Comer gives her husband a daily shower as he sits on the toilet.

MERYL COMER: Get some cologne, and you're good to go.

SUSAN DENTZER: Comer counts herself lucky that, at age 62, she's more able than most spouses of Alzheimer's patients to cope.

MERYL COMER: Think of an 80 year-old woman doing this to an 85-year-old man.

SUSAN DENTZER: Comer also says she's more fortunate than most, since she can afford to hire nurses and other aides to help out.

CAREGIVER: Brush your teeth, Dr. Harvey.

MERYL COMER: Medical Assistant Marvin Angeles (ph) has worked with the family for three years.

CAREGIVER: That's it. That's it. You almost got it.

SUSAN DENTZER: Still, just coordinating the care Angeles and other members of the team provide is a job in itself. To keep track, Comer logs daily notes in a book.

MERYL COMER: Were you easy today? I'll give you a two today. How about that?

SUSAN DENTZER: Whatever its complexities, Comer says prefers home care-giving to placing Gralnick in a nursing home, where on average half of all patients have Alzheimer's. That's a path she's already tried and rejected, partly because the costs of top facilities with private-duty nursing range from roughly $100,000 to nearly $200,000 a year.

One disease, two patients

SUSAN DENTZER: Comer's story echoes that of millions of families across the country coping with the ravages of this mostly untreatable and so far incurable disease. They're part of an informal care-giving network that provides the equivalent of tens of billions of dollars of care for free and sustains a burden many would find unimaginable.

Dr. Sam Gandy is a top neurologist at Thomas Jefferson University and chief scientific adviser to the Alzheimer's Association.

DR. SAM GANDY, Thomas Jefferson University: Caregivers are typically exhausted, depressed, withdrawn, overwhelmed.

MERYL COMER: This is for you. Ready?

DR. SAM GANDY: They may have exhausted their financial resources, in addition to their emotional resources. There's actually always a second patient with Alzheimer's disease, because the caregiver requires attention by the physician, as well.

SUSAN DENTZER: The second patient in this case, Comer, was a long way from that when her husband first fell ill.

MERYL COMER: Hello, I'm Meryl Comer, on special assignment in Tokyo.

SUSAN DENTZER: Then a TV newswoman, she spent her days interviewing business leaders, Washington political figures, and even presidents.

Divorced from her first husband and with a young son, Comer had married Gralnick in 1980. He was then at the peak of a prestigious career as a physician and scientist specializing in blood-related cancers at the National Institutes of Health.

But in the mid-1990s, Gralnick was diagnosed with early onset Alzheimer's and eventually had to leave NIH. In what was left of his mind, it was a long goodbye.

MERYL COMER: For five years, he carried around his briefcase. And every morning I got him up, saying, "Love, you have to get up. Your patients are waiting." He carried around his research papers, shuffled them around. It was heartbreaking. That's what he cared about; that was his world. And we stayed in that world with him until he didn't care about it anymore.

SUSAN DENTZER: Comer eventually quit her job and became Gralnick's full-time caregiver. As often happens with Alzheimer's patients, he'd also become paranoid, delusional, and occasionally even violent.

MERYL COMER: All personal care was a confrontation. When the mind's dementing, they don't understand personal care, so they take it as if you're attacking them. I had my front teeth knocked out in the hospital.

But I was the one who got there early in the morning to bathe him, shave him, dress him, because I could get closer. I just missed the left hook, so to speak.

Determined to reveal Alzheimer's

SUSAN DENTZER: As Gralnick grew sicker, the couple's social isolation grew, too.

MERYL COMER: The behaviors are inappropriate. Inhibitions are the first to go. One of the chapters of the book that I have yet to write is, "Is That Your Husband Peeing on the Barbecue?" Subtitled, "Social Improprieties and Why Invitations Stop Coming." You get embarrassed. You protect them. You pull them away. Nobody sees them. Nobody sees the horror at night.

SUSAN DENTZER: Comer told us she was determined to show us some of that horror, so we lent her a camera to record scenes when we were not there. She captured one typical nighttime calamity, when her six-foot, two-inch husband, weighing 200 pounds, falls to the floor and can't get up.

MERYL COMER: I'm going to try to get you up, Harvey. I'm going to get behind you, lovey. Harvey, sit up for me.

HARVEY GRALNICK: No, no, no, no, no.

MERYL COMER: Harvey, please help me, love. Harv, I can't do it. Honey, I can't do it. Here, I'm going to call the fire department. OK, honey? I've got to call somebody to come help us.

I'm told to call 911 and say it's a non-emergency, and then I break into tears because I can't do it. And I've watched these two burly men wrestle with this man to get him up off the floor

Medicare won't pay any of those long-term care bills, and Medicaid will only pay them for low-income people who've exhausted their assets. But Comer's reluctance also stems from her belief that even supposedly top-notch facilities don't always provide high-quality care.

MERYL COMER: In the facilities, his feet would get infected and swell up because he was walking in his own urine at night. We haven't had any problems here.

When will the help come?

SUSAN DENTZER: Four-and-a-half million patients in the U.S. are struggling with Alzheimer's today, and millions more are likely to develop the disease in coming years, so you might think that support for caregivers like Comer would be increasing. But at the federal level, says Steve McConnell, who oversees advocacy and public policy for the Alzheimer's Association, that's not the case.

STEPHEN MCCONNELL, Alzheimer's Association: There is a very high awareness of Alzheimer's disease among members of Congress and the administration. Many of them have seen it in their own families. But for some reason, there's a kind of head-in-the-sand approach to it, that they see the problem but they're not doing much about it.

SUSAN DENTZER: And in fact, says McConnell, the Bush administration has proposed eliminating several key programs to support Alzheimer's caregivers. Comer and other Alzheimer's disease advocates are now working to reverse those cuts in Congress.

Meanwhile, with her husband nearing the end stages of Alzheimer's, but possibly still able to live a long time, we asked Comer what her greatest hope was now.

MERYL COMER: I hope that I don't wear out. Caregivers have a very bad rate. They tend to die before the patients, statistically, because of the intensity. So my wish for Harvey is that I just don't wear out, or give up, or there's an episode where I can't manage it somehow.

SUSAN DENTZER: Until then, she says, they'll manage as best as they can.

MERYL COMER: That's all we can do. As good as it gets, Harv.

Press Release Source: ElderCarelink

1137.Desire to Fill Social Needs for Elderly Change Face of Respite Care
Tuesday August 1, 6:00 am ET http://finance.yahoo.com/
Aging Population Drives 'Social' Model for Temporary Care

ASHLAND, Mass., Aug. 1 /PRNewswire/ -- Respite care -- care that provides a short-term reprieve for full-time caregivers -- has often been used by those in need of support with daily living, or to help care for those who suffer from chronic disabilities or illness such as Alzheimer's disease. But as today's population ages, respite care may be seeing a shift in focus toward social needs. Seniors, while still dependent on loved ones for care, are living longer and leading more active lives. As such, they are as likely to require companionship and recreational activities as medical care or assistance with daily living activities.

While demand for respite care has grown significantly over the last five years, respite care that provides interaction with peers has added to that demand. "There is more readiness on the part of Baby Boomers who are serving as primary caregivers to their aging parents to seek out ways for their loved ones to remain engaged socially during planned time away," said Robert F. Brooks, CEO of ElderCarelink. "As today's caregivers -- and those in their care -- better understand the part that social interaction plays in maintaining mental and physical health, respite care that focuses on filling social needs will be increasingly valued."

The growth of the social respite care model has lead to an upsurge in community-based programs, not-for-profits, private organizations, and volunteer-based organizations such as Meals on Wheels, or companionship services to fill the demand. Below are some of the respite care resources available in many communities that are likely to focus on social components. It is always important to ask questions regarding licensing, insurance, training, and background checks for staff while seeking respite care.

-- Private Respite Care. Your community or local organization may have a
Caregiver Registry. Respite care agencies can also offer private care
that is often not part of government program.
-- Volunteer Services. Non-profit and faith-based organizations are rising
to meet caregiver needs and may offer no-cost respite care for
families, usually for those who are income eligible.
-- Adult Day Care. In addition to providing cost-effective alternatives to
home care for elderly with medical needs, adult day care programs can
provide variety of social networking and recreational activities.
-- State Coalitions. Consisting of public and private organizations and
community members, coalitions provide resources for temporary care and
other caregiver resources.

About ElderCarelink
ElderCarelink, a leading provider of qualified lead generation services within the eldercare industry, assists families in finding a multitude of senior services, including respite care, assisted living, nursing homes, adult day care, private duty nursing, care management and homecare in all 50 states. More about finding eldercare assistance or joining our network of providers can be found at www.eldercarelink.com .

Media Contact:
Ken Housman
508-881-3440
contactus@ElderCarelink.com

This press release distributed by PRWEB (http://www.prwebdirect.com/), a service of eMediaWire.

Public release date: 1-Aug-2006　http://www.eurekalert.org/

Contact: Wendy Davis
wdavis@usapple.org
U.S. Apple Association

1138.UMass Lowell research shows benefits of apple juice on neurotransmitter affecting memory
Lowell -- For those who think that apple juice is a kid's drink, think again. Apples and apple juice may be among the best foods that baby boomers and senior citizens could add to their diet, according to new research that demonstrates how apple products can help boost brain function similar to medication.

Animal research from the University of Massachusetts Lowell (UML) indicates that apple juice consumption may actually increase the production in the brain of the essential neurotransmitter acetylcholine, resulting in improved memory. Neurotransmitters such as acetylcholine are chemicals released from nerve cells that transmit messages to other nerve cells. Such communication between nerve cells is vital for good health, not just in the brain, but throughout the body.

"We anticipate that the day may come when foods like apples, apple juice and other apple products are recommended along with the most popular Alzheimer's medications," says Thomas Shea, Ph.D., director of the UML Center for Cellular Neurobiology and Neurodegeneration Research.

The study will be published in the August issue of the international Journal of Alzheimer's Disease. The abstract is now available online at http://www.j-alz.com/issues/9/vol9-3.html .

The role of acetylcholine in the brain is not a new area of research. Alzheimer's medication studies start with the premise that increasing the amount of acetylcholine in the brain can help to slow mental decline in people with Alzheimer's disease. Testing a similar hypothesis, the UML research team found that having animals consume antioxidant-rich apple juice had a comparable and beneficial effect.

In this novel animal study at UML, adult (9-12 months) and old (2-2.5 years) mice, some specially bred to develop Alzheimer's-like symptoms, were fed three different diets (a standard diet, a nutrient-deficient diet, and a nutrient-deficient diet supplemented with apple components (in this case, apple juice concentrate was added to their drinking water).

Among those fed the apple juice-supplemented diet, the mice showed an increased production of acetylcholine in their brains. Also, after multiple assessments of memory and learning using traditional Y maze tests, researchers found that the mice who consumed the apple juice-supplemented diets performed significantly better on the maze tests.

"It was surprising how the animals on the apple-enhanced diets actually did a superior job on the maze tests than those not on the supplemented diet," remarks Dr. Shea.

Earlier studies by Shea's research team had strongly suggested apples must possess a unique mix of antioxidants that improve cognition and memory via inhibition of oxidation in the brain. Those results encouraged Shea to evaluate the neurotransmitter effect, as is done in the current study. Medications given to humans with Alzheimer's disease have been shown to inhibit the production of specific enyzmes (cholinesterase inhibitors) that break down acetylcholine in the brain. The end result in the animal study is similar ・there are more of these critical messengers remaining in the brain to enhance memory.

The results obtained were from the animals consuming moderate amounts of apple juice --comparable to drinking approximately two 8 oz. glasses of apple juice or eating 2-3 apples a day. The findings also suggest that the apple-supplemented diet was most helpful in the framework of an overall healthy diet.

Shea concludes, "The findings of the present study show that consumption of antioxidant-rich foods such as apples and apple juice can help reduce problems associated with memory loss."

Shea also notes that a human clinical study evaluating consumption of apple products will begin in the near future.

###
This study was sponsored through an unrestricted grant by the U.S. Apple Association and the Apple Products Research and Education Council.

UMass Lowell, www.uml.edu, a comprehensive university with a national reputation in science, engineering and technology, is committed to educating students for lifelong success in a diverse world and conducting research and outreach activities that sustain the economic, environmental and social health of the region. UML offers its 11,000 students more than 120 degree choices, internships, five-year combined bachelor's to master's programs and doctoral studies in the colleges of Arts and Sciences, Engineering and Management, the School of Health and Environment, and the Graduate School of Education.

1139.Neuren Selects New Compound Targeted for the Oral Treatment of Parkinson's and Related Neurological Diseases
Wednesday August 2, 6:03 am ET http://finance.yahoo.com/
Key points:
- NNZ-2591 has shown preclinical efficacy in animal models of Parkinson's disease
- NNZ-2591 showed long term beneficial effects in Parkinson's disease, in addition to short term symptomatic relief
- NNZ-2591 was shown to be orally neuroprotective and safe in animals at over 15 times the effective dose
- NNZ-2591 is a member of a new class of Neuren compounds and has been selected for development through to human clinical trials


SYDNEY, Australia, Aug. 2 /PRNewswire-FirstCall/ -- Neuren Pharmaceuticals (ASX: NEU - News) announces a new lead candidate, NNZ-2591, from its diketopiperazine (DKP) family, which has shown efficacy in a preclinical model of Parkinson's disease (PD) and in other animal models of brain injury. This is now Neuren's third lead candidate, after Glypromate? and NNZ-2566, which are both currently in human trials.

Importantly in the Parkinson's disease model, NNZ-2591 was administered after onset of Parkinsonian symptoms and the beneficial effect in the behavioural tests remained for weeks after the cessation of drug treatment. This suggests the compound produced a long-term benefit in this model of the disease, rather than just temporary symptomatic relief.

NNZ-2591 did not show any liability for drug-drug interactions or any safety concerns following wide screening. The compound did not display any adverse or unwanted pharmacological effects when orally administered to rats at doses over 15 times higher than the effective dose for neuroprotection. In addition, in an experimental model of stroke, NNZ-2591 has also been shown to reduce brain damage when given orally, an important feature for chronic neurodegenerative diseases where treatment is usually prolonged.

These observations have lead to the selection of oral NNZ-2591 as a lead candidate to treat chronic neurological disorders, such as Parkinson's disease and other neurological diseases, such as Alzheimer's disease. NNZ-2591 is now in manufacturing scale-up as a precursor to formal toxicology.

Dr Mike Bickerdike, Head of Preclinical Development, said: "This is a new molecule from our research pipeline and its progression to lead candidate status broadens Neuren's development portfolio. Along with the oral NNZ-2566 program announced recently, we're now able to target chronic conditions, such as Parkinson's disease and Alzheimer's disease, with two lead candidates, oral NNZ-2566 and now oral NNZ-2591."

NNZ-2591 is distinct from Neuren's other compounds, Glypromate? and NNZ-2566, coming from a different chemical class, and displaying distinct pharmaceutical and pharmacological properties. Glypromate? and NNZ-2566 are currently in human clinical trials for acute brain injury, specifically, cognitive impairment and traumatic brain injury respectively.

Mr David Clarke, CEO, said, "This is an exciting step for the Company. NNZ-2591 has all the right characteristics for a very promising candidate and has gone through a rigorous selection process over the last 12 months. NNZ- 2591 will now follow the Company's well-tested drug development programme used for Glypromate? and NNZ-2566, both candidates that are currently in human trials. NNZ-2591 however will be targeting a new area of brain disease, with new potential markets."

Parkinson's disease is a progressive, degenerative neurological condition that affects the control of body movements. In addition, up 50% of Parkinson's patients go on to develop some form of dementia. It is estimated that approximately 1-2 people per 1,000 have Parkinson's, with the incidence increasing to one in 100 over the age of 60. In Australia there are approximately 40,000 people with Parkinson's, with one in seven people being diagnosed with Parkinson's before the age of 50 years. Alzheimer's disease has a reported 4.5 million cases a year in the US and an estimated market worth of US$2.5 billion.

The majority of work to date on NNZ-2591 has been funded by a New Enterprise Research Fund grant from the Foundation for Research Science and Technology in New Zealand.

1140.Strategies That Teach A Caregiver To Manage A Loved One’s Illness Also Helps In Coping With Death

University of Pittsburgh
8/1/2006 10:17:30 AM
http://www.webwire.com/default.asp

PITTSBURGH, Auggust 1, 2006 ? An intervention aimed at preventing depression and easing the burden of caring for a relative with dementia also help to prevent complicated grief and depression following the death of the loved one, according to a University of Pittsburgh-led study. The findings, which are published in the August issue of the American Journal of Geriatric Psychiatry, could help the millions of American families caring for relatives with dementia. Approximately 4.5 million Americans with Alzheimer’s disease live at home with 75 percent cared for by family members.

The study, initially designed to establish methods for preventing depression and increasing coping skills during the caregiving process, sought to determine who among caregivers were at risk for complicated grief and depression after their care-recipients died. Surprisingly, the interventions aimed at helping the caregiver cope while the care-recipient was living also helped the caregiver cope with the recipient’s death, preventing complicated grief and depression. According to principal investigator and lead author Richard Schulz, Ph.D., professor of psychiatry at the University of Pittsburgh, the finding was totally unexpected.

Complicated grief most often occurs following the death of someone in a very close and loving relationship. Key features include a sense of disbelief regarding the death, anger and bitterness over the death, recurrent pangs of painful emotions with intense yearning and longing for the deceased, avoidance of situations and activities that are reminders of the loss, and a preoccupation with thoughts of the loved one, often including distressing, intrusive thoughts related to the death. Since it is a newly characterized condition, not yet included in the American Psychiatric Association’s Diagnostic and Statistical Manual, little is known about how to treat and prevent complicated grief. In fact, report the authors, the results of this study are the first to demonstrate the effectiveness of such interventions -- which include education, skills training and group support -- on preventing complicated grief and depression after death.

Twenty percent of the caregivers in the study experienced symptoms of complicated grief after their loved ones died. Most of these did not receive the interventions, had depressive symptoms and/or saw the caregiving process as positive, usually because they derived a sense of purpose from the situation, and were most likely to experience severe depression and complicated grief post-death.


“Taking care of a relative with dementia can be very stressful. Most caregivers respond well to their loved one’s death, seeing it as a relief for the patient, which is why we focused on helping during the caregiving process, rather than after,” said Dr. Schulz, who is associate director of the University of Pittsburgh Institute on Aging and director of the Center for Social and Urban Research. “Given that in our previous studies we have found that a large number, some 30 percent of caregivers, are still at risk for severe depression after the death of their loved one, it’s encouraging to know that these interventions can help both before and after death.”

The Resources for Enhancing Alzheimer’s Caregiver Health (REACH) study followed 1,222 caregivers and their loved ones in Boston; Birmingham, Ala.; Memphis, Tenn.; Miami; Philadelphia; and Palo Alto, Calif., between 1996 and 2000. During the course of the study, 265 of the care-recipients died; 217 of their caregivers were followed for this study.

According to the authors, the caregivers were generally representative of individuals who provide in-home care for relatives with Alzheimer’s disease. They were an average of 64 years old; 84 percent were women; and nearly half were caring for a spouse. Care-recipients were on average 81 years old and 54 percent were men.

Caregivers were initially randomized to receive either six months of an active intervention or a control intervention, and were assessed at the onset of the study and at six, 12 and 18 months. The caregivers whose loved ones died during the study were assessed following the death, around 15 weeks post-death, and at six, 12 and 18 months.

The researchers found that reducing caregiver burden, treating depression prior to death and providing supportive psychosocial or skills training caregiver interventions helped the caregivers to better manage with their loved one’s deaths.

“Our findings show that caregiving is closely intertwined with the bereavement experience that follows. Family members caring for relatives with advanced disease would not only benefit from traditional caregiving interventions designed to ease the burden of care but also from pre-bereavement treatments that would better prepare them for the impending death of their loved one,” said Dr. Schulz.

Co-authors of the study include: Kathrin Boerner, Ph.D., Lighthouse International, N.Y.; Katherine Shear, M.D., formerly of the University of Pittsburgh and now at the Columbia School of Social Work, New York City; Song Zang, M.S., University of Pittsburgh; and Laura N. Gitlin, Ph.D., Thomas Jefferson University, Philadelphia.

The study was supported by grants from the National Institute on Aging, the National Institute of Nursing Research, the National Institute of Mental Health and the National Heart, Lung and Blood Institute, all of the National Institutes of Health.

Aug. 2, 2006, 1:33PM　　http://www.chron.com/
1141.Lexicon gets OK to start test of Alzheimer's drug
Human trials to begin in U.K. by end of summer

By BRETT BRUNE
Copyright 2006 Houston Chronicle

British authorities have given Lexicon Genetics permission to begin its first human trial of a therapy that it developed. The drug is intended to treat Alzheimer's and other cognitive disorders.

Lexicon's chief executive, Arthur Sands, said Tuesday that the United Kingdom Medicines and Healthcare Products Regulatory Agency has approved Lexicon's trial application. He said the test would begin by the end of the summer in the U.K.

Clearance from the British equivalent of the U.S. Food and Drug Administration marks the biopharmaceutical firm's move into independent drug development. The transition is coming 11 years after Lexicon began industrializing and commercializing gene-knockout technology in The Woodlands.

In mice and embryonic stem cells, the company disrupts, or knocks out, genes that may hold keys to identifying and treating human diseases.

The coming trial for the small-molecule drug ? a chemical compound that can be delivered in pill form ? will involve about 80 healthy human volunteers and last about one year, Sands said. He said additional studies could take another four to seven years.

Sands would not say how much the first-phase trial is expected to cost. Nor would he disclose the name of the firm doing the testing.

In a conference call the company held with stock analysts Tuesday, chief financial officer Julia Gregory said the Lexicon's recent financing agreement with Azimuth Opportunity gives Lexicon "flexibility in managing our cash needs as we advance our lead drug programs into human clinical trials."

Azimuth agreed in June to buy up to $75 million of common stock in the coming 18 months.

By the end of the year, Sands said, Lexicon plans to apply to the FDA for another human clinical study. That drug is intended to treat irritable bowel syndrome and other gastrointestinal disorders.

Also Tuesday, Lexicon reported a net loss of $17 million for the second quarter, up from a loss of $15 million in the same period last year. On a per-share basis, the loss was 26 cents, compared with 23 cents.

Lexicon said it took in $16.2 million in revenue, compared with $13.9 million in the second quarter of 2005. Part of that increase is attributable to money coming in from the Texas Enterprise Fund: Last July, the fund awarded Lexicon $35 million to establish a library of knockout mouse embryonic stem-cell lines for the nascent Texas Institute for Genomic Medicine.

Lexicon said Tuesday that it expects to lose $16 million to $18 million in the third quarter. It also reduced its projected net loss for 2006, to between $57 million and $60 million.

Previously, it anticipated losing $67 million to $70 million this year.

Shares of Lexicon closed at $4.41 Tuesday, unchanged from Monday's close.

brett.brune@chron.com

1142.Missing woman's death raises awareness about Alzheimer's
Last Updated: 8/2/2006 10:14:56 PM　http://www.kare11.com/
Authorities found the body of a missing Deephaven woman Wednesday in a rugged part of Wyoming. Her family hopes this tragic story will lead to some good down the road.

Julie Webster, 58, had been diagnosed with early-onset Alzheimer's, but to many she didn't look or act like someone who had the disease. She loved to play tennis and walk her dog five times a day. And her family noticed little change in the past year.

"She was a little bit quieter than normal but never would I have thought she'd be doing this," says daughter Robin Carter.

But experts say the face of Alzheimer's is changing. About 4.5 million people are currently diagnosed with the disease. About 500,000 of them are under the age of 60.

"It really does stop people in their tracks," says Mary Birchard of the Alzheimer's Association in Minnesota. "Often people aren't able to work, it changes their family dynamics, oftens changes their plans."

Webster left her Deephaven home early Friday morning to pick up her daughter at the Twin Cities airport. She apparently got confused and ended up in Saint James, which is about 120 miles southwest of the Twin Cities. A surveillance camera videotaped her alone at a gas station there.

Later Friday night she bought gas again in Gillette, Wyoming, which is 650 miles from Saint Peter.

Authorities found Webster's car Tuesday near Buffalo, Wyoming. They found her body Wednesday in a rugged area nearly a mile from the car. She apparently slid down an incline.

"It appears when she got down there, she realized that was not a way to be able to get out and it looks like she attempted to come back up the incline but couldn't," says Hennepin County Sheriff Pat McGowan.

Authorities do not suspect foul play. An autopsy is expected this week to determine the cause of death.

Birchard says it was a sad day at the Alzheimer's Association office in Edina.

She says it's important for families to know the disease manifests itself differently in different people, and some days are better than others.

"It could've been that on that particular day she was more disoriented than previous days, and that's not something you could really have prepared for," Birchard says.

"She may have felt she was driving only an hour or two, and in fact she might've been on the road for several days," she adds.

Experts say about 60 percent of Alzheimer's patients do wander away at some point during the disease. The Alzheimer's Association has a 24/7 helpline to assist families with that issue and many others. The number is 1-800-232-0851.

By Joe Fryer, KARE 11 News.

(Copyright 2006 by KARE 11. All Rights Reserved.)

1143.NC Scientists learn more in preventing Alzheimer's & Huntington's Diseases
August 2, 2006　 http://www.cherokeesentinel.com/

Scientists at North Carolina State University have effectively lifted the veil from an important protein that is linked to the prevention of neurodegenerative diseases like Alzheimer's and Huntington's.

Dr. John Cavanagh, professor of molecular and structural biochemistry, teamed with colleagues from the Mayo Clinic and Duke University to describe the shape of the protein, calbindin-D28K. Understanding a protein's structure allows researchers to learn more about how it functions and interacts with other proteins, which, in this case, may provide clues to developing drugs to halt the diseases.

The research appears in the July 2006 edition of Nature Structural and Molecular Biology.

Calbindin-D28K is a protein that either grabs calcium from areas that have too much or serves as an on/off switch for further chemical reactions. It is known for its flexibility; it is found in the kidneys, pancreas, ocular nerve and in abundant quantities in the brain. Recent studies show, Cavanagh says, that it acts as a bodyguard in the brain, binding to and inhibiting caspase 3, a protein that stimulates plaque formation and tangle formation, which are hallmark characteristics of neurodegenerative

disease. Until now, however, the structure of calbindin-D28K remained a mystery.

"If you don't know the shape of the protein, you can't figure out how it works," Cavanagh says. "It took a long time about five years but we've characterized the structure of this protein and found where it binds caspase-3. Insight into how it binds to caspase-3 might lead to a way of exploiting those interactions to develop therapeutics."

It took a long time to characterize calbindin D28K, Cavanagh says, because it was initially a challenge to force cells to make enough protein in order to do the requisite studies. Additionally, many parts of the protein are very similar and so are extremely difficult to distinguish from each other.

The research team used nuclear magnetic resonance to get a high-resolution picture of what the protein looks like. In this painstaking technique occurring inside machines that have magnetic fields several hundred times greater than the Earth's magnetic pull radio waves are bounced off the approximately 5,000 nuclei in the protein. "When you hit a nucleus with a

radiofrequency pulse, it resonates, sort of making its own little noise, like a tuning fork," Cavanagh says. "The frequency at which the nuclei resonate after being hit with a pulse is very specific to their specific position in the protein. So after we hit all of them with a pulse, it's like hitting all the keys of a piano at the same time and it's just an awful mess. And remember, we're doing this for 5,000 separate keys. Yet, we're able to untangle this mess to find the specific frequency of each nucleus and relate that to where it lies in the protein."

Cavanagh isn't satisfied with this knowledge, however. He says the shapeshifting protein sometimes contains no calcium. When it grabs calcium, it changes its shape.

"This could be why the protein plays so many different roles," Cavanagh says. "Proteins that change shape usually serve as on/off switches, but this protein also grabs calcium and takes it elsewhere. Now we're working to determine the structure of this protein when it has no calcium."

The National Institutes of Health, the American Foundation for Aging Research and the Kenan Institute for Engineering, Technology & Science supported the research.

1144.The occasional curry 'could prevent Alzheimer's'
By Daily Mail reporter

23:13pm 2nd August 2006

Reader comments (5)

Curry could help improve mental agility and stave off Alzheimer's disease, it has been claimed.

Scientists found those who ate the dish as little as once every six months did better in tests than those who had it never or rarely.

It is thought that curcumin, the part of the spice turmeric which gives curry its distinctive yellow colour, is responsible for the effects.

Although previous studies have suggested curcumin helps ward off Alzheimer's, it was not realised that even small quantities could have an effect.

Dr Tze-Pin Ng, from the National University of Singapore, who led the research, told New Scientist magazine it was remarkable 'that apparently one needs only to consume curry once in a while' to improve mental performance.

Alzheimer's affects 450,000 in the UK, robbing them of their memory and faculties.

Colouring agent

Previous research has suggested curcuma inhibits the build-up of so called amyloid plaques - harmful protein deposits - in the brains of those with the disease. It is used in many Indian dishes and also as a colouring agent in Western foods.

Turmeric, from which it comes, is ground from the root of a plant of the ginger family, which grows wild in the Himalayas.

Although a regular in spicy dishes such as chicken tikka masala, turmeric powder itself has a subtle, almost bland, taste.

The researchers looked at the curry consumption of 1,010 Asians aged 60 to 93 who did not have Alzheimer's and gave them mental agility tests. The findings may explain why rates of the disease are lower in India than in the West.

Curcumin has also been found to fight cancer.

Last year, researchers from Texas found that when used in combination with other drugs, it can help stop the spread of breast cancer to other parts of the body.

Other tests have shown it can help shut down a protein that plays a key role in the spread of prostate cancer.

Dr Ng now wants to confirm his findings with a controlled clinical trial comparing the effects of curcumin and a placebo.

1145.Art boosts Alzheimer's patients' spirits
By ROBERT WELLER, Associated Press Writer
Thu Aug 3, 2:57 AM ET
http://news.yahoo.com/

DENVER - Not a word is spoken as five aging artists sit at a table in a small room and draw. Talking is discouraged, since it can be distracting: The artists are Alzheimer's patients in the first stages of the dementia disorder that afflicts an estimated 4.5 million Americans.

One patient, Jim Lash, 83, isn't moving. His brush is still.

"He was hung up. I suggested he go on to another part of it," said aide Jeanne Hill, and he did.

Getting Alzheimer's patients to sit for 45 minutes is a challenge under any circumstances and for some of the artists the choice of colors has to be limited.

The group is part of the Memories in the Making program that began in 1988 in Orange County, Calif. There are now dozens of chapters in 26 states and experts say the artwork has provided an extraordinary outlet for Alzheimer's patients.

"One of the things that emerged was that even with the loss of memory the capacity for imagination still has it place," said Dr. Gene Cohen, the director of the Center on Aging, Health & Humanities at George Washington University who has studied the effect of art on people with Alzheimer's.

"Art is a wonderful activity that taps into imagination," Cohen said. "That is one reason there has been increasing attention to art for people with Alzheimer's. Even as memory fades the imagination has the capacity to be robust."

The illness affects parts of the brain that control thought, memory and language. Its cause remains unknown and there is no cure, though some drugs can slow the illness in its early and middle stages.

There is research that suggests artwork helps Alzheimer's patients. A small study last year of 12 people, ages 65 to 85, found that weekly sessions helped Alzheimer's patients focus their attention for 30 to 45 minutes and that completing artwork brought them "pleasure and satisfaction."

"This was particularly encouraging, given that most individuals with dementia have difficulty with attention and concentration and are unable to initiate, maintain, or complete a task without assistance and cueing," according to the study led by Clarissa Rentz, program director for the Cincinnati chapter of the Alzheimer's Association, and Jennifer Kinney, a gerontology expert at Miami University of Ohio.

The only activity that comes close to helping Alzheimer's patients the same way is music, the researchers said.

There is no indication the good feelings last, but few dispute the benefits of the art therapy.

"It is an opportunity to express themselves even after some of their standard human communications abilities of expression have gone," said Peter Reed, director of care services for the Alzheimer's Association.

Just being around people brings a smile to Lash, who can remember the day he went to work as a paper hanger ? the same day Wendell Wilkie was nominated for president by the Republican Party in 1940.

"It's annoying that I can't remember the names of people I met six hours ago," said Lash, who produced two small watercolors of lions.

"It's better than sitting home and just doing nothing," he said.

For those who have problems carrying out movements, facilitators will use a hand-over-hand technique, which guides the artist so he or she can do it on their own. Volunteer aides can help artists identify objects and provide the words to help them express their feelings.

For retired Army officer Alex Zenz, 78, artwork is "an escape."

"I can do what I want to do," Zenz said as he drew a copy of Robert Campaign's "Master of Females" from a book.

Zenz's wife, Dolores, said art is "a way for him to let out steam. He had a number of tough years in the military, in Korea and Vietnam."

The paintings and drawings of Alzheimer's patients like Cohen and Lash sell at Memories in the Making-led auctions throughout the country, helping fund efforts to fight the disease.

"I really like what I am doing," Lash said. "I always say that if I can see anything I can draw it."

1146.Cortex AMPAKINE Drugs Can Reverse Age Related Memory Decline in an Animal Model
http://www.engelpub.com/

University of California, Irvine investigators demonstrate how AMPAKINE drugs boost the brain's own protein for fighting age-related deficits in memory mechanism

IRVINE, Calif.--(BUSINESS WIRE)--Aug 2, 2006 - In the August 2006 issue of The Journal of Neurophysiology, Drs. Christine Gall and Gary Lynch and their research staff reported that it was possible to use AMPAKINE compounds to reverse age-related declines in cognitive functions in old rats, returning their cognitive ability to that seen in young rats. The authors attributed this effect to the ability of AMPAKINE drugs to increase endogenous brain-derived neurotrophic factor (BDNF) in the neurons in the brains of older rats. The study used two of Cortex Pharmaceuticals' (AMEX: COR) high impact AMPAKINE drugs that are in preclinical development testing at the company. When an antagonist to BDNF was co-administered with the AMPAKINE compounds, the older rats returned to age-related cognitive impairment level.

Dr. Gall said, "This is a significant discovery because these results indicate the exciting possibility that AMPAKINE compounds could be used to treat learning and memory loss associated with normal aging."

Cortex is developing both high and low impact AMPAKINE drugs that bind at different sites on the AMPA-receptor of neurons. The high impact compounds under development are orally active and therefore the up-regulation of BDNF with these drugs is a significant finding not only for restoring memory declines as a result of aging, but also for other neurodegenerative diseases such as Huntington's Disease, Fragile X, Parkinson's and Alzheimer's disease, where elevation of BDNF may produce disease modifying effects in the patient populations.

The article by Drs. Gall and Lynch can be found by accessing the following website link: http://jn.physiology.org/cgi/content/abstract/96/2/677.

About Cortex Pharmaceuticals

Cortex, located in Irvine, California, is a neuroscience company focused on novel drug therapies for neurological and psychiatric disorders. The Company is pioneering a class of proprietary pharmaceuticals called AMPAKINE compounds, which act to increase the strength of signals at connections between brain cells. The loss of these connections is thought to be responsible for memory and behavior problems in Alzheimer's disease. Many psychiatric diseases, including schizophrenia, occur as a result of imbalances in the brain's neurotransmitter system. These imbalances may be improved by using the AMPAKINE technology. Cortex has alliances with N.V. Organon for the treatment of schizophrenia and depression and with Les Laboratoires Servier for the development of AMPAKINE compounds to treat the neurodegenerative effects associated with aging and disease, including Mild Cognitive Impairment, Alzheimer's disease and anxiety disorders. (http://www.cortexpharm.com/)

Forward-Looking Statement

Note - This press release contains forward-looking statements concerning the Company's, and others' research and development activities. The development of commercially successful products based on success of such activities depends on a number of factors, including the risks that the Company's proposed compounds may at any time be found to be unsafe or ineffective for the indications under test and that pre-clinical and clinical studies may at any point be terminated, suspended or take substantially longer than anticipated to complete. As discussed in the Company's Securities and Exchange Commission filings, the Company's proposed products will require additional research, lengthy and costly clinical testing and regulatory approval. AMPAKINE compounds are investigational drugs and have not been approved for the treatment of any disease.

Contact Cortex Pharmaceuticals, Inc. Roger G. Stoll, Ph.D., 949-727-3157 or The Investor Relations Group Damian R. McIntosh / Dian Griesel, Ph.D. Media: Lynn Granito 212-825-3210

Last Updated: Wednesday, 2 August 2006, 23:48 GMT 00:48 UK
http://www.bbc.co.uk/
1147.Dementia risk predictor devised

A method to predict a middle-aged person's chance of developing dementia has been devised by scientists.
The test calculates risk by assessing factors such as blood pressure level, body mass index and cholesterol levels, along with age and education.

The work, published in the journal Lancet Neurology, is based on a Finnish study that revealed several midlife risk factors were linked to dementia.

A high-risk result, said the team, could encourage lifestyle changes.

A method to predict a middle-aged person's chance of developing dementia has been devised by scientists.
The test calculates risk by assessing factors such as blood pressure level, body mass index and cholesterol levels, along with age and education.

The work, published in the journal Lancet Neurology, is based on a Finnish study that revealed several midlife risk factors were linked to dementia.

A high-risk result, said the team, could encourage lifestyle changes.

The scientists used data from the Cardiovascular Risk Factors, Ageing and Dementia study.

This research assessed 1,409 middle-aged people from Finland and then looked at them again 20 years later for signs of dementia, including Alzheimer's disease and vascular dementia.

Scientists discovered that along with the known risk factors of age and a low-level of education, high blood pressure, high cholesterol and obesity also meant people had a higher chance of suffering from dementia.

Using these results, the team developed a score-based system to predict the likelihood of a middle-aged person developing dementia in later life.

Risk scores

Lead researcher Miaa Kivipelto, from the Aging Research Center, Karolinska Institute in Sweden, said: "The idea is to have a simple tool to predict the risk for diseases, like you have for cardiovascular diseases or diabetes.

"But for dementia there has been nothing like this. The idea to put this information together and have an overall estimation for dementia risk is new."

The predictive test takes information about age, number of years spent in education, sex, body mass index, blood pressure level, cholesterol level, physical activity and genetic factors and assigns each with a risk score related to their association with dementia.

It is remarkable that one can start to protect oneself from dementia that much earlier

Rebecca Wood, Alzheimer's Research Trust

Then, combining these, the patient can be given an overall score, indicating the probability of them developing dementia.

Dr Kivipelto said: "We hope physicians could use this system to find people who are at a higher risk of developing dementia at later life."

Once these people have been identified, she added, they could be advised to change their lifestyle, or be given drugs, so as to lower their weight or blood-pressure levels.

"It is also an easy way to see how much you can do yourself to lessen your risk of dementia."

Rebecca Wood, chief executive of the Alzheimer's Research Trust, said: "It is remarkable that one can start to protect oneself from dementia that much earlier.

"To be able to identify a group of people at higher risk and who might be able to introduce lifestyle changes to reduce their risk is very exciting.

"The proposed test is still a somewhat blunt instrument, because it picks up too many people who may not develop dementia so much more work is needed to improve and validate its results."

Professor Clive Ballard, director of research at the Alzheimer's Society, said: "New developments that encourage living a healthy life style are an important step towards combating dementia.

"We recommend that people take regular exercise; eat healthily; make sure they get their blood pressure checked and take part in social activities."

The Mental Health Foundation said that the general public must take responsibility for their diets if they are to avoid dementia in later life.

Posted on Thu, Aug. 03, 2006email http://www.macon.com/mld/macon/

1148.Alzheimer's cruelly robs from the old and young
By Alline Kent
TELEGRAPH COLUMNIST
Our son has a friend up the street named Adam. Together they ride bikes and jump on the trampoline. They eat ice cream and play touch football in the front yard.

But while Adam is witty and funny, and a loyal friend, he also has a serious side. This fall, you might see Adam on the side of the road selling lemonade or fruit from the pear trees in his yard.

And if you do, I hope you will stop, and make a purchase or a donation. Because what Adam will be doing is trying to raise money not for a new bike, but to help stop a terrible, horrible disease that has impacted his life.

Chances are that it has impacted yours as well.

Roughly 4.5 million Americans are living with Alzheimer's. Adam's grandmother has had the disease for the past 10 years. It has affected her so severely that she can't finish her sentences, can't even tie her own shoes. The stories that so many of us have heard from our grandparents, about their experiences during the Depression or world wars, Adam will never hear.

But while the disease has ravaged and robbed her mind, the tragedy doesn't stop there. In Central Georgia, according to the 2000 census, there are around 43,000 people who care for someone with Alzheimer's. Then there are the people like Adam and his family, the ones who support the primary caregivers.

The ripples of impact keep growing and growing of those affected by the debilitating disease.

"It is just so devastating," said JaLynn Hudnall, Adam's mom. "I remember, growing up, spending summers at my Grandma's house. My kids won't know what that's like. She doesn't know them, she doesn't know who I am anymore."

Hudnall explained how the stress of caring for someone afflicted with Alzheimer's wears on the caregiver and the rest of the family.

"She is your mom, but it is hard to remember that. You look at her, a grown adult, and she is so childlike. To her, I am still an infant, so when I tell her who I am, it is very traumatic," she said.

"It is especially hard on my dad, who still takes care of her in their home. I can't imagine what it must be like for him to see someone he has been married to for 54 years in this condition. And even for my mom, can you imagine what it must be like to basically have amnesia and be surrounded by people you do not recognize, telling you they are related to you and you have no memory of them?"

"The only way we can do something about this disease is to talk about it," Hudnall said. "The disease and the caregiver issues. It really is insidious, hateful, and affects not only the person but the spouse, the kids and the neighbors."

Hudnall is helping to organize this year's Georgia National Memory Walk, which will be Friday, Sept. 22, at the Georgia National Fairgrounds in Perry.

Registration is at 5 p.m. and the walk begins at 6 p.m. The memory walk is the largest the Alzheimer's Association has, held nationwide every fall.

And what can you do?

Well, first mark the date on your calendar and plan to be there. You may walk but you don't have to. You can just come enjoy the fun. It is going to be a fun night, with beach music and dancing and plenty of food and activies for the kids.

"Every year we want it to get bigger and better so that people won't want to miss it," Hudnall said. "It is going to be a great evening and we are going to raise money too."

Better yet, you may form a team and work together to raise money. Tell people why you are taking this action, talk about Alzheimer's and how it has affected your life - put a face on this disease like Adam did for our family.

The estimates are that by 2030 there will be 12-to-16 million more people diagnosed with Alzheimer's disease.

"I am not raising money for my mom, I am raising money for Erika and Adam, for our kids," Hudnall said. "It is only through education and research that we can get to the point where we can manage this disease."

Six percent of the funds raised goes to research, with about 80 percent staying here in the area for services and programs such as Project Safe Return, a bracelet system that identifies both the patient and the caregiver in case of an emergency.

"I just think this is such a horrible, horrible disease," Hudnall emphasized. "It takes away the person you knew and loved, and it does not discriminate - rich, poor, black or white, it doesn't matter."

Get your team together and plan to be at the Memory Walk. For more information about how you can get involved with the Georgia National Memory Walk, contact JaLynn Hudnall at 827.0750.

Do it for all the Adams and their grandmamas.

Alline Kent's columns appear three days a week. She may be contacted via e-mail at AllineKent@cox.net, or by calling 396-2467.

Thursday, Aug. 3, 2006 82° & Clear Search Website Google Ads (advanced search)

Posted Online: August 3, 2006 http://daily-journal.com/

1149.Nuns lead study in Alzheimer's
Comment on this article

Study focuses on cure

By Tom Dunkel

The Baltimore Sun

In some respects, the School Sisters' motherhouse operates as a senior citizens center -- staff nurses and physical therapists, organized games and Sister Clara Beall's hobby room.

Five worktables are squeezed into the former chapel, surrounded by storage cabinets and mounds of supplies.

"The good holy nuns think it's a bit of a mess," acknowledges Sister Clara, 73, who can be found amid the clutter from dawn until dark, filling pottery molds, running the sewing machine, doing fine-detail painting that's too difficult for hobby room attendees.

About 15 sisters show up Monday, Wednesday and Friday mornings. Some are physically and mentally sharp. Half use walkers or wheelchairs. A few have Alzheimer's.

"Deterioration is hard to watch," Sister Clara says. "These were once vital women."

She can spot the first flickers of dementia before a diagnosis. Sisters mismatch paint colors or talk to long-dead mothers.

It's as if the mind turns a corner, says Sister Clara -- and she finds easier craft work for that sister to do. There's no such thing as failure in her hobby room.

Sister Mary Agnes Klug -- a small, scrappy Orioles fanatic -- manages the motherhouse gift shop.

"I like to keep busy. It keeps my mind off myself," Sister Mary Agnes says.

Customers can buy hobby room crafts, used books and bric-a-brac, greeting cards, Blessed Mother figurines, and bargain-basement junk food.

Sister Mary Agnes keeps a safe distance from the hobby room: It's for "retired people." She also has an aversion to taking naps -- they're for "older people." Sister Mary Agnes is 97.

Sometimes Sister Genevieve Kunkel, 95, tends the gift shop. The two have known each other since prep school. Both went to the College of Notre Dame and became School Sisters in the 1930s.

Years later, neither woman hesitated when Dr. David Snowdon solicited donors for his Nun Study.

Long sessions

Snowdon has about a dozen full-time employees in his "Nun Study." One of his first hires was Sister Gabriel Mary Spaeth, a School Sister from Milwaukee. At 74, she says she's "amazed at and intrigued by" the workings of the brain.

Every nun gets tested each year, in two hour-long sessions over two days. The first involves basic skills: doing step-ups on raised blocks, walking a line as fast as possible, buttoning a sweater.

The second component is a mental aptitude exam that many sisters dread. It entails replicating complex drawings and answering questions about a long story read aloud.

About 7 percent of Snowdon's subjects have dropped out. The testing got too fatiguing or too embarrassing. An ever-dwindling majority, though, stuck with him.

Test subjects with muddled minds often freeze on memory questions. At other times there are heartbreaking flashes of clarity.

Sister Gabriel Mary recalls one nun who spoke gibberish, then suddenly stopped and whimpered, "Help me."

Despite their involvement with the Nun Study, the School Sisters -- like any family -- struggle with the realities of Alzheimer's. There are sisters who mistakenly believe the disease is a byproduct of old age or that it's contagious. They're sometimes taken aback by Alzheimer's patients, who in later stages can lose inhibitions or become aggressive.

"Some of the sisters were offended by some of the behavior they were seeing," says Diane Wit, director of education for the Greater Maryland chapter of the Alzheimer's Association. "If a sister would curse, they would reprimand her or make her feel bad or argue back."

Leaders of the motherhouse

The leaders of the motherhouse recently formed a Dementia Study Committee. They plan to hold an "awareness day" to educate all sisters. They're considering aesthetic changes that will make the medical unit more like home than hospital: softening the lighting, eliminating overhead intercoms.

But the greatest resource they draw upon is intangible.

"I love sitting with the sisters who have Alzheimer's," Sister Bernadette says. "They teach us about living life in the moment. I think they're a gift to us. The gift they give is the simplicity, their unconditional love."

The $5 million grant funding the Nun Study ends in February. Some within the National Institute on Aging think David Snowdon has hit a wall. They contend that it would serve him well to add a group of younger nuns.

"People bring that up pretty regularly to me," he says.

Snowdon is uncomfortable with bureaucrats but enjoys giving briefings to the School Sisters.

"In the future," Snowdon tells his motherhouse audience, "I see us getting into Parkinson's and other brain diseases."

He takes questions. The first hand that shoots up is Sister Mary Agnes'.

"Most of us in the study are in the older phase," she says. "Aren't you planning on getting a younger group to start up with?"

"I don't want to go out and sign up Notre Dame sisters just to get sheer numbers," Snowdon says.

Snowden feels like a man surrounded by surrogate grandmothers to whom he's fiercely loyal. He attends sisters' wakes, stays overnight at motherhouses, joined the College of Notre Dame's trustees. When his brother contracted cancer, the sisters included him in their prayer chains.

The sisters also know that questions -- like prayers --sometimes go unanswered. Alzheimer's disease could be a perpetual puzzle. Science may never unravel those brain tangles.

A cure is a matter of faith, they say. And God's will.

1150.Brain imaging identifies best memorization strategies, details differing parts of brain used in each

Visual study, word play among most effective memory techniques

By Brenda Murphy-Niederkorn
http://news-info.wustl.edu/

Aug. 3, 2006 -- Exploring exactly why some individuals' memory skills are better than others has led researchers at Washington University in St. Louis to study the brain basis of learning strategies that healthy young adults select to help them memorize a series of objects. Using functional magnetic resonance imaging (fMRI), the researchers uncovered brain regions specifically correlated with the diverse strategies that subjects adopt.

Brenda Kirchhoff, research associate in psychology in the University's School of Arts and Sciences, conducted this study in the then-Washington University lab of Randy L. Buckner, now a professor of psychology at Harvard University and investigator at the Howard Hughes Medical Institute. Their findings have been published in the July 20, 2006, issue of Neuron. (Kirchhoff is the article's first author and Buckner is senior author.)

"Randy and I were interested in exploring individual differences in memory ? why some people are better at learning new information than others," said Kirchhoff. "Our main goal was to determine the learning strategies that people use and their relationship to memory performance. Secondly, we wanted to know if individual differences in learning strategies were associated with individual differences in brain activity."

What they found was that test subjects used two main self-selected strategies to learn new information. Use of the strategies was associated with better memory performance. Furthermore, individual differences in learning strategies could be correlated with MRI-detected biological activity in distinct brain regions.

Using the Washington University population as test subjects, Kirchhoff studied 29 right-handed, healthy young adults, ages 18-31, all of whom had normal or corrected-to-normal vision and reported no significant neurological history. Participants were given interacting object pair images and told to study them in anticipation of a memory test. For example, interacting objects included a turkey seated atop a horse and a banana positioned in the back of a dump truck. No other instructions were provided so that the subjects would choose their own encoding or learning strategies.

While earlier pilot studies had indicated that individuals use a variety of strategies to help them memorize new information, the following four strategies were the main strategies used by participants in this study, according to Kirchhoff, including:

1) A visual inspection strategy in which participants carefully studied the visual appearance of objects.

2) A verbal elaboration ? or word-based strategy ? in which individuals constructed sentences about the objects to remember them.

3) A mental imagery strategy in which participants formed interactive mental images of the objects ? similar to animated cartoons.

4) A memory retrieval strategy in which they thought about the meaning of the objects and/or personal memories associated with the objects.

Visual and verbal strategies improved memory

Selection of the first two strategies described above ? visual inspection and verbal elaboration ? resulted in improved memory results, according to Kirchhoff.

"Those individuals who used the first two strategies often had better memory performance than those who used them rarely or not at all," said Kirchhoff. "There's a great deal of variability in strategy use when people are free to choose their own learning techniques. We also discovered that individual people use multiple strategies to learn new information."

In addition to behavioral analyses of these learning strategies, Kirchhoff recorded the participants' brain activity patterns during learning using functional MRI.

"From brain imaging data, we were able to find a significant correlation between different learning strategies and brain activity," said Kirchhoff. "We were excited to see that differences in brain activity patterns between people could be explained in part by differences in learning strategy use."

During functional MRI analyses of study participants, researchers focused on regions of the brain that previously had been shown to play important roles in processing information about words and objects. People who used a word-based learning strategy often had greater activity in left anterior brain regions thought to play important roles in thinking about words than people who used this strategy less frequently. In contrast, people who used a learning strategy based on studying the visual appearance of the object pairs often had greater activity in a left posterior brain region thought to play an important role in viewing and retrieving information about objects than people who used this strategy less frequently.

Changes in brain activity

"One very interesting aspect of these findings is how they reveal that not all of us memorize information in the same way. Differences in memorization strategies emerge both behaviorally and in brain activity patterns," said Buckner. "There have been a number of innovations in the last several years in medical technology that allow us to see brain activity patterns in individuals rather than averaged groups of people. These tools now allow us to see individual patterns of brain activity and how they differ from one person to the next.

"This is some of the earliest research to explore these individual learning strategies at both the behavioral level and brain level. The work is a testimony to the innovative and thorough approach that Brenda pursued. She undertook a very careful multilevel approach beginning with behavioral differences and eventually targeting the brain. Research has been undertaken to study individual differences in cognition and memory previously. Brenda's work established a new path to pursue those differences at the brain level."

While this research is in its earliest stages, further studies may help provide behavioral modification treatments for individuals with memory impairment, including adults afflicted with age-related memory loss and early onset Alzheimer's disease.

"In the future, we are interested in studying the memory performance of older adults and people with memory impairments to determine if they use different learning strategies than those selected by young, healthy adults," said Kirchhoff. "The next step would be to see if training in the use of different learning strategies would help to improve their memory."

"It's an open question as to what degree the differences in memory of older adults and those with Alzheimer's disease can be modified by the learning strategies they adopt," said Buckner. "It's possible that the strategies adopted by younger adults could be adopted by older adults. We could then look to see if any of those new strategies accounted for memory improvement in older adults."

DGDispatch

1151.Triflusal Might Slow Dementia Progression in Patients With Mild Cognitive Impairment: Presented at ICAD
By Ed Susman

MADRID, SPAIN -- July 19, 2006 -- Treatment with the anti-platelet drug Triflusal appears to reduce the risk of conversion to Alzheimer's disease in patients with mild cognitive impairment, doctors said here at the 10th International Conference on Alzheimer's Disease and Related Disorders (ICAD).

While the risk reduction was a statistically significant (P =.024) 47%, researchers said the results should be treated with caution due to methodological problems in the randomized, double-blind, placebo-controlled clinical trial.

The study failed to show significance in its primary endpoint -- reduction in the Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-cog), said lead investigator Teresa Gomez-Isla, MD, head, Memory Disorders Unit and Alzheimer's Research Laboratory, Santa Creu I Sant Pau Hospital, Barcelona, Spain.

"Even though the trial failed to show a significant reduction in scores on the ADAS-cog, the small decline that we did see may have contributed to the slower conversion to Alzheimer's disease in the patients taking trifusal," said Dr. Gomez-Isla. She reported a fall of about 2 points in the ADAS-cog among patients on Triflusal.

The study was designed to recruit up to 534 patients, but the trial was halted due to slow enrollment. A total of 128 patients were randomly assigned to placebo and 129 were assigned to receive Triflusal 900 mg a day. The patients were followed for 13 months. During this period, 25 patients in the placebo group progressed to Alzheimer's disease compared with 16 patients in the Triflusal group.

"The study demonstrated a reduced likelihood of progression to dementia in the trifusal as compared with the placebo group," she said in her poster presentation on July 18th and at a press briefing. "The observed risk reduction for progression to dementia of 47% may be clinically relevant."

Dr. Gomez-Isla said that an analysis of the genotype of the patients found a significantly higher prevalence of the apolipoprotein-E 4 allele -- a genotype shown to increase susceptibility to Alzheimer's disease -- and this finding could also have skewed the results.

"These results," she said, "should be interpreted with great caution and require further confirmatory studies with apolipoprotein-E 4satatus as a balancing correlate."

[Presentation title: A Randomized, Double-Blind, Placebo Controlled-Trial of Triflusal in Mild Cognitive Impairment. Abstract P3-46]

08/04/06　 http://www.sun-herald.com/
1152.Hurricane preparation tips for Alzheimer'S caregivers

Beyond all of the press encouraging Floridians to prepare for hurricane season, we must also focus on families living with special needs, especially caregivers and families coping with Alzheimer's disease.

In addition to the standard activities everyone should take, the Alzheimer's Association wants caregivers of people living with Alzheimer's disease to take a few steps in preparing for hurricanes. The Florida Gulf Coast Chapter of the Alzheimer's Association recommends:

Advance preparations:

* Consult with your physician and pharmacy about what mechanisms they have in place for continuity of care and prescription needs in the event standard communications lines are down.

* If your loved one lives in a residential facility, meet the staff and learn about their hurricane procedures. Find out about their evacuation plan.

* Prepare an emergency kit (see below for item suggestions).

* Enroll in the Alzheimer's Associations's SAFE RETURN Program.

* Keep all medications organized and in a safe and accessible place.

* If you have a cell phone, keep it charged and store your emergency contact numbers, including your local Alzheimer's Association. Have an additional pre-charged battery.

* If you do not have a cell phone, keep an emergency call list with your medications.

* Identify and visit the options you have in case you need to evacuate to a shelter. Speak with those who will be managing the shelter before the need to go there occurs. This way you can discuss any special needs you may have ahead of time.


If a hurricane is coming your way:

* Get to a safe place. If you need to evacuate, do not delay.

* Alert others (family, friends and medical personnel) that you are changing locations.

* Be sure there are other people who have copies of the person with dementia's medical history, medications and physician information.

* Purchase extra medications.

Emergency kit:

* Consider preparing an emergency kit in advance. Keep it in a watertight container and store it in an easily accessible location.

* Easy on/off clothing (a couple of sets).

* Supplies of medication.

* Toiletries/dentures.

* Velcro shoes/sneakers. Back-up eyeglasses.

* Incontinence products.

* Extra identification items for the person, such as an ID bracelet and clothing tags.

* Copies of legal documents, such as a power of attorney.

* Copies of medical documents of individual's condition and current medications.

* Copies of insurance and Social Security cards.

* Use waterproof bags to hold medications and documents.

* Physician's name, address and phone numbers. Recent picture of the person with dementia. Lotion (good for soothing person). Favorite items or foods. Liquid meals.

* Pillow, toy or something else to hug.

During an evacuation:

Persons with dementia are especially vulnerable to chaos and emotional trauma. They have a limited ability to understand what is happening and they may forget what they have been told about the disaster. Be alert to potential reactions that may result from changes in routine, traveling or new environments including: agitation, pacing, wandering and delusions or hallucinations.

Inform others around you (hotel or shelter staff) that your loved one has dementia and may not understand what is happening. Do not leave the person alone. It only takes a few minutes to wander away.

Changes in routine, traveling and new environments can cause agitation and wandering behaviors including hallucinations, delusions and sleep disturbance. Remain calm. The person with dementia will respond to the tone you set.

Tips for preventing agitated behavior:

* Reassure the person frequently. Take their hand or put your arm on their shoulder and tell them things are going to be fine.

* Redirect the person's attention if they begin to become upset. Move the person to a safer or quieter place. Make sure the person takes their medications as scheduled. Schedule regular meals. Avoid detailed explanations. Provide additional assistance with all activities of daily living. Pay attention to cues of agitation (fidgeting, pacing).

* Remind the person they are in the right place.

Contact Information: Alzheimer's Association 24/7 helpline is 800-272-3900. Go online for more information at www.alz.org OR www.nbc.noaa.gov.

Written by Gloria J.T. Smith -- President of the Alzheimer's Association Florida Gulf Coast Chapter.

By GLORIA J.T. SMITH

Alzheimer's Association

1153.Alzheimer's disease, drinking not linked, study says
By Molly McElroy
ST. LOUIS POST-DISPATCH
08/03/2006　http://www.stltoday.com/　

Drinking alcohol in moderate amounts can help the heart. But can the benefits of alcohol be extended to other body organs, such as the brain?

Alcohol is commonly believed to be harmful to the brain, as seen by slurred speech, stumbling and other drunken behaviors. But it is not clear whether acute alcohol consumption damages the brain.

"There is little proof of permanent neurological effects" from mild to moderate alcohol consumption, said John Morris, neurology professor at Washington University. He defines moderate drinking as one to two drinks every day or two.

Morris and his colleagues studied whether moderate drinking influenced Alzheimer's disease.

The researchers tracked the mental abilities and drinking habits of people with dementia and their nondemented counterparts for up to 24 years. They found no difference in drinking patterns between the two groups.

The results also showed that alcohol's effects on dementia are neither beneficial nor detrimental.

"Daily alcohol use had no influence on the development of Alzheimer's disease or the rate at which the disease progresses," Monique Williams wrote in an e-mail from Madrid, Spain, where she presented the findings at a recent conference.

But alcohol's lack of effect on mental abilities does not mean that alcohol is healthy.

"The findings should not serve as encouragement to drink alcohol," cautioned Williams, a professor and clinician at Washington U.

Risks associated with alcohol use in the elderly include injuries due to falling, slower metabolism of alcohol and interaction of alcohol with medications.

The Washington U. researchers are the first to study long-term effects of alcohol on memory within the same individuals.

Williams presented the study last month.

Aug 4, 2006 7:49 am US/Central　http://wcco.com/

1154.Good Question: Why Do Some Get Alzheimer's Young?

Ben Tracy
Reporting

(WCCO) Alzheimer's disease steals people's thoughts and erases their memories and while some think it only affects older people, there are people in their 40s and 50s with the mind-robbing disease.

This week, news that a Minnesota mother with early-onset Alzheimer's got lost and died in Wyoming shocked many. She was just 58 years old.

So why do some people get Alzheimer's so young?

"The face of Alzheimer's is changing," said Mary Birchard, the executive director of the Twin Cities Alzheimer's Association. "It is not someone in a nursing home who is 95 years old. It is people who look way too much like you and I."

Early-onset Alzheimer's strikes people before the age of 65. It accounts for more than 5 percent of Alzheimer's cases, which means as many as 500,000 younger people are living with the disease.

People in their late 30s can get early-onset Alzheimer's and the symptoms tend to be the same as Alzheimer's in older people. Those signs include memory loss and disorientation to time and place.

It also includes getting lost, like the Minnesota mother.

"We do know that six out of 10 people with Alzheimer's at some point wander or get lost," Birchard said.

It is unknown exactly what causes Alzheimer's disease, but there is a genetic link to early-onset Alzheimer's disease.

It is generally inherited through a defective gene. Researchers have pinpointed it to chromosome 1, 14 or 21.

Experts expect to see more cases of early-onset Alzheimer's with the aging baby boomer population.

"We're projecting almost a quadrupling of the number of people with Alzheimer's disease in the next 25 to 30 years and that will include early-onset as well," Birchard said.

Studies show Alzheimer's is the second most-feared disease after cancer.

New research out this week may help predict who is at greater risk. High blood pressure, cholesterol and obesity are all on the list.

(? MMVI, CBS Broadcasting Inc. All Rights Reserved.)

1155.LV chosen as training ground for treating Alzheimer's
August 4 - August 10　　http://www.inbusinesslasvegas.com/
By Cristina Rodriguez / Staff Writer

A simple and rapidly spreading therapy for Alzheimer's patients now has a national training base in Las Vegas.

And it is easy to see why the Canadian founders of Cognitive Retention Therapy decided this summer to establish a U.S. headquarters. They expect hundreds of elder-care providers to seek training in upcoming years, and Las Vegas will be a convenient destination, said John Asby, program director of the Calgary-based company.

In one year, 60 providers with 220 clients have started using the drug-free techniques, which promise to reverse memory loss associated with dementia.

Therapists merely talk with the patients, using written exercises and field trips that remind individuals about their lives. For example, one retired pilot was told to read paragraphs about pilot training or the Wright Brothers aloud, then to answer multiple-choice questions. He then progressed to visiting an aerospace museum.

"It's simplistic to look at it in its form, and the results are amazing," said Julie Buss, program director for CRT at Care4Life, a Las Vegas home health company that has signed on 10 CRT clients in four months. It was also her enthusiasm for the program that guided CRT officials to set up shop in Las Vegas.

No specific research on CRT has been conducted, though a study is in the works with the Arizona-based research center Sun Health, Ashby said.

But experience has shown the methods improve scores on the Mini Mental State Examination, a measure of cognitive mental status, by about four points, he said.

"Generally speaking, (the scores of Alzheimer's patients) don't go up at all, they just go down," Ashby said.

The science is based on the research of his mother, Dr. Mira Ashby, who was awarded Canada's highest civil honor for research on the learning process in people with brain injuries.

John Ashby and Sue Jaspar, executive director of the CRT program, two years ago began perfecting their system through trial and error.

The basic concept is that a brain stores memories in different parts. CRT uses the example of a lemon: The taste of a lemon is stored in one section, while the size and shape are stored in another.

"You do not actually lose information, you just cannot find it," Ashby said. "The pathway is lost, and you can't put the memory together. This reinforces new pathways. Your brain wants to be able to remember."

CRT gives therapists packets of exercises called modules. Most are generic ? like ones on the 1920s, '30s or '40s ? and are designed to apply to a large number of elderly clients.

Anecdotal results show individuals regain their self sufficiency and return to normal activities that were hindered by memory loss, like golfing or telling jokes at the dinner table.

"There's a reengagement with the family, and they do things they've stopped doing," Jaspar said. "They stand a lot taller, their confidence is improved, and they are participating in their own disease process."

The sessions are currently only available through private payment. Leaders hope that upcoming studies will help the therapy qualify for Medicare reimbursement and that other insurance companies may follow.

Care4Life charges $65 an hour and meets with clients twice per week, and it gives a $10-per-session discount to individuals who are using the agency's home health service, Buss said.

The 1 1/2-day training sessions will take place at Acacia Springs, the independent living facility where Care4Life's office is based. Geriatric care managers, psychologists and nurses who specialize in dementia care are expected to be interested in the training, Ashby said.

And as simple as the therapy sounds, he predicts that individuals will seek out professionals to administer it.

"These structured exercises are very, very difficult for the average person to do," he said. "If it was as simple as sitting down with Mom and Dad and having a jolly old conversation, I would assure you everybody would do that."

Posted on Sat, Aug. 05, 2006　　http://www.bradenton.com/mld/bradenton/
1156.Alzheimer's mobile clinic brings free services
HERALD STAFF REPORT
BRADENTON - The Florida Gulf Coast Chapter of the Alzheimer's Association invites the public to visit its mobile office, the Memory Mobile. Free services through the fully equipped mobile office will be available at the following days and locations:

? Aug. 7-8 10 a.m.-2 p.m., College Park Club,

5612 26th Ave. W., Bradenton. Information: 756-5571.

? Aug. 9-11, Alterra Clare Bridge, 6101 Point West Blvd., Bradenton. Information: 795-5533.

Services available to visitors include memory screenings, information and referral services, Family Care Assistance, Safe Return for Wanderers, and a variety of literature related to Alzheimer's disease and caregiver concerns. Visitors can also view caregiver training videos or talk with an Alzheimer's Association Program Specialist about their families' specific needs.

The Memory Mobile is made possible through funding provided by the Florida Department of Elder Affairs and the Area Agency on Aging.

1157.Middle-Aged Women Care for Older Generation
By Faiza Elmasry
Washington DC
04 August 2006
http://www.voanews.com/english/portal.cfm
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Their kids are grown and they're back at work, but many middle-aged women find they are still juggling, trying hard to strike a balance between advancing in their careers and caring for their aging parents. This daunting new challenge can be made easier if both sides - care givers and takers - are prepared for it.

Gina Petruccelli is the primary caregiver for her 84-year old mother. "People have asked me, 'Why do you do it?' and I think, 'How could I not?'," she says.

The 49-year-old flight attendant told ABC Morning News how she takes care of her mother, who had suffered two major strokes. Her mother, Millie, says she appreciates what her daughter is doing for her. "She has been very, very helpful and it has been rather strenuous because she has her job and she worries about me," she says.

Being committed to taking care of her mother, Petruccelli admits, has negatively affected her career. "There are opportunities that I haven't explored because it would necessitate a move," she says. "I've got a lot of responsibilities with her."

Gina Petruccelli is one of a growing number of American women who juggle careers and caring for their elderly parents. According to the Family Caregiver Alliance, the typical caregiver is a 46-year-old woman who is employed outside the home and spends more than 20 hours a week caring for a mother who lives nearby.

Business executive Mary Lou Quinlan says because many adult daughters are dedicated to their parents' caregiving, they are not advancing in their careers as much as they would like. Some even consider quitting their jobs to be a full-time caregiver. Quinlan - who's written magazine columns and books about working women - does not recommend that.

"You need your salary," she point out. "You need your benefits, maybe your benefits could even help your parent. Women find that their job is their haven. It's the escape and the normalcy that they are going to crave as things get tough."

To help balance their family and work responsibilities, she recommends women discuss their situation openly with their supervisor. "The good news is that your boss may be in the same seat because all of us will be facing this," she says. "But when you go to your boss, think of it as a business plan. I mean, how can I do a 'win-win plan' so that I ask perhaps for part-time, leave, or maybe you can take on a job that nobody wants to do that you can do on your days off. But try to hold on to part of that job because you're going to need it."

Juggling work and family is just one of many challengers caregivers face, according to psychologist Barry Jacobs. "The burden of care often falls on either the oldest or youngest daughter," he says. "Sometimes that causes friction among the siblings as to who is providing care and who isn't stepping up and providing care." He points to psychological challenges, as well. "Sometimes the relationship with their parents is good and they want to give back to their parent by taking care of them. But in some families, the relationship with their parents has not been good and adult children feel very burdened by taking care of a parent who they have resentment towards and they don't really want to provide that care. Sons and daughters can, over time, be prone to having marital problems with their own marriages because of providing care to a parent."

To help adult children deal with those stresses, Jacobs wrote The Emotional Survival Guide For Caregivers: Looking After Yourself and Your Family While Helping an Aging Parent. In it, he notes that when there is no hope of a full recovery or when a disease changes the parent's personality, many caregivers struggle with depression and anxiety.

He recalls one of his clients - a woman in her 80s who had had a stroke and had a certain amount of dementia as a result. "I remember talking to her 3 daughters, who were in their 50s and early 60s. And the daughters said to me that they feel that the mother that they knew was dead, and the woman that was still alive was a stranger." Jacobs says he hears that sentiment frequently. "When you have an older parent who has Alzheimer, dementia or any other disease which affects their cognition and personality in many ways, the family is being asked to provide care for someone who is very different than the person they have always known and loved. They have to hold on their memories of the person as they knew that person, but also see the person's personality now as a manifestation of the disease. It's not that the person is willfully trying to be difficult or paranoid."

The psychologist recommends that caregivers seek social support and explore community services and programs that would help ease the burden. "In the United States," he observes, "many churches, synagogues and mosques have support services available for people caring for aging parents. It could be respite services or transportation services or even financial help. In terms of government programs, through what are called the Area Agencies on Aging, which exist in every county of the United States, there is funding available to help family caregivers provide care for elderly citizens and the funding can be used for buying equipment, hiring home health aides, getting some sort of respite care."

In addition, Jacobs says, children of aging parents should learn about the health consequences of getting older so they will know what to expect. And, he says, parents can help their children by starting early on to plan for their later years. They can explore various support options, discuss the best arrangements with their family and make important decisions themselves while they can, instead of leaving the entire burden to their children.

Monday, August 7, 2006 - Page updated at 12:00 AM
http://seattletimes.nwsource.com/html/home/
Growing Older

1158.What to look for in dementia-care facilities
By Liz Taylor

Special to The Seattle Times


Related

More Liz Taylor

"Dementia" is a $10 word for a disorder that permanently, progressively, relentlessly kills a person's brain cells.

Slowly, it takes away memory and the ability to reason, learn, make good judgments, communicate and operate day-to-day. Personality and behavior change unpredictably. Without a cure, the person usually dies eight years after diagnosis. The most common cause is Alzheimer's. Little in life prepares us to care for someone with a dementing illness. It requires the patience of a saint, the boundless energy of a puppy and the ability to think fast and shift gears quickly. Few of us ? I'm not one ? have the personality for it long-term.

The good news is that there's been a sea change in our understanding of dementia in the past several years. At the forefront is the Alzheimer's Association, a nonprofit that operates in every state and can provide families with an amazing array of information and resources about dementing illnesses.

Because the disease begins so insidiously, families are the first caregiving foot soldiers. But the burden can be relentless, and some older caregivers actually die prematurely from the stress.

At some point, you may need to turn the responsibility over to others.

What do you look for in a facility that cares for people with dementia? Here are some of the basics:

Good dementia care comes from good leadership, says Patricia Hunter, director of programs and policy for the Alzheimer's Association in Seattle. "The environment isn't as important as the people who are in charge, and every person ? the manager, the aides, the housekeepers and everybody in between, plus the residents ? counts."

How is the staff trained? Although the state mandates basic dementia training, how is that translated into practice? Is each staff committed to the facility's mission and philosophy of care ? or do only the administrator and marketing person know what it is? Just because "memory loss" or "Alzheimer's" is in a facility's name doesn't mean the staff is qualified.

Is there enough staff? There's no minimum staff-to-resident requirement by law, so ask about each facility's practice, then compare the answers. The more demented the residents, the more numerous the staff should be.

How many people are on the night shift and are they awake and available to help?

"One of the characteristics of Alzheimer's is a disturbed sleep/wake pattern. Those with the disease are often awake at night," explains Nora Gibson, executive director of ElderHealth Northwest, which operates two residential-care facilities.

What is staff turnover? "I really like it when I hear that an aide has been with a facility for, say, 10 years," says Hunter, "and that she loves her job."

Is staff assigned to specific residents, or do staff members "float"? Good care requires strong, consistent relationships between caregivers and residents.

What are the facility's discharge criteria? What specific situations trigger a resident being asked to leave? Get specific examples.

How are resident assessments done?

Resident assessments are also critical, says Hunter. What effort does the staff go through to know each resident's "life story" ? children, spiritual beliefs, work experiences, hobbies, current interests? This builds bridges between caregivers and residents, providing clues about what care will be needed.

As you tour, watch to see whether the staff interacts with residents on a personal level. Are they talking to residents or just to each other? Do the residents seem alert and active? Are they moving around freely? Are special features, such as "country kitchens" for use by residents, really used, or are they just decorative?

Can residents go outside? People with dementia lose their ability to tell time. Having access to light and the outdoors helps them retain their natural rhythm ? yet this is often the first thing that gets cut when budgets are tight.

"What's been missing in dementia care is evidence-based design," says John Shoesmith, vice president of Wattenbarger Architects, specialists in designing older adult environments. "What works and doesn't? It wasn't until 1989 that the dementia environment began to be studied."

So now we know, he says, that small settings are good for people with dementia, but choice is even better. If you've seen one person with dementia, you've seen one person with dementia ? meaning there's no single answer. What works depends on each person's background and personality. The more choices there are for activities, programs, privacy, going outside, talking to others, dining, the better.

You also want to look for an environment, he says, that:

? Promotes safety and security. Are hallways cluttered with carts? Is there poor lighting? Confusing hallways?

? Encourages independence. Can the older person continue to take care of his own needs as long as possible?

? Maximizes orientation. Are there easy-to-understand clues that help residents find their way?

For more information about dementia care and dementia-training options for staff, contact the Alzheimer's Association in Seattle at 800-848-7097 or www.alzwa.org.

Liz Taylor's column runs Mondays in the Northwest Life section. A specialist in aging and long-term care for 30 years, she consults with families and their elders. E-mail her at growingolder@seattletimes.com or write to P.O. Box 11601, Bainbridge Island, WA 98110. You can see all of her columns at www.seattletimes.com/growingolder/.

Copyright ? 2006 The Seattle Times Company

1159.Alzheimer's drugs offer modest improvements, equal effectiveness
08/08/2006　http://www.xagena.it/
The Alzheimer's drugs Aricept ( Donepezil ), Razadyne ( Galantamine ) and Exelon ( Rivastigmine ) can lead to small improvements in mental functioning and the ability to carry out everyday activities in people with mild to moderate forms of the disease, according to a review of recent studies.
Although the three drugs work in slightly different ways, the few head-to-head studies of the drugs, found them equally effective, according to review author Jacqueline Birks of the University of Oxford.

The review is published in The Cochrane Library, a publication of The Cochrane Collaboration.

Birks' review included 13 high-quality studies involving 7,298 patients from North America, Europe and Australia. The studies compared the three drugs against placebo treatment, with 2,228 patients in the Aricept studies, 2,267 in the Razadyne studies and 2,803 in the Exelon studies.

The effects of the drugs were not very large when measured across the 13 studies, Birks found. In one measure of how well the drugs worked, for instance, patients across the studies improved by an average of less than three points on a 70-point scale that tracks mental functioning.

" There is nothing to suggest the effects are less for patients with severe dementia, although there is very little evidence for other than mild to moderate dementia," she said.

Side effects caused about 29 percent of the patients taking the drugs to leave the studies, compared with 18 percent dropout among the patients taking a placebo. The most common side effects were nausea, vomiting and diarrhea.

Birks found fewer reported side effects among patients taking Aricept, but she suggests that this may have to do with the way Aricept and the other two drugs are prescribed.

Razadyne and Exelon have a "ramp-up" period in which patients take increasingly higher doses to get to a therapeutic level of treatment. Birks says the two drugs may be as tolerable as Aricept if they are gradually introduced over a course of three months.

In a second review focusing on Aricept only, Birks and researcher Richard Harvey found that a 5 milligram a day dose of the drug was only slightly less effective than a 10 milligram a day dose, with fewer side effects.

In another, newly updated Cochrane review, Clement Loy of Garvan Institute of Medical Research in Australia and colleagues concluded that Razadyne can improve or maintain mental functioning at a 16 milligram a day dose.

The three drugs are from a class of medicines called cholinesterase inhibitors. They boost chemical signaling in a group of brain neurons that are typically destroyed during the course of Alzheimer's disease.

Birks said there is no way to know ahead of time whether the inhibitors will work on a particular Alzheimer's patient, but some researchers recommend starting the treatment as soon as possible after a diagnosis.

George Grossberg, at the Saint Louis University School of Medicine, said there is ample evidence that "the earlier one starts the better" for slowing the progression of the disease.

" In fact, patients who come to drugs later, even as little as six months later, never catch up with those who were on drug from the outset," of their diagnosis, Grossberg said.

Although the review of Aricept showed that the drug can be effective even 52 weeks after the start of treatment, Birks says more long term studies of the medicines are needed.

" As Alzheimer's disease generally progresses slowly and clinical course of five to 10 years is not unusual, clinical trials of six or 12 month duration are of limited use," she noted.

Longer trials could also provide more information on whether these drugs are cost-effective treatments. For the moment, there is only limited data on how these drugs affect the overall cost of care for Alzheimer's patients, Birks found.

Source: Center for the Advancement of Health, 2006

XagenaMedicine2006

Monday, August 07, 2006　http://www.webmd.com/　
1160.Eye Doctors May Someday Screen for Alzheimer's
A simple x-ray can help diagnose a broken arm.
A needle biopsy confirms the presence (or absence) of cancer.
Male-pattern baldness is diagnosed with a glance.

Sadly, one of the biggest challenges regarding Alzheimer's Disease is the inability to definitively diagnose it. Although there are surveys and checklists used to score whether or not an individual's behavior is consistent with Alzheimer's Disease, there is no definitive clinical test that can be applied to living patients. A postmortem brain biopsy is the only surefire way to establish a concrete diagnosis.


A new test developed by researchers at Boston's Brigham and Women's Hospital may be able to detect early dementia using a painless, noninvasive eye test. The test, developed by a team led by Harvard's Dr. Lee Goldstein, uses a laser beam to scan the lens of the eye for deposits of beta-amyloid, a protein found in the brains of those who have Alzheimer's disease.


The lens analysis technique has been successful in a trial using mice: a brief pulse of infrared light into the eyes of four mice with Alzheimer's and four healthy control mice. The laser scan accurately identified which of the animals had the condition. The laser beam detects very earliest stages of amyloid deposits in the lens. Dr Goldstein and his colleagues believe that the test could eventually be used to detect Alzheimer's disease at its earliest stages in humans, and that it may also be able to track disease progression and monitor how people respond to treatments.

Early detection leads to early treatment. Let's hope this device works just as well for humans.

1161.Write Your Care Plan Before You Need It
08/08/2006　http://www.saworship.com/index.php
by Starr Calo-oy

Why should you take the time to plan your care for the golden years? With the growing number of elderly every year, it is imperative to prepare and organize all important paperwork ahead of time so that your exact wishes can be carried out regarding your care, which will also make it easier for your adult children.

"Baby boomers" or "the sandwich generation" ? there are various labels used to describe this demographic group ? and the facts speak for themselves. Census studies by the Administration on Aging, AARP and the National Alzheimer's Association have revealed that in the year 2000 there were 281,421,906 people living in the U.S. Of that number, 45,797,200 were over the age of 65. Within this population, 52% are mentally or physically handicapped and 33.4% are severely disabled.

The most amazing statistic of all is that only 4.1% of our more than 45 million citizens over 65 are currently in nursing homes. This means that a staggering 43 million families are currently wrestling with what to do about finding appropriate care for their parents or are struggling to care for them themselves. This is not a problem that will go away; the numbers of the aged in our population are climbing every year, and it is estimated that by the year 2030, there will be 85 million Americans over the age of 60. We still have a long way to go before we peak.

If we take into consideration the fact that people are living longer (according to the Census Bureau, the average age at death in the year 2000 was 85), we can see that there are millions of Americans between the ages of 38 and 67 who are of necessity making decisions about arranging care for their elderly parents or grandparents.

Many of these caregivers have children of their own and the responsibilities of caring for them, both in the home and on the job; they want to help their parents, but they are simply overwhelmed. All too often, they suffer from a tremendous burden of guilt that keeps them from making important and sound decisions about their parents' care until it is too late ? and their own health, careers or marriages are sacrificed in the meantime.

Now that you know why and you feel convicted, let's talk about how to do it. The following is a check-list to help you make your wishes known and to organize all vital paperwork to keep in one place:

1) Go to an office supply store, like Mailboxes, Etc. or your local post office and purchase a Living Will packet and fill it out according to the instructions. You can spend much more money if you prefer to enlist the help of your attorney, but it's really not necessary because the forms are very user friendly. Make a copy for your Power of Attorney and your attorney and get it to them. Make a folder marked "Living Will" and place the document in it.

2) If you have decided to invoke a DNR (Do Not Resuscitate) order and not enlist the aid of any artificial methods of keeping you alive such as a breathing machine, etc., you can pick up the legal document at the places listed above. Follow the instructions, fill in the blanks, mark a folder "DNR" and place it inside.

3) In the event you become mentally or physically disabled and if you have sufficient finances available for private care, decide if you want to be cared for in your own home by a private nurse or agency, in a residential care home or specific nursing home. Write down your wishes and contact information if applicable and place the sheet in this folder. Make sure your POA and/or attorney has a copy of it and that you have expressed your wishes to all of your family members to avoid future conflict in the event that you are no longer able to verbalize your choices.

4) Make a folder marked "Family Attorney," if you have one, and write down his contact information on it and place the page in this folder. (Make sure all information in the folders are legible; print clearly or type the information.)

5) Make a folder for your financial planner or accountant, if you have one, with contact information.

6) Do the same for your power of attorney. If you don't have a POA designated, pray and ask the Lord to direct you to one. It can be one of your adult children that you trust implicitly, a trusted friend in good health or another family member that you believe will carry out your wishes if you become incapacitated. Make sure your family attorney understands the type of POA you need to carry out your wishes regarding your care and your personal finances and belongings and that your POA needs to have access to all of your holdings for your future care. The POA expires at the time of your death. You need to have the POA notarized in the presence of two witnesses who do not have any interest in your affairs. The attorney will go into more detail regarding the rules.

7) You need to make a folder marked "Bank Accounts." Designate a sheet for each bank account you have with all contact information, passwords, balances, account numbers and the person's name that you primarily deal with. Update these as needed.

8) If you have a current will, make a folder marked "My Current Will" and place a copy of it in the folder. If you want to update it, call your attorney and make an appointment to talk to him and get it done. Place another copy of the will with your POA and in your safe deposit box, if you have one, but be sure to mention this on another piece of paper to include inside the folder.

9) If you are married, place your marriage certificate in a folder so named. Your spouse will need this if you pass away first so he/she can file for benefits.

10) Place your current health, life and funeral insurance policies in folders so named. If you have been dealing with a particular agent, write the name and all contact information on a sheet of paper and place it in the folder.

11) If you have funeral arrangements made with a specific funeral home make a folder and place all paperwork relating to it inside along with contact information.

12) Make a list of all of your current credit cards and the passwords and balances on each and place the list in a folder marked "Credit Card Information Sheet."

13) If you own any property, write the details down and place the sheet in a folder marked "Property."

14) If you have a pension or retirement plan with any of your former employers, write down who are they and how they can be contacted and make a folder marked "Retirement Plan" and place the paper in this folder.

15) If you have any CD's or IRA's, write down who you have them with and any specific account numbers and passwords if applicable.

16) Make a list all of your assets and debts and place them in a folder marked appropriately.

Place all of the folders in a plastic, portable file box for future reference. This file box will contain your very life so you must make sure it's kept in a safe place. The attic is a great place if you have one and can get up there!

This will take time to gather but you and/or your family, POA and attorney must have the information at any given time so get it done. Don't put it off.

If you are doing this for a loved one and he has dementia or cannot communicate with you for this information, you need to initiate a search of his home and/or office. Enlist the help and legwork of your family. You may need to divide up the list among several people. Call a family meeting with a few of the more organized and diligent members. Schedule the next meeting with them (have them bring their weekly planners or calendars with them) before they leave. Tell them that you will all report on your findings at the next meeting.

This may sound like a lot of unnecessary work but if you've never been through it, you have no idea how important it is to get it done right. If you have been through it and not been this organized, then you will appreciate our attention to the small details.

The Word of God says it so perfectly: "Commit your works to the Lord, and your thoughts will be established" (Proverbs 16:2-4).

1162.Evotec's Alzheimer's drug OK in phase 1
HAMBURG, Germany, Aug. 8 (UPI) -- U.S. firm Evotec said Tuesday EVT 101, a potential treatment for Alzheimer's disease, looked promising in a phase 1 trial.

"In all subjects EVT 101 was well absorbed, achieved good exposure levels, and was very well tolerated with no significant adverse events," Evotec said in a statement.

The trial involved 90 healthy subjects who received single and multiple ascending doses of EVT 101.

The compound, which is an NR2B subtype-specific NMDA receptor antagonist, also appeared to have a good pharmacokinetic profile, achieving an eleven-hour half-life.

"The good tolerability of EVT 101 is significant given the unfavorable side-effect profile of non-selective NMDA antagonists," Evotec said.

1163.Multiple Newly Published U.S. and European Peer-Review Studies Support Statin Drug Potential Therapeutic Use in Alzheimer's Disease; Nymox Has Global Patent Rights for Statin Drugs for the Treatment and Prevention of Alzheimer's Disease
HASBROUCK HEIGHTS, N.J., August 8 /CNW/ - Nymox Pharmaceutical
Corporation (NASDAQ: NYMX) holds U.S. and global patent rights for the use of
statin drugs for the prevention and treatment of Alzheimer's disease (AD),
including for patients at risk for AD because of vascular-related risk factors
or disease. Three newly published peer-review studies from the Karolinska
Institute in Sweden and the Sun Health Research Institute in Arizona have
provided new clinical trial and research data supporting statin use for
Alzheimer's and elucidating how the statin drugs are believed to produce these
beneficial effects on the brain. In addition, a widely circulated report in
yesterday's Washington Times (August 7, 2006) quotes experts referring to the
promise of statin drugs for Alzheimer's patients.
Statins are a class of cholesterol-lowering drugs that are the
biggest-selling prescription pills in pharmaceutical history with estimated
2004 global sales of $26 billion. Alzheimer's disease is the leading cause of
dementia in the elderly, afflicting an estimated 4.5 million people in the
U.S.
A review of epidemiological studies from the Karolinska Institute in
Stockholm concluded that influencing the serum lipid profile may reduce
dementia risk (Acta Neurol Scand 2006; 185: 50-57). A double-blind
placebo-controlled randomized trial of 1 year exposure of atorvastatin from
the Sun Health Research Institute demonstrated a statistically significant
improvement in cognition and memory among patients with mild to moderate
Alzheimer's after 6 months of treatment, which persisted for one year (Acta
Neurol Scand 2006; 185: 78-86). A further new report from the Karolinska
Institute reviewed the relevance of statins to the regulation of dementia
pathogenesis, suggesting that statins may confer multiple effects due to the
production of mevalonate pathway intermediates (Acta Neurol Scand 2006; 185:
115-118).
The potential for statin drugs to treat or reduce the risk of Alzheimer's
disease (AD) has also been bolstered by several other recently published
studies and reviews in leading medical and scientific journals. One study
followed 3,334 people over the age of 65 for an average of seven years and
found that regular statin use was associated with a rate of deterioration less
than half of that of untreated patients (Neurology 2005; 65:1388-1394). A
second three year study of 342 AD patients found evidence that statins slowed
the progression of AD (J. Neurol. Neurosurg. Psychiatry 2005; 76:1624-1629).
Recent expert articles reviewing the clinical and scientific evidence in the
field have also highlighted the potential of statin drugs for the treatment or
prevention of AD: J.Neurochem. 2006; 97:716-723; Restor. Neurol. Neurosci
2006; 24:79-95; Neuromolecular Med. 2006; 8:319-328; The American Journal of
Medicine 2005; 118: 48S-53S; The Lancet Neurology 2005; 4:841-852; Current
Opinions in Lipidology 2005;16: 619-623; The Lancet Neurology 2005; 4: 521-2.
The potential use of statins to treat Alzheimer's disease (AD) has been
widely reported in the peer-reviewed medical literature, both in terms of
clinical data, (such as Arch Neurol (2005; 62:1047-51); Neurology (2005;
64:1531-8); Arch Neurol (2005; 62:753-7); J Neurol Sci (2005; 229-230:147-50);
Arch Gen Psychiatry (2005; 62:217-24)) and possible mechanisms through which
statins may prevent or slow the progression of Alzheimer's disease (such as J
Neurosci Res (2005; 82:10-19); J Biol Chem (2005; M505268200); PLoS Med (2005;
2:e18); J Neurosci (2005; 25:299-307)).
More information about Nymox is available at www.nymox.com, email:
info@nymox.com, or 800-936-9669.
This press release contains certain "forward-looking statements" as
defined in the United States Private Securities Litigation Reform Act of 1995
that involve a number of risks and uncertainties. There can be no assurance
that such statements will prove to be accurate and the actual results and
future events could differ materially from management's current expectations.
The conduct of clinical trials and the development of drug products involve
substantial risks and uncertainties and actual results may differ materially
from expectations. Promising early results do not ensure that later stage or
larger scale clinical trials will be successful or will proceed as expected.
Such factors are detailed from time to time in Nymox's filings with the United
States Securities and Exchange Commission and other regulatory authorities.

For further information: Nymox Pharmaceutical Corporation Roy Wolvin,
1-800-93NYMOX www.nymox.com

1164.Professor explores Alzheimer's causes
Deborah Halber, News Office Correspondent
August 8, 2006　MIT

Some people live to be 100 without falling victim to Alzheimer's disease. Li-Huei Tsai, who joined MIT this spring as Picower Professor of Neuroscience, wants to know why.

Amyloid beta or Abeta (a protein fragment that accumulates in the brains of Alzheimer's patients) is a telltale sign of the disease, which affects 4 million Americans, most over age 65. Normally, the body manages to break down and eliminate these fragments, but in the aging brain, they tend to form insoluble plaques.

To add to the mystery, some people function relatively normally with plaques nestled among their neurons, while others are virtually incapacitated. "There are people with a significant plaque load who can keep up with their daily lives," said Tsai, who has appointments in the Department of Brain and Cognitive Sciences and at the Picower Institute for Learning and Memory. "Obviously, other factors are determining whether they have full-blown Alzheimer's."

Tsai, who as a child in Taipei witnessed her beloved grandmother's descent into dementia, is determined to unravel the thorny questions associated with neurodegenerative and psychiatric disorders.

Tsai uses a combination of molecular, cellular and biochemical approaches to study Alzheimer's disease and psychiatric and developmental disorders. She focuses on a kinase (kinases are enzymes that change proteins) called Cdk5. Cdk5, paired with the protein p35, helps new neurons form and migrate to their correct positions during brain development. But Cdk5, paired with an aberrant form of p35 called p25, also is implicated in age-related neurodegenerative diseases.

Psychiatric diseases such as schizophrenia and the neurodegenerative diseases of old age are as devastating as they are elusive. Their very intractability is one of the things that attracted Tsai to the field 10 years ago when she abruptly switched from cancer research to neuroscience.

"There are still a lot of unknowns," Tsai said. "I think causes for psychiatric disorders are still very much unclear."

And getting fuzzier. There is no definitive diagnosis for Alzheimer's, and as more sophisticated cognitive tests are developed, the line between whether or not memory loss and personality changes are tied to Alzheimer's becomes more and more blurred.

For the 5 percent of the population with an inherited tendency toward Alzheimer's, genes are the culprit. But for the 95 percent of the aging population in which the disease arises spontaneously, the role of Abeta plaques becomes murkier.

Tsai, along with many other researchers, is eagerly awaiting the results of anti-amyloid studies in humans. A handful of therapies -- based on antibodies, enzymes or preventing plaques from aggregating into characteristic Alzheimer's clumps -- seem to be effective in animal models. "The question is, if you get rid of the plaques, will you prevent Alzheimer's?" Tsai said.

Major pharmaceutical companies are betting heavily that the answer is yes. They all have therapeutics in the pipeline based on one or more of the anti-plaque approaches. But Tsai wonders if eliminating plaques is sufficient to prevent or cure the majority of Alzheimer's cases.

Tsai's laboratory has developed an innovative mouse model that exhibits the onset of Alzheimer's symptoms in a fraction of the time previously possible. She uses this and other techniques to zero in on the trigger of the cascade of events that leads to Alzheimer's.

Tsai believes that a combination of genetic and environmental factors involving a variety of biological systems ultimately underlies Alzheimer's. Treatment, she predicts, will likely be a cocktail of drugs such as the ones used for AIDS and some cancers. Tsai hopes such a treatment based on the fundamental knowledge spawned by her lab will emerge in the not-too-distant future.

1165.Reduced brain volume may predict dementia in elderly people
08/09/2006　XagenaMedicine2006

Reduced volume, or atrophy, in parts of the brain known as the amygdala and hippocampus may predict which cognitively healthy elderly people will develop dementia over a six-year period.

New strategies may be able to prevent or delay the onset of Alzheimer's disease, the most common cause of dementia among older adults.

Accurate methods of identifying which people are at high risk for dementia in old age would help physicians determine who could benefit from these interventions.

There is evidence that adults with Alzheimer's disease and mild cognitive impairment, a less severe condition that is considered a risk factor for Alzheimer's disease, have reduced hippocampal and amygdalar volumes.
However, previous research has not addressed whether measuring atrophy using magnetic resonance imaging ( MRI ) can predict the onset of Alzheimer's disease at an earlier stage, before cognitive symptoms appear.

Tom den Heijer, of the Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues used MRI to assess the brain volumes of 511 dementia-free elderly people who were part of the Rotterdam Study, a large population-based cohort study that began in 1990.
They screened the participants for dementia at initial visits in 1995 and 1996 and then in follow-up visits between 1997 and 2003, during which they asked about memory problems and performed extensive neuropsychological testing.
The authors also monitored the medical records of all participants.

During the follow-up, 35 participants developed dementia and 26 were diagnosed with Alzheimer's disease.

People with severe amygdalar or hippocampal atrophy had the highest risk of developing dementia or Alzheimer's disease over the course of the study, which followed participants for an average period of six years. " Concerning the extent of atrophy, we found in those destined to develop dementia volume reductions between 17 percent and 5 percent, depending on how long before the diagnosis of dementia the MRI was conducted," the authors report. " In persons with mild to moderate Alzheimer disease, volume reductions compared with healthy elderly persons are between 25 percent and 40 percent, suggesting that atrophy rates accelerate in patients with Alzheimer disease."

" Our study suggests that structural brain imaging can help identify people at high risk for developing dementia, even before they have any memory complaints or measurable cognitive impairment," they write. " However, we must bear in mind that most people with atrophy did not develop dementia, even after six years. Further prospective population studies are therefore required to find additional biomarkers, including other brain imaging parameters, that alone or in combination with clinical and genetic characteristics can help separate those who are at risk for developing dementia from those who are not."

Source: Archives of General Psychiatry, 2006

XagenaMedicine2006

1166.Who should take the car keys away from Alzheimer's patients?

By Diane C. Lade
South Florida Sun-Sentinel
Posted August 9 2006

A doctor told Marilyn Pennachio that her father's increasingly bizarre behavior was due to Alzheimer's disease, and then prescribed a medication to ease the symptoms. He suggested her father shouldn't live alone in his Lauderdale Lakes apartment any more, and shouldn't drive.

But Pennachio said she needed more out of that office visit -- more on living day-to-day with an incurable disease that only would get worse. And she said she needed more specifics about what to do if her father refused to give up the car keys, especially since the elderly man told the doctor that he had no intention of doing so.

"They evaluate you, they send you away, but then what does the caregiver do?" said Pennachio. "I wanted to say, `So how can I stop this man from driving, doctor? This is my loved one, my father, and I am taking on all this responsibility.'"

One group of medical professionals agrees that it's time for doctors and other health professionals to take a more active role in helping dementia patients and their families cope. The American Association for Geriatric Psychiatry recently released a checklist that, for the first time, outlines nonmedical but critical things practitioners should discuss with their patients and families.

At the top are safety issues, including whether a patient should continue driving -- an emotional topic doctors often are loath to broach.

Kathy Townley, of Boynton Beach, agreed that doctors should be the ones to tell Alzheimer's patients when to give up the keys.

"Doctors have more clout than we do," said Townley, who took a caregiver education class at North Broward Medical Center.

She has an elderly relative with Alzheimer's who refused his family's pleas to stop driving, despite three near accidents. Yet while he was angry when his doctor told him the same thing, Townley said he then agreed to stay off the roads.

"[Doctors] need to be proactive in terms of telling people how to deal with issues on a practical basis," she said.

In addition to recommending that doctors address concerns about driving, the association's checklist urges physicians to help caregivers deal with stress, plan for assisted living or nursing home care, and encourage patients to stay active and healthy for as long as possible.

"When it comes to this whole issue of the doctor-patient relationship ... we need to improve our ability to be empathetic listeners," said Dr. Christopher Colenda, association president and dean of the College of Medicine at Texas A&M University. "We need to be able to say the right thing at the right time in the right manner."

The checklist recommendations, more than a year in the making, are separate from the physician guidelines for testing, diagnosis and treatment. The checklist could be used by any doctor or health professional -- not just psychiatrists -- who regularly deals with Alzheimer's patients, Colenda said.

Physicians are bracing for an explosion in Alzheimer's cases during the next decade, as Baby Boomers retire. The chances of developing the disorder increase with age, with some studies suggesting one of two people over age 85 are at risk.

"We don't have a cure, and we're a long ways from one," said Dr. Marc Agronin, a geriatric psychiatrist who directs the Memory Center at the Miami Jewish Home and Hospital for the Aged. "We've been focused on screening and behavioral issues. We have to be equally focused on lifestyle and safety issues."

The stop-driving talk remains a stumbling block for most doctors, even though they're often best qualified to judge driving ability and whose opinions the patients are most likely to respect.

A recent survey of more then 3,800 midlife and older adults by The Hartford insurance company and the Massachusetts Institute of Technology found 92 percent thought their doctor was the one who should tell them if they should hang up the keys.

The American Medical Association also has been advocating more involvement by doctors in their patients' decisions about driving. Three years ago, the AMA drafted a guide on driving cessation and next year an AMA-trained team will make appearances at Florida medical conventions to encourage physicians to use it.

Florida is one of six states where physician reports to licensing bureaus are confidential and one of 30 states where physicians are immune from legal action by their patients in such cases, according to the American Association of Motor Vehicle Administrators.

Three states -- California, Nevada and Pennsylvania -- have laws holding physicians responsible if they do not report specific medical conditions and one of their patients later causes a crash. The California law is the only one specifically mentioning Alzheimer's disease.

Drivers age 80 and older in Florida must take a visual exam to renew their licenses, but no driving tests are tied to cognitive ability. A license is automatically suspended only when a driver racks up 12 points in a 12-month period, with points given for traffic tickets or accidents. Police, physicians, judges and the general public, however, can report at-risk drivers to the licensing bureau's Medical Review Board, which decides if a retest is necessary. The state has rescinded about 30,000 licenses for medical reasons.

The Memory and Wellness Center at Florida Atlantic University in Boca Raton has one of the few South Florida programs to evaluate older drivers through computer and road tests. Program Director Denise Sparks is seeing more referrals from neurologists and hopes the care guidelines will encourage other doctors to deal with driving.

The fact that Medicare and most private insurance does not cover the $275 test battery keeps some away. "A lot of rehabilitation centers don't do driving evaluations because it's not profitable," said Sparks.

8/9/2006CommunityHEALTH AND FITNESS
1167.Too much weight ups your Alzheimer's risk
By Gregg Schwartz
http://www.toledofreepress.com/
People who are overweight or obese in their 40s have a greater risk of developing Alzheimer's disease later in life, a new study suggests.

“The implication is that keeping a healthy weight in middle age is linked to good outcomes in old age,” said study author Rachel A. Whitmer, a research scientist at Kaiser Permanente of Northern California.

Whitmer and other researchers are finding increasing evidence that Alzheimer's and other forms of dementia are often linked to physical, and sometimes preventable, causes.

“There has been a whole bunch of recent evidence that being overweight is bad for the brain,” she said.

Even when compensating for common health problems that can contribute to Alzheimer's, such as diabetes and cardiovascular disease, fat itself seemed to play a surprisingly important role in the development of the brain disease, Whitmer said.

The new findings were to be presented recently at the American Academy of Neurology annual meeting in San Diego.

Whitmer's research is part of a larger study, started in 1964, that followed nearly 9,000 Kaiser Permanente patients for up to 30 years. The participants were evaluated by measuring the thickness of skin folds both below the shoulder and at the back of the upper arm.

Those with the thickest shoulder measurements were nearly three times as likely to develop Alzheimer's disease as those in the lowest group. For arm measurements, those in the highest group were two and a half times as likely to develop the disease.

Whitmer said future studies are needed to examine the molecular mechanisms that seem to link obesity and Alzheimer's disease.

Maria Carrillo, director of medical and scientific relations for the Alzheimer's Association, said the findings aren't surprising.

She suggested that overweight people aren't as physically fit, so arteries can get clogged and restrict blood flow. And, she added, overweight people are probably not eating right. “Studies have shown that healthy eating can contribute to brain health,” Carrillo said.

Alzheimer's disease is at epidemic proportions, Carrillo said, with 4.5 million Americans diagnosed. As the population ages and people live longer, that number is expected to reach 16 million by 2050.

Gregg Schwartz is a personal trainer at Wildwood Athletic Club, 2865 N. Reynolds Road.

1168.Alzheimer's disease: two forms of mild cognitive impairment identified
10/08/2006　XagenaMedicine2006

Mild cognitive impairment ( MCI ), a transitional stage between normal cognition and Alzheimer's disease, exists in two different forms.

Using a new imaging procedure that creates 3-D maps of the brain, researchers at the University of Pittsburgh School of Medicine and the University of California, Los Angeles ( UCLA ) determined specific areas that had degenerated in people with MCI.
Depending on the person's symptoms, more tissue was lost in the hippocampus, a brain area critical for memory and one of the earliest to change in Alzheimer's disease, indicating two different paths of progression to Alzheimer's disease.
The finding could lead to better diagnosis and treatment of patients with MCI, perhaps delaying or preventing the onset of dementia.

Mild cognitive impairment is categorized into two sub-types, currently distinguished based solely on symptoms.
Those with MCI, amnesic subtype ( MCI-A ) have memory impairments only, while those with mild cognitive impairment, multiple cognitive domain subtype ( MCI-MCD ) have other types of mild impairments, such as in judgment or language, but also have either mild or no memory loss. Both sub-types progress to Alzheimer's disease at the same rate.
Until now it was not known if the pathologies of the two types of MCI were different, or if MCI-MCD was just a more advanced form of MCI-A.

Researchers found that the hippocampus of the patients with MCI-A was 14 percent smaller than that of the healthy subjects, nearly as great as the 23 percent shrinkage seen in Alzheimer's disease. But, the hippocampus of those with MCI-MCD most resembled that of the controls, showing only 5 percent shrinkage.

Using highly accurate Magnetic Resonance Imaging ( MRI ) data from six patients with MCI-A, 20 with MCI-MCD and 20 with Alzheimer's disease who were seen at the University of Pittsburgh's Alzheimer Disease Research Center and 20 healthy controls, researchers created 3-D mesh reconstructions of each participant's hippocampus that allowed them to see where the hippocampus had deteriorated.
This study is the first to use such modeling technology to visualize changes in the brains of people with MCI. Prior studies have only been able to measure the volume of the hippocampus and estimate atrophy through noticeable volume loss.

" These vibrant images produced by 3-D modeling have proven what we suspected ? there are at least two transitional states that lead to Alzheimer's disease," said James T. Becker, at the University of Pittsburgh School of Medicine and lead author of the study. " Now we can investigate these pathways and develop treatments that, we hope, may slow or stop the progression of Alzheimer's."

Alzheimer's disease affects as many as 10 percent of people older than 65, and delaying or preventing the onset of dementia is an important medical priority. "We can now see the pattern of brain damage in people with MCI and we can use these new types of images to monitor how different therapies may be working," said Paul M. Thompson, at the University of California, Los Angeles. " By imaging the brain like this, we can explore the progression of diseases, and see if therapies are protecting the brain."

The study is published in the Archives of Neurology.

Source: University of Pittsburgh Medical Center, 2006

Source: American Association of Naturopathic Physicians (AANP)
Released: Wed 09-Aug-2006, 09:45 ET

1169.A “Leaky” Blood-Brain Barrier and Alzheimer’s

Medical News Keywords
ALZHEIMER'S DISEASE; BLOOD-BRAIN BARRIER (BBB); NATUROPATHIC PHYSICIAN
Contact Information

Available for logged-in reporters only
Description

While no one knows the precise underlying cause leading to Alzheimer’s disease, a new study finds that a “leaky” blood-brain barrier (BBB) ? and levels of water-soluble antioxidants ? may offer clues to unlocking this haunting disease.

Newswise ? Alzheimer’s disease (AD) affects 4.5 million Americans according to the National Institutes of Aging; the direct and indirect costs of the disease exceed $100 billion each year. As the wave of baby boomers continues to age it is apparent that the number of people with AD will increase, along with the costs for care. While no one knows the precise underlying cause leading to the characteristic pathology of the disease, a new study finds that a “leaky” blood-brain barrier (BBB) ? and levels of water-soluble antioxidants ? may offer clues to unlocking this haunting disease.

The Study
The study was led by Gene Bowman, ND, of the Oregon Center for Complementary and Alternative Medicine in Neurological Disorders at Oregon Health & Science University, Portland, OR. Co-investigators were Joseph Quinn, MD, Jeffrey Kaye, MD, Milar Moore, BS, and Dana Waichunas, BS, all of the Layton Aging and Alzheimer’s Disease Center, Portland, OR; and Balz Frei, Ph.D., of the Linus Pauling Institute of Oregon State University, Corvallis, OR.

The study was supported by NIH-T32 Kirschstein Award, United States Public Health Service grants AG16835, AG05144, AG08017, RR00334, the United States Department of Veterans Affairs, and The Dana Foundation.

Although the manuscript describing the findings is under development, conclusive findings will be presented by the lead author at the 21st Annual Meeting of the American Association of Naturopathic Physicians (AANP) (http://www.Naturopathic.org), being held August 9-12, 2006 at the Oregon Convention Center, Portland, OR.

Methodology
Thirty-six participants (mean age 70 + 7 years) diagnosed with mild to moderate Alzheimer’s disease (Mini-Mental Status Exam 19+5) participated in a prospective biomarker study. The evaluation of the participants included clinical assessments, brain imaging, and cerebral spinal fluid (CSF) along with plasma collection for a period of one year. The participants were evaluated at baseline, three months and 12 months. The researchers employed the CSF-albumin index to determine blood-brain barrier integrity. CSF and plasma levels of ascorbic acid (AA) and uric acid (UA) were also measured.

Results
The researchers observed the following:

§ As expected, the concentration of AA was higher in the CSF compared to the plasma reflected by a CSF-to-plasma ratio of AA greater than 1.0 in all cases, with an average of 4.0. In contrast, the concentration of UA in the CSF was lower than plasma reflected by a CSF-to-plasma ratio of UA was less than 0.25 in all subjects.

§ The mean CSF-albumin index was 7.2. However, in 22% of the study participants, the CSF-albumin index was greater than 9.0, indicating blood-brain barrier disruption.

§ There were no correlations appreciated between plasma AA and age, gender, APOE status, MMSE at baseline or rates of clinical decline at 12 months. However, a positive correlation did exist between plasma AA and hippocampus volume at baseline and at 12 months. Study participants in the upper 25% of plasma AA at baseline showed the least temporal-lobe volume rate of decline at 12 months.

§ CSF-to-plasma AA ratio inversely correlated with hippocampus volume rate of decline and temporal-lobe volume rate of decline at 12 months. An inverse correlation between CSF-to-plasma AA ratio and CSF-albumin index, and a positive correlation between the CSF-to-plasma UA ratio and the CSF albumin index was significant.

Conclusion
Blood-brain barrier integrity is generally thought to be perturbed in cerebrovascular disease, but preserved in AD. Although BBB impairment is not thought to be a primary mechanism of disease it may be an important modifier of treatment and outcome.

The study found BBB impairment in a significant minority of subjects with AD. Furthermore, BBB disruption may be clinically significant by allowing antioxidants to “diffuse down” their respective concentration gradient facilitating unabated oxidative processes in the brain that underlie AD pathology. The relationship between this phenomenon, BBB impairment and maintenance, and the neurodegenerative process remains to be clarified.

The American Association of Naturopathic Physicians (AANP) was founded in 1985 to provide alternative methods for healing human diseases and disorders than have been traditionally offered in the United States. Members of the AANP must have graduated from one of North America’s six accredited graduate schools of naturopathic medicine.

For more information about naturopathic physicians, log on to http://www.naturopathic.org/

1170.Tests may predict progression to Alzheimer's
Thu Aug 10, 2006 6:15 PM BST
By Will Boggs, MD

NEW YORK (Reuters Health) - Deficits in certain neurological and psychological areas strongly predict conversion to Alzheimer's disease (AD) in individuals with mild cognitive impairment, research shows.

"The use of specific neuropsychological tests are useful for making an early diagnosis of AD and will most likely play an important role in determining which patients in the pre-clinical/pre-symptomatic stages of the disease will receive the most benefit from drug therapies aimed at modifying the course of incipient AD," Dr. Matthias H. Tabert told Reuters Health.

Tabert and colleagues from Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, classified a group of patients according to the type of mild cognitive impairment present and examined whether baseline neuropsychological measures were predictive of conversion to AD.

The authors observed that patients who converted to AD scored lower than nonconverters on all measures of memory and so-called "executive function" abilities (i.e., overall reasoning and functioning).

The two groups differed on some tests of "visuospatial ability" -- the type of skills that give you an accurate mental picture of where you are going when you drive a car, for example.

They also differed on some tests of language, but not on tests of attention.

Within 3 years, 50 percent of the patients with "multiple-domain" deficits and memory deficits converted to AD, the researchers note, compared with only 10 percent of patients with single-domain amnesic mild cognitive impairment.

The final predictive model was 86 percent accurate in predicting the conversion to AD, the investigators say.

"Our findings strongly support the use of physician referral for detailed cognitive testing of verbal memory and executive function in patients with mild cognitive impairment," Tabert said.

SOURCE: Archives of General Psychiatry August 2006.

Thursday, August 10, 2006 ?http://seattlepi.nwsource.com/

1171.Scientists make discovery in Alzheimer's

By LAURAN NEERGAARD
AP MEDICAL WRITER

WASHINGTON -- Scientists have discovered molecular janitors that clear away a sticky gunk blamed for Alzheimer's disease - until they get old and quit sweeping up.

The finding helps explain why Alzheimer's is a disease of aging. More importantly, it suggests a new weapon: drugs that give nature's cleanup crews a boost.

"It's a whole new way of thinking in the Alzheimer's field," said Dr. Andrew Dillin, a biologist at California's Salk Institute for Biological Studies who led the new research.

The discovery, published Thursday by the journal Science, was made in a tiny roundworm called C. elegans.

What do worms have to do with people? They're commonly used in age-related genetics research, and the new work involves a collection of genes that people harbor, too. Dillin's team from Salk and the neighboring Scripps Research Institute already is on the trail of potential drug candidates.

About 4.5 million Americans have Alzheimer's, a toll expected to more than triple by 2050 as the population grays. The creeping brain disease gradually robs sufferers of their memories and ability to care for themselves, eventually killing them. There is no known cure; today's drugs only temporarily alleviate symptoms.

Nor does anyone know what causes Alzheimer's. The lead suspect is a gooey protein called beta-amyloid. All brains contain it, although healthy cells somehow get rid of excess amounts. But beta-amyloid builds up in Alzheimer's patients, both inside their brain cells and forming clumps that coat the cells - plaque that is the disease's hallmark.

Thursday's study reveals one way that cells fend off amyloid buildup, and that natural aging gradually erodes that detoxification process.

"Every pathway we can discover that modifies amyloid provides us with new drug targets," said Dr. Sam Gandy, a neuroscientist at Philadelphia's Thomas Jefferson University and an Alzheimer's Association spokesman. "This now opens up a new pathway" for developing anti-Alzheimer's drugs.

Worms can't get Alzheimer's. So Dillin's team used roundworms that produce human beta-amyloid in the muscles of the body wall. As the worms age, amyloid builds up until it eventually paralyzes them; they can wiggle only their heads.

Then the researchers altered genes in a pathway called insulin/IGF-1, long known to be key in controlling lifespan. Making the worms live longer protected them from paralysis.

So in slowing down normal aging, something also slowed the buildup of toxic amyloid. But what?

Enter those cellular janitors, two proteins in that gene pathway.

One, named HSF-1, breaks apart amyloid and disposes of it, the researchers discovered. Natural aging slows HSF-1, so it can't keep up with the necessary detoxification.

Another protein called DAF-16 jumps in to help buy a little more time, by clumping extra amyloid together in a way that makes it less toxic.

That was a key finding, Dillin said: Until recently, scientists thought amyloid clumps, or plaques, were the bigger problem. His research supports more recent findings that smaller amyloid tendrils inside cells are the really poisonous form.

"We think probably the HSF-1 is the preferred way" to dispose of amyloid, Dillin said. "By the time you see the plaques, it's too late."

Mammals, including people, have these same proteins. Dillin now is repeating his experiment in mice to be sure they work the same way.

Scientists already are creating drugs to try to rid the brain of amyloid. These cleanup proteins point to a novel way to do that. The hope: Create drugs that boost their effects, and amyloid might not build up in the first place. Dillin said some initial drug attempts are showing promise in his worms.

The proteins won't be the brain's only natural amyloid scrubbers, noted Gandy, whose own research points toward involvement of another age-related gene.

The study is key for an additional reason, he added.

"We all knew that aging increases the risk for Alzheimer's," but not why, Gandy explained. "Now there's a direct link. ... It gives the molecular connection between aging and Alzheimer's."

And this process of "toxic aging" likely plays a role in still other neurodegenerative diseases, Dillin said, citing similar research with Huntington's disease.

1172.Books, blog help doctor cope with Alzheimer's

By Linda McIntosh
UNION-TRIBUNE COMMUNITY NEWS WRITER
August 10, 2006
http://www.signonsandiego.com/
CARLSBAD ? Don Hayen spent his life as a doctor, first in the Navy and later in private practice as a dermatologist in the Tri-City area.

But he always considered himself a storyteller at heart.

Hayen used to tell stories to his grandchildren on car trips. The tales were from his childhood growing up in a small Kansas town during the 1940s.

One of his favorites was about the time he and some high school buddies took a case of gin from a bootlegger's garage and buried it in a ditch as a lark.

Although national Prohibition was repealed in 1933, Kansas state laws were not changed until 1948.

Hayen ended up in the sheriff's office with his father.

The story turned into Hayen's first novel, published earlier this year, called “Moonshine Harvest.”
The 72-year-old Carlsbad resident finished the book about the time he found out he was in the early stages of Alzheimer's disease.

But that's not keeping him from writing a sequel, due out next year.

“Moonshine Harvest” centers on a 15-year-old boy who finds the town drunk hanging from a railroad bridge and suspects the sheriff and a local bootlegger are involved.

Hayen has gotten calls from people in his hometown of Marion, Kan., asking who the characters are.

The book, published by BookSurge, won the Editor's Choice Award at the 2005 San Diego State University Writer's Conference and was nominated as a finalist in the Unpublished Young Adult Competition of the 2005 San Diego Book Awards.

“I wanted to tell a good story and bring back what it was like living in a world so different from now,” Hayen said.

Hayen talks about going hunting and fishing, wandering the countryside and learning by trial and error under the guidance of parents who grew up on the frontier.

“There's value in young people looking back in history and seeing what people went through. It helps them understand the way older people think,” he said.

The sequel follows the boy in the first book during a major flood in Kansas in the early 1950s.

Hayen plans to keep writing and remembering as long as he can.

“The process of writing is like inventing,” he said.

As a doctor, Hayen twice won the Physician's Writer Contest for Medical Economics magazine. But his fiction is a different kind of writing that he feels will help him cope with Alzheimer's.

Hayen is set on helping others with Alzheimer's and writes a blog he calls “The Trip Over, A Journal Through Early Alzheimer's” at www.thetripover.com.

“It's a way for us to help each other,” Hayen said.

Hayen encourages others to tell their stories as he has done in his book.

“When you write, you feel like you're a whole different person. It's like you're in the story and it tells itself,” he said.

Hayen's wife, Jane, has heard her husband's stories at family reunions during their 50 years together and always wanted him to put them down on paper.

“It's good for him. He's always thinking of what might be in his next story,” she said.

In his dedication to “Moonshine Harvest,” Hayden called it a “legacy to his grandchildren ... who begged for just one more story.”

For information about the book, go online to www.moonshineharvest.com.

1173.Microglia, a natural defence mechanism for Alzheimer's disease
12/08/2006　XagenaMedicine2006

Researchers at Universit? Laval and the research centre at CHUQ ( Centre Hospitalier Universitaire de Qu?bec ) has discovered a natural defence mechanism that the body deploys to combat nerve cell degeneration observed in persons with Alzheimer's disease.

Investigators Alain R. Simard, Denis Soulet, Genevieve Gowing, Jean-Pierre Julien and Serge Rivest describe this major discovery in the journal Neuron.

Alzheimer's disease is characterized by the accumulation of amyloid proteins in the brain. These proteins form plaques around which microglia, the central nervous system's immune cells, aggregate. These microglia appear to be incapable of eliminating the plaques, and this has led some researchers to postulate that microglial action produces an inflammation causing neuronal death. The fact that Alzheimer's patients are prescribed anti-inflammatory drugs results from this concept of the disease.

For Serge Rivest and his team have observed that, although the brain's resident microglia do appear to be poorly equipped for combating amyloid plaques, an entirely different case prevails for another type of microglia: those derived from bone marrow stem cells.

Using tests conducted with transgenic mouse models of Alzheimer's disease, the investigators have demonstrated that bone marrow-derived microglia infiltrate amyloid plaques and succeed in destroying them most efficiently. These newly-recruited immune cells are specifically attracted by the amyloid proteins that are the most toxic to nerve cells.

According to Rivest, anti-inflammatory drugs should not be administered in cases of Alzheimer's disease, as they interfere with this natural defence mechanism. On the contrary, he adds, a way must be found to stimulate the recruitment of a greater number of bone marrow-derived microglia.

Serge Rivest's team also had recourse to genetic engineering, in order to manufacture microglia that can anchor themselves more solidly to plaques and that are equipped with enzymes with more efficient plaque-destroying capability.

" Stem cells should be harvested from the patients themselves, thus limiting the risks of both rejection and adverse effects," says Rivest. " While this cellular therapy will not prevent Alzheimer's, by curbing plaque development, we believe that it will help patients prolong their autonomy and cognitive capacity. We believe that this is new and powerful weapon in the fight to conquer Alzheimer's."

Source: Canadian Institutes of Health Research, 2006

1174.Calories and Alzheimer’s
08.11.06 http://www.sciencentral.com/index.php3

Scientists are finding that reducing calories might be a way to slow the progression of Alzheimer's disease. This ScienCentral News video explains how a study in mice is offering new clues in fighting the disease.

Alzheimer's brake?

Calorie-restriction -- consuming 30-percent fewer calories than normal -- is the only scientifically proven way to slow the process of aging in organisms ranging from yeast to mammals. Now a new study in mice shows that through a similar mechanism, calorie restriction may also slow or prevent Alzheimer's disease.

"A decrease in amount of calorie intake might have a causal effect in prevention of Alzheimer's disease," says Giulio Pasinetti, professor of psychiatry and neuroscience at Mount Sinai School of Medicine. He and his team conducted the study in a strain of transgenic mice destined to develop Alzheimer's-like symptoms. The mice that were fed a calorie-restricted diet, mainly by a reduction in their carbohydrate intake, over a period of six months, had fewer disease symptoms than their normal-diet counterparts.

"With this kind of calorie restriction we were able to improve memory function ? I would say five-fold times more efficient," says Pasinetti. The amount of beta-amyloid peptides, molecules that cause the build-up of characteristic Alzheimer's plaques, was also much lower in the brains of the mice on the low-calorie diet.

Since calorie restriction has been found to increase the expression of proteins known as sirtuins, Pasinetti and his team tested whether or not one of these proteins could be responsible for the reduction of Alzheimer's symptoms in these mice. As they reported in the Journal of Biological Chemistry, they synthesized a sirtuin called SIRT1 and applied it to brain cells in the laboratory to see whether they'd see similar results to those with calorie restriction.

"Excitingly, we have been able to demonstrate that just the SIRT1 molecule, once re-introduced into brain cells was capable to recapitulate almost the same identical features of calorie restriction," says Pasinetti.

They found that SIRT1 actually works by preventing the cleavage of beta amyloid precursor molecules. If the molecules aren't cleaved, they can't join together to form plaques, keeping Alzheimer's symptoms from appearing. "Through the regulation of SIRT1, we might be in a position to cure the disease," says Pasinetti.

Other mammals, including humans, also have a gene with nearly the same sequence and function as the mouse SIRT1. Pasinetti says that preliminary findings in monkeys confirm these results, which makes it more likely that they'll hold true in people.

Normal lab mouse diets consist of around 20-percent protein, 20-percent fat, and 60-percent carbohydrates. For the purposes of calorie restriction in this experiment, the carbohydrates were the main macronutrient reduced. Pasinetti says that this was important to maintain their general health and prevent the mice from developing insulin-resistance ? a precursor to diabetes.

The calorie restriction was initiated between four and five months of age, when the mice were in the first stages of developing Alzheimer-type symptoms. Pasinetti says that this corresponds roughly to the stage of Mild Cognitive Impairment in people, which isn't Alzheimer's yet, but is a high-risk condition for developing it. Since drug intervention at a late stage of the disease is unlikely to ever be successful because of the intensity of damage done, prevention is the main goal.

Although he says it's too soon to know whether calorie restriction can prevent Alzheimer's in people, the results of his studies have already convinced Pasinetti to change his own behavior.

"I decided personally and my family, definitely to have a major reduction in the total amount of food that actually we eat," he says.

While the weight of the evidence is building that drastically cutting calories might just be worth it, eventually it might not prove necessary. Pasinetti says that the ultimate goal is to design a pill that imitates calorie restriction without actually requiring us to eat less ? leaving us both with healthy minds and healthy appetites.

Pasinetti's research was published in the July 2006 issue of the Journal of Biological Chemistry. The research was funded by the National Science Foundation, National Institute on Aging, Veteran's Administration, Dana Foundation for Brain Research, Cornell Center for Aging Research, and Atkins Foundation.

1175.Exercise Helps Sustain Mental Activity As We Age; And May Prevent Dementia-Like Illnesses

American Psychological Association
8/11/2006 9:40:39 AM

Researchers will next zero in how much and what types of exercise keeps us cognitively young


August 11, 2006, NEW ORLEANS ? Based on a review of studies on exercise and its effect on brain functioning in human and animal populations, researchers find that physical exercise may slow aging’s effects and help people maintain cognitive abilities well into older age. Animals seem to benefit from exercise too and perform spatial tasks better when they are active. Furthermore, fitness training ? an increased level of exercise ? may improve some mental processes even more than moderate activity, say the authors of the review.

Findings from the review will be presented at the 114th Annual Convention of the American Psychological Association (APA).

Varying opinions still exist on the benefits of exercise and activity, said authors Arthur F. Kramer, PhD, Kirk I. Erickson, PhD and Stanley J. Colcombe of the University of Illinois at Urbana ? Champaign, “but our review of the last 40 years of research does offer evidence that physical exercise can have a positive influence on cognitive and brain functions in older animal and human subjects.” Different methodologies were examined to comprehensively study what effects exercise can have.

The researchers first examined the epidemiological literature of diseases to determine whether exercise and physical activity can at certain points in a person’s lifetime improve cognitive ability and decrease the likelihood of age-related neurological diseases, like Alzheimer’s. The authors then reviewed longitudinal randomized trial studies to see if specific fitness training had an affect on cognition and brain function in older adults. Finally, animal studies were examined to understand the molecular and cellular mechanisms responsible for exercise effects on the brain as well as on learning and memory.

Based on a review of the epidemiological literature, the authors found a significant relationship between physical activity and later cognitive function and decreased occurrence of dementia. And the benefits may last several decades. In a few of the studies that examined men and women over 65 years old, the findings showed that those who exercised for at least 15-30 minutes at a time three times a week were less likely to develop Alzheimer’s Disease, even if they were genetically predisposed to the disease.

By examining the human intervention studies, a relationship was also found between fitness training and improved cognition, more efficient brain function and retained brain volume in older people, said Kramer. He cautions that different fitness training regimens and aspects of mental functions need further study to solidify a causal relationship. But, he added, there are some preliminary positive findings. In a four year study looking at the relationship between physical activity on cognition and brain function in 62-70 year olds, “those who continued to work and retirees who exercised showed sustained levels of cerebral blood flow and superior performance on general measures of cognition as compared to the group of inactive retirees,” said Kramer.

Other studies confirmed the evidence that fitness does have positive effects on brain function in older adults. A study of older adults who were randomly assigned to either a walking group or a stretching and toning control group for six months found that those in the walking group were better able to ignore distracting information in a distractibility task than those in the control group. “Aerobically trained older adults showed increased neural activities in certain parts of the brain that involved attention and reduced activity in other parts of the brain that are sensitive to behavioral conflict,” said Kramer.

Animal studies also provide support for the aging benefits of physical activity. Analyzing the effects of exercise in animal populations provides a unique window into learning about exercise-induced neurological and cognitive plasticity ? the ability of parts of the brain to function in place of other parts of the brain, said Dr. Kramer. Some of the animal studies reviewed used voluntary-wheel running experiments to show the existence of performance benefits of wheel running on hippocampus-related spatial learning tasks. Moreover, a few studies found that aged rodents that exercised in a water maze learned and retained information about a hidden platform better than age-matched controls.

Exercise also protected both young and aged animals from developing some age-related diseases as indicated by increases in certain neurochemical levels that can offset or prevent certain pathological diseases.

“From this review we have found that physical and aerobic exercise training can lower the risk for developing some undesirable age-related changes in cognitive and brain functions,” said Dr. Kramer, “and also help the brain maintain its plasticity - ability to cover one function if another starts failing later in life.”

More research is needed to know exactly how much and what types of exercise produce the most rapid and significant effects on thinking and the brain; how long exercise effects last following the end of training; or how much exercise is needed to get continued benefits, said Kramer.

Presentation: "Fitness Training and the Brain: From Molecules to Minds," Arthur F. Kramer, PhD, Stanley J. Colcombe, PhD, Kirk Erickson, PhD, and Paige Scalf, PhD, University of Illinois at Urbana - Champaign

Session 2028 - Invited Symposium: Optimal Aging and Cognition - Moderators of Cognitive Change and Decline, 8:00 - 9:50 AM, Friday, August 11, Morial Convention Center, Second Level, Meeting Room 278

Full text of the article is available from the APA Public Affairs Office

Dr. Kramer can be contacted by phone at (217) 244-1933 or by e-mail.

# # #

The American Psychological Association (APA), in Washington, DC, is the largest scientific and professional organization representing psychology in the United States and is the world’s largest association of psychologists. APA’s membership includes more than 150,000 researchers, educators, clinicians, consultants and students. Through its divisions in 54 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance psychology as a science, as a profession and as a means of promoting health, education and human welfare.

1176.New biomarkers could help doctors spot Alzheimer's and other neurodegenerative diseases
August 11, 2006 　http://www.physorg.com/
Neurodegenerative diseases like Alzheimer's and Parkinson's in their early stages can be difficult for physicians to spot, and many diagnoses are incorrect. A finding by researchers at the University of Washington and Harborview Medical Center may soon help in the diagnosis of such diseases.

The researchers have used an advanced technique to identify proteins in the human body, known as biomarkers, that can indicate whether a patient has a particular neurodegenerative disease, or determine the progression of a disease. Searching for biomarkers is nothing new, but the researchers used a cutting-edge proteomics system, called iTRAQ, that relies on isotopic labeling of protein molecules. The system could help a physician determine the amount of a biomarker a patient may have in his body, which can help with diagnosis.

In a large multi-site study, the researchers identified more than 1,500 potential biomarkers in cerebrospinal fluid from patients with one of three neurodegenerative diseases: Alzheimer's, Parksinson's, or dementia with Lewy bodies (DLB). Researchers identified different sets of potential biomarkers corresponding to each disease; each of the proteins are linked specifically to one of the diseases. The results appear in the new issue of the Journal of Alzheimer's Disease.

"We're getting very close to being able to use these biomarkers for the clinical diagnosis of Alzheimer's and Parkinson's disease, and dementia with Lewy bodies," said the study's lead author, Dr. Jing Zhang, associate professor of pathology at the UW. His lab is at Harborview Medical Center. "This is a major improvement on other biomarker detection techniques."

Alzheimer's, Parkinson's, and other neurodegenerative diseases affect millions of people in the United States, and the toll of the diseases is expected to worsen as the Baby Boomer generation grows older. Though researchers and clinicians are learning more and more about the diseases, there is still uncertainty in the diagnosis and treatment of these conditions.

The biomarkers identified in this study need to be tested in a larger population of patients before becoming part of a full diagnostic tool, Zhang said, but these results are promising. The extensive number of proteins that the research team found in patients with neurodegenerative diseases will likely help researchers create a large panel of biomarkers that could be used in a clinical diagnosis and in monitoring disease progression.

The multi-site study also included researchers from Oregon Health and Science University in Portland; Baylor College of Medicine in Houston; the Fred Hutchinson Cancer Research Center in Seattle; and Applied Biosystems in Framingham, Mass.

Source: University of Washington

1177.Scientists Discover Age-regulated Cellular Activities that Protect Against Protein Aggregation
http://www.bio.com/
08/11/06 -- The research, led by Professor Jeffery Kelly of Scripps Research and Professor Andrew Dillin of the Salk Institute's Molecular and Cell Biology Laboratory, is being published August 10, 2006 as an article in an advanced, online edition of the journal Science.

Alzheimer's disease now strikes more than one in 30 Americans, and about half the population that lives past 85 acquires Alzheimer's. Approximately one million Americans have Parkinson's disease, including three out of every 100 people over age 60. Aging is the most important risk factor for both of these diseases.

The new study-conducted in a C. elegans model, a roundworm that expresses a protein whose aggregation appears to cause Alzheimer's disease-showed that toxicity from protein aggregation is "drastically reduced" when aging is slowed by modulating the insulin growth factor (IGF) signaling pathway.

Moreover, the researchers found two novel independent activities promoting this cellular survival. The first protective mechanism disassembles and cuts up protein aggregates. Surprisingly, the second protective mechanism enables the formation of larger aggregates from smaller ones that appear to be more toxic.

Unexpected Findings

Kelly, who is the Lita Annenberg Hazen Professor of Chemistry at The Scripps Research Institute, a member of its Skaggs Institute of Chemical Biology, and dean of graduate and postgraduate studies, stresses that this novel work was a synergetic collaboration between the research groups at the two institutions.

The Dillin lab at Salk was interested in investigating the connection between cell aging and the onset of proteotoxicity. So, the group set out to determine if the aging process in the worm could be slowed by using RNA interference (RNAi), a naturally occurring process known to suppress certain gene activity in living cells, to lower the activity of the IGF signaling pathway. Indeed, this approach worked and the researchers discovered that if aging was delayed, the onset of proteotoxicity was also postponed.

"In switching this pathway on and off, we also found that we altered the high molecular weight aggregates-the plaque buildup in the animals," explains Dillin.

But the researchers also noticed an unexpected phenomenon. "Curiously," Dillin continues, "some animals were totally protected from proteotoxicity despite having high molecular weight aggregation buildup, while other animals were extremely sensitive to proteotoxicity even though they had no detectable high molecular weight aggregates."

Dillin was eager to further investigate these unexpected findings, so he contacted Kelly at Scripps Research, whose lab had the expertise to examine and analyze these aggregates.

Opposite Activities

Intrigued, Kelly's colleague Jan Bieschke, in collaboration with Ehud Cohen of the Dillin laboratory, did additional experiments perturbing individual components of the IGF signaling pathway. They focused on two downstream transcription factors, heat shock factor-1 (HSF-1) and DAF 16, to see what effect they had on aggregation. The results were surprising.

"When we inhibited only HSF-1, the result was a tremendous amount of aggregate buildup; when we selectively inhibited DAF 16, there were almost no aggregates observed," Kelly says. "That clued us in to the fact that these two transcription factors must be controlling effectively opposite activities."

His group had been using aggregation assays for a long time, and it occurred to him and his colleagues to add samples of the worm's ground-up tissue to these assays as a way of even more sensitively detecting how these transcription factors were controlling aggregation in the animal. The Scripps Research team subjected the worm contents to aggregation assays, using fluorescent dyes that emit light when amyloid is present to read out the extent of aggregation. "It turned out that this worked really well," Kelly says.

When Cohen and Bieschke examined the results, they expected to see less aggregation in the worms when insulin signaling was inhibited. In fact, what they saw was more.

Teasing apart the results, the researchers concluded that two mechanisms were protecting the worms against protein-aggregation-associated proteotoxicity. One mechanism was taking the aggregates apart and degrading them into small pieces; the second mechanism was taking smaller, lower-molecular-weight aggregates and transforming them into high molecular weight aggregates of lower toxicity.

Kelly says that this second finding is "quite surprising" in that heavier aggregates seem to be protective for the cell, albeit in a transient fashion-until the cell can "re-group" to dispose of the aggregates. "What we expected was that the amount of aggregates would correlate with toxicity in these worms, but there was no correlation."

"This second finding is clearly a shift in paradigm," says Dillin. "For nearly a year in this work, we assumed that large aggregates were the toxic species; however, our data proved otherwise. These results further support a shift in thinking for this field regarding the toxicity of small aggregates and lays the framework for new avenues to combat age-onset protein aggregation diseases, such as AD, Parkinson's, Huntington's, and ALS, owing to the protective biological activities discovered."

What Next?

"Now, we want to use this mechanistic information to discover the macromolecular basis for these activities and to discover small molecules that will delay the aging program and thus delay the onset of proteotoxicity associated with these diseases by modulating aggregation and disaggregation activities," Kelly states. "The hope is that, by manipulating the protective mechanism inherent in cells, we can find a single entity-a single drug-that would be useful for a variety of neurodegenerative diseases where protein aggregation leads to neurodegeneration."
In addition to Kelly and Bieschke at Scripps Research and Dillin and Cohen at Salk, Technician Rhonda Perciavalle of the Salk Institute also made significant contributions to the Science study, titled "Opposing Activities Protect from Age Onset Proteotoxicity."
"This has been a wonderful, synergetic collaboration," says Kelly. "This work could not have been done solely in their lab or in ours. Fortunately, scientists at Salk are just down the road and have always been great neighbors."
Source: Scripps Research Institute

12 Aug 2006 http://www.medindia.net/home.asp
1178.Aging Critical For Alzheimer's Disease
Alzheimer's disease is usually accepted as a hazard of aging, but researchers actually do not know whether neurodegenerative diseases are a consequence of aging or not. Researchers at the Salk Institute for Biological Studies and the Scripps Research Institute have now conducted a study that proves it is aging that is critical for diseases like Alzheimer's.

Harmful beta amyloid aggregates accumulate when aging impedes two molecular clean-up crews from getting rid of these toxic species.

This finding opens the door for development of drugs preventing build-up of toxic protein aggregates in the brain. The study appears in the Aug. 10 issue of Science Express, the advanced online edition of the journal Science.

"Aging is the most important risk factor for neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease," says senior author Andrew Dillin, Ph.D., an assistant professor in the Salk Molecular and Cell Biology Laboratory. "Our study revealed that the age onset of these diseases is not simply a matter of time but that the aging process plays an active role in controlling the onset of toxicity," he explains.

Beta amyloid production occurs in all brains, but healthy cells clear away excess amounts. Brains of people with Alzheimer's disease, on the other hand, are unable to control beta amyloid accumulation. For years, scientists have scrambled to find out why.

To answer this vexing question, Dillin analyzed protein aggregation in the roundworm, a streamlined organism that, like mammals, uses the insulin/IGF-1 pathway to control lifespan but can be rapidly manipulated genetically. Dillin used roundworms that produce human beta amyloid peptide in body wall muscles. As the worms aged, the protein formed toxic aggregates causing paralysis.

Then researchers experimentally decelerated aging in engineered worms by lowering activity of the insulin/IGF-1 pathway and asked whether it was simply the passage of time--not aging per se--that favored protein aggregation. It wasn't: chronologically "old" worms crawled around happily, while counterparts whose insulin/IGF-1 pathway was normal could only helplessly wriggle their heads.

However, close inspection of the data revealed a surprise: "Worms with reduced insulin signaling seemed perfectly fine although they had high molecular weight aggregates, while worms with an accelerated aging program were extremely sensitive to the toxic effects of beta amyloid but we couldn't detect any large fibrils," explains postdoctoral researcher and co-lead author Ehud Cohen, Ph.D.

Intrigued, Dillin turned to an expert on beta amyloid biochemistry, Jeffery Kelly, Ph.D., a professor of chemistry at Scripps and a member of its Skaggs Institute of Chemical Biology.

Together they found that cells use an unexpected two-pronged strategy to rid themselves of harmful aggregates. Kelly explains, "One pathway disaggregated beta amyloid fibrils, while the other actively packed them into high molecular weight aggregates. But the latter only kicks in when the cell is left with no other options."

The surprise was that very high molecular weight species were actually less toxic than smaller aggregates. "For a long time large protein aggregates were considered the toxic species," explains Cohen. "The fact that cells protect themselves by temporarily storing small fibrils as high molecular weight aggregates marks a clear paradigm shift."

Two proteins controlled by insulin/IGF-1 signaling orchestrate detoxification--HSF-1, which takes care of aggregate break-down, and DAF-16, which mediates formation of safer, super-sized aggregates as debris accumulates. "We assumed that DAF-16 and HSF-1 would do the same job, but they don't. This is extremely exciting because it gives us two unique opportunities to attenuate beta amyloid-mediated toxicity by manipulating the activity of these factors," says Dillin.

New model for neurodegenerative diseases

Half of all people who reach age 85 will likely be affected by Alzheimer's disease, and the onset age ? usually around 75 ? is almost the same for all sporadic neurodegenerative aggregation diseases. Thus, Salk researchers have developed a model that explains why these disorders diseases occur late in life.

Throughout life, brain cells produce aggregation-prone beta-amyloid fragments that must be cleared. "This process is very efficient when we are young but as we get older it gets progressively less efficient," says Cohen. As the affected individual reaches the seventh decade of life the clearance machineries fail to degrade the continually forming toxic aggregates and the disease emerges. In individuals who carry early onset Alzheimer's-linked mutation, an increased "aggregation challenge" leads to clearance failure and the emergence of Alzheimer's much earlier ? usually during their fifth decade.

"It was very satisfying when the biochemical data from Jeffery's lab and genetic results from our lab came together," recalls Dillin. Both scientists are continuing the collaboration by searching for small molecules that delay the aging program and boost protective mechanisms.

Other contributing authors were co-lead author Jan Bieschke, Ph.D., formerly at Scripps and now at Max Delbrueck Center in Berlin, and research assistant Rhonda M. Perciavalle.

Source: Eurekalert

Medindia on Alzheimers Disease
"If any one faculty of our nature may be called more wonderful than the rest, I do think it is memory. There seems something more speakingly incomprehensible in the powers, the failures, the inequalities of memory, than in any other of our intelligences," wrote Jane Austen, the English writer. This most wonderful gift, if you loose, can make your life chaotic.

August 12, 2006 http://www.futurepundit.com/
1179.THC Blocks Alzheimer's Plaque Formation
Old hippies who haven't toked for decades might come back to the stoner life. Marijuana active ingredient tetrahydrocannabinol blocks the formation of beta amyloid plaques which are suspected as a cause of Alzheimer's disease.

LA JOLLA, CA, August 9, 2006 - Scientists at The Scripps Research Institute have found that the active ingredient in marijuana, tetrahydrocannabinol or THC, inhibits the formation of amyloid plaque, the primary pathological marker for Alzheimer's disease. In fact, the study said, THC is "a considerably superior inhibitor of [amyloid plaque] aggregation" to several currently approved drugs for treating the disease.

The study was published online August 9 in the journal Molecular Pharmaceutics, a publication of the American Chemical Society.

According to the new Scripps Research study, which used both computer modeling and biochemical assays, THC inhibits the enzyme acetylcholinesterase (AChE), which acts as a "molecular chaperone" to accelerate the formation of amyloid plaque in the brains of Alzheimer victims. Although experts disagree on whether the presence of beta-amyloid plaques in those areas critical to memory and cognition is a symptom or cause, it remains a significant hallmark of the disease. With its strong inhibitory abilities, the study said, THC "may provide an improved therapeutic for Alzheimer's disease" that would treat "both the symptoms and progression" of the disease.

The development of better tests for amyloid plaque formation probably will provide the ability to predict the development of Alzheimer's many years in advance of obvious symptoms. For people who face the threat of losing their memory 10 years hence if THC can prevent or delay that outcome use of THC might be worth it. Though quite a few people won't want to go through every day of their lives high on THC.

THC works better than commercial drugs currently on the market.

"When we investigated the power of THC to inhibit the aggregation of beta-amyloid," Janda said, "we found that THC was a very effective inhibitor of acetylcholinesterase. In addition to propidium, we also found that THC was considerably more effective than two of the approved drugs for Alzheimer's disease treatment, donepezil (Aricept ?) and tacrine (Cognex ?), which reduced amyloid aggregation by only 22 percent and 7 percent, respectively, at twice the concentration used in our studies. Our results are conclusive enough to warrant further investigation."

Alzheimer's is a terrible disease. It gradually robs you of your identity. People who face the prospect of losing their memories should be allowed a great deal of latitutde in terms of what they can do to protect themselves from that fate. I expect drugs, antibodies, and vaccines will all come to market in the next 10 years that stop and reverse beta amyloid plaque formation. Use of THC for this purpose will be transitory at best. But will any government even allow clinical trials of its effectiveness against Alzheimer's?

1180.Few know about Alzheimer's

Aug. 14, 2006 12:00 AM　　http://www.azcentral.com/

SCOTTSDALE

Last week I discussed some of the latest research on the causes and potential treatments of Alzheimer's disease.

Now comes new research with profound implications about the latest public attitudes and knowledge of the disease

As you read about the study, think about how you might respond.

Major changes in longevity have occurred in the past several decades. As my parents aged, they were concerned about cancer and heart disease. Better medicine is helping to forestall these chronic conditions.

My parents paid little attention to dementia and Alzheimer's, which today are on the rise.

One in 10 Americans older than age 65 has Alzheimer's, and that increases to 50 percent for the population over 85.

With increased longevity, the Alzheimer's Association expects the number with the disease to increase from the current 4.5 million Americans to as many as 16 million by 2050.

With the estimated cost of lifetime care for an individual with Alzheimer's at $174,000, that represents more than $780 billion nationwide currently.

Even assuming no inflation and no scientific breakthroughs, that amount could balloon to nearly $3 trillion by 2050.

How we think about it
Metlife Foundation just released a study, Alzheimer's Disease: What America Thinks. It commissioned a national telephone survey to assess Americans' perceptions of Alzheimer's.

More than 93 percent of respondents said they know a little about the disease, though only 26 percent said they know a lot about it. The youngest respondents were least knowledgeable. Women were more knowledgeable than men.

Three other important findings:

At least one-third of the respondents had a family member and/or friend with Alzheimer's.

62 percent said they are at least somewhat concerned that they will have to someday provide care for someone with the disease.

Nine of 10 Americans have not made a plan for the possibility of getting Alzheimer's. While 62 percent are concerned about providing care, they fail to make any plans.

Basic steps for us all
There are some basic steps each of us can take. We can make financial arrangements for insurance, housing, skilled care and respite care. The study found that 83 percent had not many any financial arrangements.

If you develop the disease, how do you want to be cared for?

The survey found that 72 percent had not considered what care options are available. Do you know the care options that are available in your community?

Sixty-four percent said they had not talked to their family about the disease or what might be done if they developed Alzheimer's. Having a conversation about the possibility of the disease and what care you want would be a good first step.

As a part of that conversation, designating who would take care of your affairs is important. The survey found that only 58 percent had made that designation. Should your spouse or your child be designated? You may want to include a series of alternatives in case the one you designate is unable to do so.

Universal ed needed
My reading of the study suggests that we all need to become more informed about Alzheimer's and how we can lessen the impact, since it cannot yet be cured.

Just as important is to understand the financial, personal and legal arrangements that are possible. I will do my part by sharing information as I receive it.

You also can contact your local chapter of the Alzheimer's Association.

I talked with Deborah Schaus, executive director of the Desert Southwest Chapter about their programs. She described a range of educational services available.

They can be reached at:

1028 E. McDowell Road, Phoenix, 85005.

(602) 528-0545.

www.alzdsw.org.

Deborah also reminded me of the 24/7 hotline: 1-800-272-3900.

Struggle for a cure
In keeping with my sharing, another promising research study was reported out of the Madrid Conference on Alzheimer's.

Scientists have developed a once-a-day pill that may cure Alzheimer's. The drug, PBT2, works by preventing the build-up of a protein called amyloid.

Amyloid protein build-up in the brain is one of the possible causes of Alzheimer's.

Researchers in Victoria, British Columbia, reported that tests on mice showed that levels of Beta-amyloid, also known as Abeta, dropped by 60 percent within 24 hours of a single dose of PBT2, and memory performance improved within five days.

Remember, this is still the early stage of a laboratory study with mice.

In previous columns, I have discussed how you might personally ward off Alzheimer's through diet and exercise. If you missed that column, e-mail me and I will send you a copy.

William Arnold is a professor emeritus at Arizona State University. Reach him at william.arnold@asu.edu.

1181.Study provides new insights into brain organisation
next article 02.08.2006　http://www.innovations-report.com/index.php　
Scientists have provided new insights into how the brain is organised - knowledge which could eventually inform diagnosis of and treatments for conditions like Alzheimer’s disease and autism.
A study by Newcastle University, UK, and the International University Bremen, Germany, debunked a prevailing theory that the nervous system should have mainly very short nerve fibre connections between nerve cells, or neurons, to function at its most effective.

Instead the study, which carried out a sophisticated computer analysis of public databases containing detailed information of worldwide anatomical studies on primate and worm brains, found that long nerve fibre connections were just as vital to overall brain function as short ones.

Much of what we know about the human brain derives from neuroscience research on primates, which are used because they have have experienced similar evolutionary stages to humans.

Brain scans of Alzheimer’s patients and people with autism have shown that they are lacking certain long-distance neural interactions, although experts have yet to discover their specific purpose.

The new study, published in the academic journal PLoS Computational Biology, found that long fibres are important because they can send messages quickly over a longer distance compared with if the same message was sent over the same distance via lots of short fibres. It also found that long fibres are more reliable for transmission of messages over longer distances.

“You can draw parallels with a train journey from Newcastle to London,” said lead researcher, Dr Marcus Kaiser, of Newcastle University’s School of Computing Science and the University’s Institute of Neuroscience.

“For example, you would get to London much more quickly and easily if you took a direct train there. However, if you had to make the journey via Durham, Leeds and Stevenage, changing trains each time, then it will take you longer to get there, and there is the possibility you would miss a connection at some point. It’s the same in the human brain.”

The computer programme, run over several days, took information about the length of nerve fibres in the primate brain and neuronal connections called axons in the brain of a species of worm known as Caenorhabditis elegans. It then tested if the total length of fibres could be reduced, by testing billions of different position arrangements. Indeed, wiring lengths could be reduced by up to 50% owing to the fact that neural systems have surprisingly many long-distance connections.

Co-researcher Dr Claus Hilgetag, an associate professor with International University Bremen’s School of Engineering and Science, said: “Many people have suggested that the brain is like a computer and that for optimum effectiveness it should have mainly short connections between the nerve cells. Our research suggests that a combination of different lengths of neural projections is essential.

“It is particularly interesting that we made the same observations in both the primate and the worm as their brains are very different in terms of shape and size.”

Although it is too early for the research to have direct clinical applications, the researchers suggest that it may eventually contribute towards insights into the diagnosis and possibly the treatment of patients with Alzheimer’s and autism if more information about neural networks - and specifically what the long and short nerve fibres do in the brain - is garnered.

One potential development could be a predictive test for the conditions, which examines and analyses a patient’s brain organisation, aiding diagnosis and possibly showing how the condition may develop over the coming years.

The study is the most comprehensive yet to look at the spatial organisation of the nervous system in primates and worms.

Claire Jordan | Source: alphagalileo
Further information: www.ncl.ac.uk

1182.Copper in high-fat diet risks mental decline

Mon Aug 14, 4:27 PM ET

CHICAGO (Reuters) - Elderly people whose diets were rich in copper and heavy in saturated fats and trans fats risked faster mental decline that could be related to the onset of Alzheimer's disease, researchers said on Monday.

In the six-year study of more than 3,700 people aged 65 or older, about 600 of the subjects consumed at least 1.6 milligrams of copper a day, along with foods heavy in saturated and trans fat. Many of those people added the equivalent of 19 years to their ages in terms of mental decline, according to the study.

While copper, zinc and iron are essential for brain development, too much copper in the bloodstream may block the body's ability to rid itself of proteins that form plaques found to clog the brains of Alzheimer's patients, study author Martha Clare Morris of Rush University Medical Center in Chicago found.

Copper, which has been found at higher levels in the blood of Alzheimer's patients, is normally consumed in animal organs like liver, and in shellfish, nuts, legumes, some fruits, potatoes and chocolate. Drinking water that travels through copper pipes can also contain copper. Many of those in the study with high copper levels got it primarily through multivitamins.

The U.S. daily recommended intake of copper is 0.9 milligrams, while study subjects with the most copper consumed at least 1.6 milligrams per day.

Trans fatty acids, or trans fats, are created when oil reacts with hydrogen gas. They prolong the shelf-life of many manufactured food products, but also contain increased levels of a cholesterol that raises the risk of coronary artery disease and stroke.


The study was published in the journal Archives of Neurology.

Previous studies have indicated people who consume foods heavy with saturated or trans fats were at up to three times the risk of Alzheimer's disease.

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

Public release date: 14-Aug-2006

Contact: Mary Ann Schultz
312-942-7816
JAMA and Archives Journals

High-fat, copper-rich diets associated with increased rates of cognitive decline in older adults
Among older adults whose diets are high in saturated and trans fats, a high intake of copper may be associated with an accelerated rate of decline in thinking, learning and memory abilities, according to a report in the August issue of Archives of Neurology, one of the JAMA/Archives journals.

Although copper, zinc and iron are essential for brain development and function, an imbalance of these metals may play a role in the development of brain plaques associated with Alzheimer's disease. Previous studies have also linked fat intake, especially that of saturated and trans fats, to Alzheimer's disease and other forms of cognitive difficulties, according to background information in the article. One recent animal study found that the consumption of copper in drinking water could amplify the degenerative effects of a high-fat diet on rabbit brains.

Martha Clare Morris, Sc.D., Rush University Medical Center, Chicago, and colleagues assessed the connection between dietary fat and dietary copper intake in 3,718 Chicago residents age 65 years and older. Participants underwent cognitive testing at the beginning of the study, after three years and after six years. An average of one year after the study began, they filled out a questionnaire about their diets. The dietary recommended allowance of copper for adults is .9 milligrams per day. Organ meats, such as liver, and shellfish are the foods with the highest copper levels, followed by nuts, seeds, legumes, whole grains, potatoes, chocolate and some fruits. Copper pipes may also add trace amounts of the metal to drinking water.

Cognitive abilities declined in all participants as they aged. Overall, copper intake was not associated with the rate of this decline. However, among the 604 individuals (16.2 percent of the study group) who consumed the most saturated and trans fats, cognitive function deteriorated more rapidly with the more copper they had in their diets. "The increase in rate for the high-fat consumers whose total copper intake was in the top 20 percent (greater than or equal to 1.6 milligrams per day) was equivalent to 19 more years of age," the authors write.

Other metals assessed in this study, iron and zinc, did not show any effects on cognitive decline in interaction with a high-fat diet. Previous studies have found higher levels of copper in the blood of patients with Alzheimer's disease, and medications that bind with copper to block its effects have shown promise treating patients with the condition.

"This finding of accelerated cognitive decline among persons whose diets were high in copper and saturated and trans fats must be viewed with caution," the authors conclude. "The supporting evidence on this topic is limited. The strength of the association and the potential impact on public health warrant further investigation." (Arch Neurol. 2006;63:1085-1088. Available pre-embargo to the media at http://www.jamamedia.org.)

###
Editor's Note: This study was supported by grants from the National Institute on Aging. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

For more information, contact JAMA/Archives Media Relations at 312/464-JAMA (5262) or e-mail mediarelations@jama-archives.org.

1183.Program nurtures Alzheimer's patients and their caregivers
By MAUREEN SIMPSON
The Bluffton Packet
Published Tuesday, August 15, 2006 http://www.islandpacket.com/
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Alma Mitchell drew a portrait of herself, then cut it up in pieces last Tuesday.

The Sun City Hilton Head resident said that's exactly how her life has felt since her husband, Eric, was diagnosed with Alzheimer's disease almost seven years ago.

Fractured. Chaotic. Unrecognizable.

But not without hope.

"This represents me being in pieces, but I'm looking out towards something," she said as she analyzed her painting of an ocean view and skyline, fragments of her face glued to various corners of the canvas. "I'm aiming somewhere, you know? Where I want to go. I might just put a cruise ship here or a door."

Though Eric died from complications related to the illness last September, Mitchell remains connected to the activities and social day programs that Alzheimer's Respite & Resource offers to caregivers and their disease-stricken loved ones.

Last Tuesday, the nonprofit organization marked the official opening of its new program site at Riverside at Belfair Retirement Community with an art class for caregivers led by Bluffton artist Amos Hummell. Mitchell was one of about a dozen in attendance.

She said that she doesn't know how she would have made it through those unending days if it weren't for the relief provided by AR&R. Aside from giving her husband back some dignity, it maintained her sanity. For that, she'll be returning the favor as a volunteer for years to come.

"This group, they have given me such wonderful support," Mitchell said, as newfound pal and fellow caregiver Maggie Wallace looked on and nodded in affirmation. "You'd go nuts if you didn't have something like this. ... I've stayed involved. You have to be. God knows they need the help."

Wallace, who moved to Bluffton from California just over a year and a half ago, has been bringing her husband, Robert, to the social day program provided by AR&R every week since she found out about it. For him, she said, it's a total joy to be able to interact with others and participate in the various recreational and craft activities provided by the program. For her, it's an inexplicable freedom to have a moment in the day when she doesn't have to worry.

"It means the world to me," Wallace said of the Tuesdays she drops Robert off for art and music therapy, exercise, games, crafts and a hot lunch. "Just to get that few hours, you know, when I can go and shop or have lunch with a friend. Just not to have to be constantly watching that he's not hurting himself or emptying the closet and folding everything in the bed. ... It takes it out of you. Sometimes I run into the bathroom and I just scream, 'Why? What did we do?'"

Edwina Hoyle, executive director of AR&R, said that caregivers of those with Alzheimer's disease and other forms of dementia have a 24-hours-a-day, seven-days-a-week job on their hands that results in a tremendous amount of stress. Studies, she said, have compared the emotional and physical toll placed on their immune systems to that of someone with advanced HIV.

"To them, it's not a burden, it's a labor of love," Hoyle said. "But it really is a very stressful endeavor to take care of somebody that's so ill both mentally and physically. ... About one-third of the caregivers who do care for their loved one at home will die before the person that they're caring for. The numbers are very staggering and frightening."

Hoyle said AR&R was founded on Hilton Head Island nearly 10 years ago by a core group of people who recognized there was a need that was not being met in terms of caring for the caregiver. As such, the organization was designed to cover the gamut of issues that arise upon diagnosis of the disease, which is debilitating for both the patient and the family.

Program assistant Cathee Stegall has been working with patients at the social day program since May, and said she knows from personal experience the effect that Alzheimer's can have on all who are connected to the disease in some way.

"My mom had Alzheimer's," Stegall said, as about six of the day program's participants worked on coloring Turkish tile. Their loved ones, only a few feet away, continued to work on their own artistic creations for the facility's open house. "If my father had a program like this, it would have added length to his days, too. He would have gotten a little time for himself to go run appointments and make sure he was having fun. ... To be able to be part of this and to give the patients and their caregivers some quality of life back. I love that."

In addition to the social day program that AR&R offers five days a week at three different locations in the area, it also offers caregiver support groups, family meetings, educational resources, presentations and referrals. In all, the organization assists 30 to 35 families in Bluffton and Hilton Head.

"We try to work with caregivers to help them think maybe five steps ahead," Hoyle said. "Their world is so in the present moment, but whether it's five weeks or five months, their loved one's abilities decline and they are going to need a different plan in place. ... We have to really provide them with enough information and resources and education about other community resources to help them be aware of other avenues."

Though Wallace, 70, has been caring for her husband for seven years now, she can't imagine reaching a point where she will turn him over to someone else's care, though many have encouraged her to get help. For now, she said, AR&R is exactly the relief she needs. It's a program that fits her specific needs and a haven for those like her husband, Robert, whose days are filled with shadow after shadow after shadow.

"It's inevitable that he's declining," she said, as she looked at her painting of a quiet, shady escape with a narrow, uphill climb. Her eyes were the only part of her portrait she chose to glue on the canvas -- angry eyes that were evidence of a seven-year battle she's yet to quit fighting. "But you thank God for the years that you did have. ... I remember all that when I tend to get a wee bit less patient than I should be. I know that he would do the exact same thing for me. I know he would."

1184.Skin Test Could Detect Alzheimer's Disease Early
Researchers working on a simple analysis that could be done in a doctor's office or outpatient clinic

By Ed Edelson
HealthDay Reporter

MONDAY, Aug. 14 (HealthDay News) -- A simple skin test that would allow detection of Alzheimer's disease in its earliest stages is working its way to reality.

The work "is based on the hypothesis that Alzheimer's disease doesn't just affect the brain but affects the body systemically," said Dr. Daniel L. Alkon, a lead author of a report on the test published online this week in Proceedings of the National Academy of Sciences.

The test zeroes in on two forms of an enzyme involved in the degradation of amyloid, the protein that accumulates in the brain of someone with Alzheimer's, said Alkon, scientific director of the Blanchette Rockefeller Neurosciences Institute at the West Virginia University Health Sciences Center.

The presence of Alzheimer's disease is indicated by a steep imbalance in the ratio of the two forms of the enzyme, MAP kinase Erk, in skin cells that are exposed to bradykinin, an inflammation-related molecule, Alkon said. That imbalance is not seen in cells of people without dementia or those with other forms of dementia, he said.

The test produced good results when run on 60 tissue samples: 30 from a tissue bank, 30 from autopsy samples of people diagnosed with Alzheimer's disease, Alkon said.

"We have seen a correlation with the duration of the disease," he said. "The earlier it is done in the course of the disease, the larger is the abnormality."

An as-yet unpublished study of the test done on 100 people showed equally good results, Alkon said.

"We are ready to expand this to thousands," he added.

Such expanded testing is essential, said Dr. Samuel Gandy, director of Thomas Jefferson University's Farber Institute for Neurosciences and chief of the Alzheimer's Association medical and scientific advisory council.

The hypothesis behind the test "is, by no means, an accepted formulation, nor have they proved it," he said.

The presence of inflammation around the amyloid clumps that form in the brain of Alzheimer's patients is well known, Gandy said. "Whether there is inflammation elsewhere in the body hasn't been established. The idea that this might be a systemic process hasn't been thoroughly investigated," he added.

Gandy said the theory is "unconventional, but it certainly is something that can be investigated by others."

"Technically, it looks perfectly sound," Gandy said of the published paper. "But certainly nothing in science is accepted until it is replicated. The real test of the pudding will be if others do the same experiment and get the same results. It would have to be robustly reproducible before we change the way we think about Alzheimer's."

Having a test for early detection of Alzheimer's disease would be extremely valuable, both Alkon and Gandy said. "All the newest medications in clinical trials are aimed at the earliest stage of the disease," Gandy said.

"Drugs now are being tested on the basis of clinical diagnosis," Alkon said. "There is a major need for an early biomarker."

More information

A major source of information about Alzheimer's disease is the Alzheimer's Association.

SOURCES: Daniel L. Alkon, M.D., director, Blanchette Rockefeller Neurosciences Institute, West Virginia University Health Sciences Center, Morgantown, W.Va.; Samuel Gandy, M.D., Ph.D, director, Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia; Aug. 14-18, 2006, Proceedings of the National Academy of Sciences

Last Updated: Aug. 15, 2006

Copyright ? 2006 ScoutNews LLC. All rights reserved.

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Source: West Virginia University Health Sciences Center
Released: Wed 09-Aug-2006, 17:00 ET
Embargo expired: Mon 14-Aug-2006, 17:00 ET
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Scientists Closer to Early Alzheimer’s Diagnosis
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A painless skin test for Alzheimer’s disease? It may seem unlikely, but scientists at the Blanchette Rockefeller Neurosciences Institute (BRNI) have isolated a substance in skin cells that may provide doctors with a quick and accurate yes-or-no answer when they suspect a patient is showing early signs of the disease. The test could be performed easily by a nurse or medical technician in a doctor’s office or outpatient clinic.

In an article to be published online the week of Aug. 14 in the Proceedings of the National Academy of Sciences (PNAS), researchers at BRNI describe a biomarker that can accurately distinguish between Alzheimer’s disease and other forms of dementia during the first one to two years of the disease’s progression.
The BRNI biomarker showed high accuracy when tested with human skin cells from a tissue bank, as well as for samples obtained in a previous, unpublished study of patients with autopsy-confirmed diagnoses. The biomarker could also potentially be used with blood samples.

“When it begins, Alzheimer's disease is often difficult to distinguish from other dementias or mild cognitive impairment,” says Daniel L. Alkon, M.D., scientific director of BRNI and coauthor of the study with Tapan K. Khan, Ph.D., assistant professor. “Potential treatments of Alzheimer’s, however, are likely to have their greatest efficacy before the devastating and widespread impairment of brain function that inevitably develops after four or more years.”

Many scientists have concluded in recent years that Alzheimer’s effects are found throughout the body, not just in the brain. By testing for signs of Alzheimer’s-related inflammation in skin cells called fibroblasts, the BRNI team has located a biomarker for the disease that can be tested without the invasive tests previously required, such as a lumbar tap.

Alzheimer’s disease stimulates a change in the enzyme, MAP Kinase Erk 1/2. When fibroblasts are tested by exposing them to Bradykinin, a common inflammatory signal, the Erk 1/2 response in skin cells of Alzheimer’s patients was sharply distinguished from the results in cells from age-matched controls. It was also differentiated from the skin cells from patients with non-Alzheimer’s dementias, such as Parkinson's disease, multiple infarct dementia and Huntington's chorea.

Drs. Khan and Alkon have created an Alzheimer’s Index that may contribute greatly to physicians’ evaluations of patients with dementia. The index is a mathematical formula that allows the scientists to convert the test results for each patient to a single number.

“The results demonstrate that when the Alzheimer’s Index agrees with the clinical diagnosis of the presence of Alzheimer’s, there is a high probability of accurate diagnosis,” Alkon said.

The molecular pathway measured by the BRNI biomarker includes the same enzyme, PKC, which is targeted by the drug Bryostatin. BRNI is currently seeking approval to begin clinical trials of Bryostatin to determine if it is useful in treating both the symptoms and neurodegeneration of Alzheimer’s disease.

The article, “An Internally Controlled Peripheral Biomarker for Alzheimer’s Disease: Erk1 and Erk2 Responses to the Inflammatory Signal Bradykinin,” appears on the PNAS website, http://www.pnas.org/cgi/doi/10.1073/pnas.0605411103.

BRNI is an independent research center, affiliated with West Virginia University, which seeks to accelerate the transfer of basic neuroscience discoveries into practical treatments for patients suffering from Alzheimer's disease and other memory disorders.

U.S. Senator Jay Rockefeller founded the institute in memory of his mother, who died of Alzheimer's disease. For more information, see http://www.brni.org.

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August 15, 2006 AA

Alzheimer's Association statement on Alzheimer "skin test"

A study published online by the Proceedings of the National Academy of Sciences describes a method of examining human skin cells that the authors feel may distinguish individuals with Alzheimer’s disease from those with other types of dementia or those with no impairment. According to the authors, “…the molecular biomarker described [in this study] could have important clinical utility for providing more certainty in the positive diagnosis of AD.”

“As of today, the validity of this ‘skin test’ technology for making or confirming any dementia diagnosis is unproven. Claims to the contrary are misleading and overstated,” says Sam Gandy, M.D., Ph.D., chair of the Alzheimer’s Association’s Medical & Scientific Advisory Council. Dr. Gandy is Director of the Farber Institute for Neurosciences at Thomas Jefferson University, Philadelphia.

The study contains very interesting though very preliminary research. The Alzheimer’s Association urges caution in interpreting the results. It is important to note that no living persons were involved in this study. The scientists used skin cells from a “cell bank” and tissue samples from autopsied patients. These findings need replication by other scientists in bigger populations.

It is important for families affected by Alzheimer’s disease to know that this research does not describe a “product” that is available to doctors or patients, nor is this technology anywhere near becoming a “product.” That will take much more research.

We do need ways to diagnose Alzheimer’s disease earlier, for example, because drugs now in the pipeline may be able to work earlier in the disease process to slow or stop the progression of Alzheimer’s. This is a high priority area for the Alzheimer’s Association, and it is why we have launched our Effective Treatment Initiative and strongly support the NIA’s Alzheimer’s Disease Neuroimaging Initiative (ADNI).

At this critical time for Alzheimer’s disease research, more federal research funds are needed to capitalize on the advances of the last decade. The Alzheimer's Association calls on Congress to appropriate $1 billion for Alzheimer’s research at the National Institutes of Health. If our elected officials are serious about saving our healthcare system and controlling the costs of Medicare and Medicaid, they have no choice but to increase ? immediately and substantially ? their investment in Alzheimer’s research.

For more information, contact the Alzheimer’s Association media line at 312.335.4078 or media@alz.org.

Aug. 11, 2006 | Health and Medicine | Science and Tech
1185.New biomarkers could help doctors spot Alzheimer's and other neurodegenerative diseases
CONTACT: Justin Reedy jreedy@u.washington.edu 206-685-0382
http://www.uwnews.org/
Neurodegenerative diseases like Alzheimer's and Parkinson's in their early stages can be difficult for physicians to spot, and many diagnoses are incorrect. A finding by researchers at the University of Washington and Harborview Medical Center may soon help in the diagnosis of such diseases.
The researchers have used an advanced technique to identify proteins in the human body, known as biomarkers, that can indicate whether a patient has a particular neurodegenerative disease, or determine the progression of a disease. Searching for biomarkers is nothing new, but the researchers used a cutting-edge proteomics system, called iTRAQ, that relies on isotopic labeling of protein molecules. The system could help a physician determine the amount of a biomarker a patient may have in his body, which can help with diagnosis.

In a large multi-site study, the researchers identified more than 1,500 potential biomarkers in cerebrospinal fluid from patients with one of three neurodegenerative diseases: Alzheimer's, Parksinson's, or dementia with Lewy bodies. Researchers identified different sets of potential biomarkers corresponding to each disease; each of the proteins are linked specifically to one of the diseases. The results appear in the new issue of the Journal of Alzheimer's Disease.

"We're getting very close to being able to use these biomarkers for the clinical diagnosis of Alzheimer's and Parkinson's disease, and dementia with Lewy bodies," said the study's lead author, Dr. Jing Zhang, associate professor of pathology at the UW. His lab is at Harborview Medical Center. "This is a major improvement on other biomarker detection techniques."

Alzheimer's, Parkinson's, and other neurodegenerative diseases affect millions of people in the United States, and the toll of the diseases is expected to worsen as the Baby Boomer generation grows older. Though researchers and clinicians are learning more and more about the diseases, there is still uncertainty in the diagnosis and treatment of these conditions.

The biomarkers identified in this study need to be tested in a larger population of patients before becoming part of a full diagnostic tool, Zhang said, but these results are promising. The extensive number of proteins that the research team found in patients with neurodegenerative diseases will likely help researchers create a large panel of biomarkers that could be used in a clinical diagnosis and in monitoring disease progression.

The multi-site study also included researchers from Oregon Health and Science University in Portland; Baylor College of Medicine in Houston; the Fred Hutchinson Cancer Research Center in Seattle; and Applied Biosystems in Framingham, Mass.

1186.Region of DNA strongly associated with Alzheimer's disease
08/17/2006　　XagenaMedicine2006

An international team of researchers, led by investigators at Washington University School of Medicine in St. Louis, are zeroing in on a gene that increases risk for Alzheimer's disease.
They have identified a region of chromosome 10 that appears to be involved in risk for the disease.

" There are a few genes that have been implicated in the development of early-onset Alzheimer's disease, but other than APOE, no genes have been found that increase risk for the more common, late-onset form of the disease," says principal investigator Alison M. Goate, at Washington University. " The region of DNA identified in our study showed evidence of replication in four independent series of experiments. I haven't seen a putative risk factor show such consistent results since the e4 variant of the APOE gene was identified as a risk factor for late-onset Alzheimer's disease more than 10 years ago."

Goate's team of researchers reported in the American Journal of Human Genetics results of a scan of more than 1,400 single-nucleotide polymorphisms ( SNPs ) on chromosome 10 to home in on susceptibility genes for late-onset Alzheimer's disease.

Since most DNA does not make proteins, the majority of SNPs have no effect on DNA function or on health and disease. However, some SNP variants can cause major health problems. An example is APOE4, a common SNP in the apolipoprotein E gene that increases risk for Alzheimer's disease.

Goate and colleagues have not yet isolated a gene on chromosome 10, but in studying the 1,400 SNPs on chromosome 10 in DNA from three series, each with approximately 400 people with late-onset Alzheimer's disease and 400 healthy, age-matched controls, her team found only one SNP that consistently showed evidence of risk for Alzheimer's disease in all three series.

" The region of DNA implicated in our study contains six genes," Goate says. " We don't know which of those genes is most likely to harbor this particular risk factor for Alzheimer's disease, but we're getting closer. We're now trying to nail down which one of these six genes is the most likely to be involved."

Goate expects between five and 10 genes eventually will be implicated as possible risk factors for late-onset Alzheimer's disease, and she says it's possible that more than one of those genes is located on chromosome 10.

" One thing we're trying to do at a functional level is to see whether any of the six genes that we've identified might be involved in pathways that we already know are related to Alzheimer's disease," she says. " For example, we know amyloid-beta peptide plays a role, so we want to see whether any of these genes might have a role in amyloid-beta metabolism.

" We don't really know the nature of this risk factor yet. What we can say is that we believe we know where it's located, and we know there are six genes in that region. But there also could be other regulatory elements within that strand of DNA that don't directly produce a protein but may somehow affect proteins produced elsewhere in the genome. At this point, we can say that there is a variant in this region of DNA that is increasing risk for Alzheimer's disease, but we can't yet say how," Goate says.

Source: Washington University School of Medicine, 2006

1187.SLS makes breakthrough in pre-clinical study for MCI treatment
Aug. 16, 2006
http://www.indiadaily.com/default.asp
Announcing a breakthrough in its pre-clinical studies for lead compounds to treat mild cognitive impairment (MCI) associated with Alzheimer's disease or Schizophrenia, Suven Life Sciences (SLS) today said it would present the pre-clinical data at the annual meeting of the Society for Neuroscience. "We are encouraged by the results of these pre-clinical studies which lead us to believe that that these selected 5HT6 antagonists may provide a novel safe and effective approach of treating diseases like MCI, Alzheimer's disease, Schizophrenia, Parkinson's and obesity," SLS CEO Venkat Jasti said in a communique to the Bombay Stock Exchange. The company said its highly selective small molecules 5-HT6 antagonists have been developed for treatment of MCI associated with Alzheimer's disease or Schizophrenia, Parkinsons and obesity. It said the pre-clinical data will be presented at the annual meeting of the Society for Neuroscience (SFN) to be held in Atlanta from October 14-18. Around 30,000 neuroscientists from across the world are expected to attend this year's SFN's annual meeting.

Wednesday, August 16, 2006
1188.Slowing Alzheimer's disease by keeping mind and body active
http://canucwhatic.blogspot.com/
Researchers have uncovered the pathways behind the protection offered by environmental stimulation in Alzheimer's disease, further confirming that enhanced mental and physical activity slows neurological decline. The paper by Ambr?e et al., "Reduction of amyloid angiopathy and Aβ plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways," appears in the August issue of The American Journal of Pathology.

Alzheimer's disease, the leading cause of senile dementia, presents with cognitive and behavioral deficiencies resulting in part from accumulation of ?-amyloid (A?) deposits within the brain (A? plaques) and its blood vessels (amyloid angiopathy). Although previous studies have shown that increased mental and physical activity can slow the progression of the disease, how such deceleration occurs has been unclear until now.

Dr. Kathy Keyvani's group at University Hospital Muenster examined the effects of environmental stimulation on the brain pathology of TgCRND8 mice. These mice, which express a mutant form of A? found in some Alzheimer's patients, develop Alzheimer-like features including A? plaques and cognitive deficits. To study the effects of enrichment, mice were housed in either standard cages or enriched cages, similar to the standard but with access to a stimulus cage containing permanent fixtures (rope and gnawing wood) as well as removable items (tunnels, balls, ladders, ramps, and exercise wheels) that were changed on a rotating basis.

Following five months of standard versus enriched housing, mouse brains were examined for signs of disease. Mice housed in the enriched environment had fewer A? plaques, smaller plaque size, and reduced amyloid angiopathy compared to mice housed in standard cages. Interestingly, there were no differences in the levels of soluble A? peptide or the transcriptional/translational expression levels of its precursor protein (APP) or the processing of APP between the two groups. So how did environmental stimulation prevent disease?

To answer this question, Ambr?e et al. performed DNA microarray analysis to determine which genes were differentially regulated in mice housed in the enriched environment compared to standard cages. Enriched mice exhibited down-regulation of pro-inflammatory genes but up-regulation of genes related to anti-inflammatory processes, protein degradation and cholesterol binding. These results were confirmed by specifically analyzing gene expression for examples in each category. Together these data suggest that an enriched environment elicits protection via pathways that prevent A? accumulation and enhance its clearance.

The authors speculate that the altered expression of inflammatory genes may shift the immune response from one that is neurotoxic to one that is phagocytic, i.e., able to clear unwanted debris, such as A?. In accordance with this, a significant enhancement of microglial activity was found by Western blot and morphometric analyses of microglia, which often surround and infiltrate A? plaques. In addition, activating cellular protein degradation pathways provides another means of removing excess A?. Finally, changes in cholesterol homeostasis, elements of which have been shown to correlate with A? deposition, may exert beneficial effects by preventing plaque formation in the first place.

These data provide strong evidence that an environment rich in mental and physical stimulation slows the progression of Alzheimer-like brain pathology. Further investigation of the pathways and individual elements involved in such protection may provide novel treatment strategies for Alzheimer's disease. Until that time, keep your running shoes and crossword puzzles handy.

August 17, 2006 Email This Story http://www.news-banner.com/index
1189.Wells County Law Enforcement Agencies Trained on Alzheimer's Related Procedures
By J.G. WALLACE
An elderly Bluffton woman runs a stop sign and is involved in a serious automobile accident. She is a lifelong local resident, yet she doesn’t know the name of the town, her address, or even where she was going.
An older man wanders off from a local nursing home, and after a confused and winding path he settles down to sleep in a cornfield. He is found the next day, cold, confused and badly dehydrated.
A woman slips out the back door of her caregiver’s home, drives off and hundreds of miles from Wells County she drives into a river and dies.
None of these scenarios are farfetched. With minor variations local law enforcement officers have dealt with each case. The common denominator; each individual involved was afflicted with Alzheimer’s Disease.
Officers from the Wells County Sheriff’s Department, the Bluffton Police Department, and the Ossian Police Department came together on Wednesday for a joint meeting at the Bluffton Police Department to learn how to better address the special needs of those with Alzheimer’s.
Sheriff Barry Story initiated the training session after being approached by the Northern Indiana Regional Office of the Alzheimer’s Association.
The main focus of the training was to educate the officers on ways to identify an Alzheimer’s patient, and to facilitate their safe return home.
Alzheimer’s is a progressive fatal brain disorder that affects 4.5 million Americans now. Studies suggest by 2015 that number will have risen to 16 million Americans.
In Indiana alone there are more than 100,000 Alzheimer’s cases, according to Olivia Reeves, an educator involved with the Alzheimer’s Association and the marketing director at River Terrace. Reeves was joined by Jana Powell, a nurse practitioner who works with Alzheimer’s patients.
Both women are involved with Safe Return, a national initiative of the association that was launched in 1993 with support from the United States Department of Justice.
The program maintains a registry of Alzheimer’s patients, and acts as an information clearing house for missing patients, helping to speed communications with law enforcement agencies.
Patients who are registered with the program are provided with special identifying jewelry, id cards, and even iron on clothing labels with a specific I.D. number.
Registering with Safe Return speeds the recovery process by providing law enforcement agencies with descriptive information, photographs, and family contact data. When someone is not registered police may be hard pressed to confirm their identity, and often caregivers are not yet aware someone is missing, so recovery can be a tedious process.
Safe Return also contacts other local agencies when someone is missing to inform other jurisdictions and widen a search.
There is a nominal $40 charge to register, but sadly only about 1200 patients are presently enrolled in Indiana, with none of them living in Wells County. There are 3 registered patients in Adams County and 4 in Huntington County.
Last year the national toll-free call center fielded 6971 cases of missing patients. The association has two main goals through Safe Return. The first is to enroll more patients. The second was demonstrated yesterday, the education of law enforcement officers.
As of 2005, the association has trained 1064 Indiana law enforcement officers.
Wandering off is a major concern for Alzheimer’s patients and their families. Finding them quickly is the key to a happy outcome. After 24 hours up to 50 percent of lost Alzheimer’s patients will suffer a serious injury or death.
The numbers involved are staggering. Up to 1 in 10 adults over 65 have Alzheimer’s, and in people over age 80 that number leaps to between 45 and 49 percent.
“They will not cry out or seek help,” explained Jana Powell. “To their way of thinking they are not lost.”
Powell said patients can be, agitated, confused, and scared. “That’s how you’re going to find them,” Powell said.
Those who wander on foot are usually found within a half mile to a mile and a half from home. Police were told to look for lost patients in trouble spots like bodies of water, brush, or fence lines. 29 percent are found in brush or briars.
Safe Return also logs information on patient’s previous wandering episodes, as patients often follow a predictable pattern, or seek out familiar places like previous residences.
Police were told to look for warning signs like automobile accidents, erratic driving, inappropriate clothing, victimization, false police reports, or shoplifting.
Alzheimer’s patients have been known to call the police after seeing themselves in a mirror, thinking an intruder is present based on a totally different perception of their appearance. They may envision themselves as they looked years before.
Police were also told to be concerned for firearms in cases involving Alzheimer’s patients. The Alzheimer’s Association reports that about 60 percent of Alzheimer’s patients have a firearm in the home, and about 44 percent of those are loaded.
Councilman Jim Phillabaum who is involved with a caregiver support group noted one Wells County patient persistently tries to open his gun safe, but fortunately lost the combination years ago.
Police were advised to look for the bracelets and other I.D. provided by the program. They were also provided with information packets and registration forms they can give to family members. For those unable to afford the program the local association has financial aid available.
In extreme cases Powell suggested police could contact the association to offer support to the families involved. Often those who care for Alzheimer’s patients are very stressed, exhausted, and feel helpless. In the short term caregivers are actually more prone to death than their charges are, because of stress related problems.
Phillabaum also noted that the B.M.V. has a confidential procedure to evaluate whether someone should still be driving. Often caregivers are reluctant to deal with those who still drive, but Phillabaum said after they find their is a confidential way to have their loved ones tested they seek to revoke their license.
That alone is not a guarantee that they will not drive anyway but it is a route families can take. Police were also advised that when dealing with an Alzheimer’s patient in a motor vehicle problem, they should issue citations as it often prompts actions from the family.
Powell and Reeves suggested treating any missing Alzheimer’s patient as an emergency situation and to not require a waiting period before taking action.
Some of the suggestions police were given for dealing with Alzheimer’s patients included:

? Maintaining good eye contact with possible patients.
? Speaking slowly and clearly, and not being loud, which may convey anger.
? Using simple words, yes or no questions, and allowing them time to respond.
? Avoiding confrontation and not correcting them or giving “reality checks.”
? Having only one officer speaking at a time.
? Not handcuffing or restraining an Alzheimer’s patient.
? Using non-verbal communication if necessary.
? Realizing that because a patient may not fully understand what is happening, they may often answer “yes,” to seem as if they are aware of the situation.

Sheriff Story said prior to the training officers had to rely mostly on common sense and had no formal training on the needs of Alzheimer’s patients. There is no formal policy in place at either the Sheriff’s Department or other local agencies.
Story said the training was very helpful for his officers and would likely benefit the Bluffton Police Department even more since most of the local patients live in Bluffton.
Chief of Police Tammy Schaffer said, “This will be a big benefit for us.” Schaffer said it is important for officers to recognize the problems of Alzheimer’s patients are much different than someone who is just elderly.
Schaffer said often officers encounter someone who is mentally ill, and the training will help them distinguish between the two conditions.
Both Schaffer and Story said that officers in their departments most likely did not know about the bracelets before and will be more likely to look for Alzheimer’s specific identification in future situations.
“I really want to encourage families to register,” Schaffer said. While the number of registered patients is discouraging at the present, Powell is hopeful that will soon change.
“People don’t really know about it (Safe Return) now, but it hasn’t been well advertised,” Powell said.
More information on Alzheimer’s is available from the Alzheimer’s Association on their web site at www.alzindiana.org, or by calling 260-420-5547. Families can register for Safe Return at www.alz.org/safereturn, or by calling 888-572-8566.

jgwallace@news-banner.com

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1190.Enhancing Gene Delivery with Nanoparticles Could Ultimately Lead to a Cure for Alzheimer's
http://www.newswiretoday.com/index.php
NewswireToday - /newswire/ - Honolulu, HI, United States, 08/18/2006 - A number of neurodegenerative disorders, such as Parkinson's or Alzheimer Disease, may potentially be treated by gene therapy, i.e. the delivery of therapeutic genes to neurons.


Currently, the most common carrier molecules to deliver the therapeutic gene to the patient's target cells are viruses that have been genetically altered to carry normal human DNA. Overall gene delivery efficiency is typically low for nonviral vectors. New research undertaken at The Johns Hopkins University offers a systematic approach to understanding the gene delivery process in neurons and explores the intracellular barriers to nonviral gene delivery and possible ways to improve their effectiveness.

The development of nonviral vectors (the delivery tools) is attractive due to the potential for improved safety, reduced ability to provoke an immune response, ease of manufacturing and scale up, and the ability to accommodate larger DNA molecules compared to viral vectors. However, synthetic systems such as polymer-, lipid- and peptide-based gene carriers are typically much less efficient in delivering genes to primary neurons compared to viral vectors. Thus, identifying bottlenecks to efficient nonviral gene delivery in transfection-resistant neurons and testing of new vectors are priorities.

Much work has been done already to improve gene delivery into central nervous system (CNS) neurons to treat neurodegenerative disorders using various gene delivery systems with several therapeutic agents. Nevertheless, so far there have been no systematic studies investigating the individual intracellular barriers, which should be the guideline for the design of future gene vectors for CNS therapy.

"In our recent study we systematically examined several potential intracellular barriers that may limit the effectiveness of polymeric gene carriers" Professor Justin Hanes from The Johns Hopkins University in Baltimore explained to Nanowerk.

Read the full article on the Nanowerk website.

About Nanowerk: Nanowerk is a leading nanotechnology information portal. Apart from its unique Nanomaterial Database?, with over 1,300 products from 90 suppliers, it provides the most complete nanotech events calendar; hundreds of links to universities, labs, researchers, associations, networks and international initiatives involved in nanotechnology; daily news; downloadable reports; and much more. The site includes a daily “Spotlight” section featuring Nanowerk-exclusive reviews and summaries of cutting-edge nanotechnology research by guest authors and Nanowerk editors. Nanowerk also publishes the nanoRISK newsletter ? a constructive contribution to the debate about the potential risks of nanotechnology.

By Michael Berger, Copyright 2006 Nanowerk LLC

Agency / Source: Nanowerk, LLC

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Friday August 18, 2006 NEWS http://www.pressconnects.com/apps/pbcs.dll/frontpage
NEIGHBORS
1191.Allies aid memory loss fight Humor, medicine, community support help Candor man

By Valerie Zehl

CANDOR -- As an amateur historian, educator and humorist, Bert White knows how to captivate an audience.

But when he speaks in public now, White, 84, introduces himself by saying, "I have Alzheimer's, so if I forget a word here and there, feel free to help me out."

And he's not kidding.

White and his family will be part of the upcoming Memory Walk to benefit the local Alzheimer's Association.

Doctors rendered their diagnosis through a process of elimination in May 2001, casting a dark shadow over the remaining years of the man who had been an English teacher, principal and interim superintendent in the Candor school district, as well as a walking encyclopedia of Civil War history.

For a while, White wrote about his descent into the disease and rallied fellow sufferers and their families with coping strategies.

He still speaks in public, but rarely.

His daughter, Lori White, who teaches in a school district just outside of Ithaca, expects him to talk to her eighth-grade class again, as he does every year.

"A lot of people have hidden from this disease, to close themselves off," she says. "He doesn't do that. He tells people up front that he has it and that it's not going to defeat him."

He disarms people with his blunt acknowledgement of the disease, and that encourages them to talk about it. Don't be afraid to make mistakes, he tells them. And don't hesitate to ask when you need help.

He also listens and learns from others with the disease. It took another Alzheimer's patient telling him about her near-death experience while driving to persuade him to put his own car keys into retirement.

Thanks in part to some clinical trials that have proven beneficial, he has lost less ground to Alzheimer's than most people would have in five years.

Medicine isn't the only factor, though. His wife Mary, 75, won the 2005 Excellence in Caregiving award from the Alzheimer's Society, Lori points out, and it was Mary's dogged research on the Internet that led to her husband participating in that research study that has helped keep him so functional and articulate.

Still, when he addressed his World War II buddies at a reunion last month, forgetting words caused him to pause from time to time.

That's when the audience came to his rescue, yelling out words to fill in the blanks for his faltering memory.

"It goes back to our days in the Army," Bert White says. "We had to do things together."

Last Updated: August 18, 2006 http://www.mcall.com/

1192.Sale or rental of house to finance parent's Alzheimer's care?
Kathy Kristof Personal Finance
Q: My mother, who is 74 years old, is in an assisted living residence. She was diagnosed with Alzheimer's about four years ago. We are concerned about her financial situation because the facility costs about $4,500 a month. So far, we have depleted about $250,000 of her retirement funds and are trying to figure out a way to maximize the rest of her money. We want her to continue to live in this residence, which she enjoys very much. She has about $200,000 left in a money market account.

Her house is worth about $300,000. It is currently unoccupied because we had it renovated, thinking that it could provide a rental income to help reduce the cost of her care. The house is now finished and ready to be rented. Lately, we have been thinking that it might be a better idea to sell the house and invest the returns more aggressively in mutual funds.

The house would rent for about $1,500 a month, but with real estate taxes and property management fees we may end up with a profit of $1,000 a month.

What do you think we should do to maximize the funds available to her? Rent the house out until she depletes her remaining funds in the money market account, then sell the house and use the proceeds to continue financing her care? Or sell the house now and invest in mutual funds?

A: There's no easy solution.

Neither the stock market nor home rentals have anything close to a guaranteed return. So, in either case, you're hoping that the return will keep up with your mother's cost of care.

If you keep the house, the tax on the income generated from it is likely to be less. Here's one scenario, although you should discuss this situation with a tax adviser to put real numbers into the discussion.

If you sell the house, you're likely to generate a taxable gain. Let's assume that the investment in the house is $100,000, including the purchase price and the cost of the renovations. So, if you sold it for $300,000, you'd be paying tax on a $200,000 gain. At a 15 percent rate, your tax would be $30,000, leaving you with $270,000 to invest.

You could earn about 5.25 percent in today's market on bank certificates of deposit. A nest egg that size would generate $14,175 a year, or $1,181 a month.

Although some of that amount might be eaten away by income taxes, the return approximates the return you expect to get from renting the house ? and CDs are a lot lower-maintenance than tenants.

Even with this income, you need to be monitoring what kind state and federal benefits are available to help pay for your mother's care. Talk to your local office on aging. You can usually find it through AARP, or listed under government services in the phone book. The aging office can tell you about social services that might help defray some costs, either now or in the future.

Figuring Out How Much Life Insurance You Need

Q: We are expecting our first child this August. For the first time in our lives, life insurance is something to think about.

I believe we have done a good job planning for retirement ? thanks in no small part to reading books and newspaper columns such as your own ? but I can find no good books about how to estimate the proper level of life insurance.

Rules of thumb, such as buying a policy worth four to 10 times your income, do not strike me as the proper way to plan for the protection of our child. Do you have any thoughts on the correct methodology or books that can help us determine the right amount of life insurance for my wife and me?

A: I wrote a series of stories a few years ago on life insurance that is posted on the Los Angeles Times Web site, http://www.latimes.com . One of those addressed the question of how much to buy.

Here's the short version: You buy life insurance to replace your income in the event that you die when others are relying on you for support. To approximate how much you need, you have to go through a what-if scenario ? and understand that you are not dealing with an exact science.

Questions to consider: What if I die tomorrow? How would my spouse pay the mortgage? If she's working, or could work but now cares for the children, what would it cost to get adequate day care? How long would my dependents need support? What assets, besides life insurance, could they draw on, and how far would those other assets take them?

This doomsday imagining should help you come up with an estimated amount that your monthly budget would fall short and for how long.

From there, my simple rule of thumb is to multiply that amount by 240. That's what will come up with the lump sum necessary to provide the required monthly income, assuming that your dependents will earn 5 percent annually on that nest egg and won't spend down the principal.

So, if the dependents needed, say, $1,500 a month, you'd need a term life insurance policy of $360,000. If they needed $4,500 a month, you'd need about $1 million in insurance.

A final note: round up ? liberally. Term life insurance is cheap, particularly when you are young and healthy. (Conveniently, that's when you need it the most.) A recent check found that a healthy 35-year-old could buy a $1 million 10-year level-premium term policy for about $500 a year.

Los Angeles Times staff writer Kathy M. Kristof welcomes your comments and suggestions but regrets that she cannot respond individually to letters or phone calls. Write to Personal Finance, Business Section, Los Angeles Times, 202 W. 1st St. 90012, or e-mail kathy.kristof@latimes.com.

1193.Solving Alzheimer’s riddle
By Shawn Conner

Publish Date: 17-Aug-2006 http://www.straight.com

Forget omega-3 fatty-acid supplements, bridge, and crossword puzzles. If you really want to prevent memory loss and Alzheimer’s disease, do everything possible to avoid a stroke. And the most effective way to do that, says Dr. Howard Feldman, is through controlling blood pressure.

“Whereas in the past as people have gotten older, doctors might have said, ‘Well, they’re getting older; we can let their blood pressure climb a bit,’ we would not say that at the present time,” explains Feldman, director of an Alzheimer’s research unit at UBC. “The interesting thing is, it looks as though the control of blood pressure in midlife?45 to 65 or 70, not late in life?determines the risk of stroke. At a time when people are still productive and feeling well, and may have absolutely no symptoms of high blood pressure, that might be the time the risk is being set up.”

In the presence of small strokes in the brain, even those that are incidental, Feldman says, “there is a 20 times?increased risk of Alzheimer’s in individuals who already have a footprint of that disease starting.” High blood pressure leads to a variety of different complications in blood vessels that in turn can lead to stroke.

Alzheimer’s is a progressive neurodegenerative disease in which nerve cells die prematurely. Victims experience loss of memory and language skills, as well as changes in mood and behaviour due to decreased ability to effectively pass messages in the nervous system and the brain. “Strokes come in different sizes and shapes,” notes Feldman, who is head of the neurology division at UBC and head of neurology at Vancouver Hospital. “They may be very clinically apparent, based on where they occur, or they may be silent. Stroke may cause specific symptoms, or it may be a background factor.

“We recognize there is likely to be a continuum that includes what we call ‘normal aging,’” Feldman says. “That then spreads into what we call mild cognitive impairment, where individuals have mild impairments that don’t interfere with daily life. If it progresses, it becomes something we know as Alzheimer’s disease.”

Fortunately, research has led to some treatments that have proven effective in battling Alzheimer’s. Feldman observes that their “modest but measurable” benefits help some but not all patients.

But anyone who has experienced the horror of not being recognized by close relatives or friends suffering from dementia?whether brought on by Alzheimer’s or other factors?has good reason to want to do everything possible to dodge such a fate. Thus, every few months a new headline appears concerning another possible preventative method to combat the disease. In Japan, manufacturers have addressed the concerns of a rapidly aging society with electronic games designed to exercise the player’s brain. According to a recent BBC News article, some scientists claim these products can help delay the onset of dementia.

“Most of the leads we have, have not been proven,” cautions Feldman. But don’t throw out your vitamin supplements yet. “I’m supportive on the grounds that a healthy lifestyle is good for a lot of different things. Which is to say everything that’s part of a healthy life?maintaining a rich network of social contacts, being mentally active, exercising, having a healthy, well-balanced diet?is risk-factor protection for Alzheimer’s. No harm comes to people for trying those things. The question is whether we can prescribe them, or know that they work, in order to justify the expense and organizational requirements from knowing that they were proven.”

A direct link between “people who age healthfully and well”, as Feldman puts it, and test groups with lower Alzheimer’s rates is difficult to prove. “It might be that people have a lot of social contacts, exercise, and so on because of some other factor, maybe that they’re generally healthier. It’s not that playing bridge or exercising protects them; it’s that they’re able to play bridge because they’re healthier, and because they’re healthier they have a lower risk of dementia.”

But prevention of stroke “has been shown unequivocally to reduce the rate of dementia”, Feldman says. “And that’s very, very important. If we can prevent stroke in the brain, even small and incidental stroke, we might have a huge impact on public health.”

Public release date: 20-Aug-2006

J. Michael McIntosh
Research professor of biology
Professor of Psychiatry
office (801) 585-3622
mcintosh.mike@gmail.com
Lee Siegel
Science news specialist
University of Utah Public Relations
office (801) 581-8993
cellular (801) 244-5399
leesiegel@ucomm.utah.edu

The Brain Institute at the University of Utah

University of Utah

1194.A new tool against brain disease Snail toxin may spur new meds for Alzheimer's, Parkinson's, depression

University of Utah researchers isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases.

"We discovered a new toxin from a venomous cone snail that may enable scientists to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh.

Discovery of the new cone snail toxin will be published Friday, Aug. 25 in The Journal of Biological Chemistry by a team led by McIntosh, a University of Utah research professor of biology, professor and research director of psychiatry, member of the Center for Peptide Neuropharmacology and member of The Brain Institute.

McIntosh is the same University of Utah researcher who ・as an incoming freshman student in 1979 ・discovered another "conotoxin" that was developed into Prialt, a drug injected into fluid surrounding the spinal cord to treat severe pain due to cancer, AIDS, injury, failed back surgery and certain nervous system disorders. Prialt was approved in late 2004 in the United States and was introduced in Europe last month.

Prialt, sold by Ireland's Elan Pharmaceuticals, took roughly 25 years to reach market after its discovery in venom from the fish-eating cone snail Conus magus or magician's cone. McIntosh says he expects it will take 10 to 20 years to develop new medications based on what is learned from the new toxin ・named alpha conotoxin OmIA (oh-em-one-ay) ・isolated from a cone snail species named Conus omaria, which lives in the Pacific and Indian oceans and eats other snails. It ranges from 1ｾ to 3ｽ inches long.

McIntosh discovered and analyzed the new toxin with help from University of Utah cone snail research pioneer Baldomero "Toto" Olivera, who is a distinguished professor of biology, and lab technicians Sean B. Christensen and Cheryl Dowell.

Other coauthors of the study are Palmer Taylor, professor and dean of pharmacology at the University of California, San Diego, and his associates ・Todd Talley, Igor Tsigelny and Kwok-Yiu Ho ・as well as Kyou-Hoon Han at the Korea Research Institute of Bioscience and Biotechnology.

Diseases that Might Benefit from the New Snail Toxin

McIntosh says the OmIA toxin will be useful in designing new medicines because it fits like a key into certain lock-like "nicotinic acetylcholine receptors" found on nerve cells in the brain and the rest of the nervous system.

"Those are the same types of receptors you activate if you smoke a cigarette," he says, explaining that nicotine in cigarette smoke "binds" to the receptor to trigger the release of a neurotransmitter, which is a chemical that carries a nerve impulse from one nerve cell to another, allowing nerve cells to communicate.

"Nicotine acts on those receptors in our brain, but they are in our brain for better reasons than to enjoy a cigarette," McIntosh says. Different forms or subtypes of nicotinic receptors control the release of different neurotransmitters. "That's important because if you had compounds to facilitate the release of one neurotransmitter and not another neurotransmitter, that opens up medicinal potential," he says.

"For instance, one receptor modifies the release of dopamine. There are inadequate amounts of dopamine in Parkinson's disease," so a medicine designed to fit into a certain subtype of nicotinic receptor would produce more dopamine and thus protect against the development of tremors and other Parkinson's symptoms. Indeed, other studies have found that smoking seems to forestall Parkinson's disease.

A medicine that could block certain nicotinic receptors could be used to help people stop smoking cigarettes, and the same method might work for alcoholism because nicotinic receptors may be involved in alcohol addiction, McIntosh says.

Other nicotinic receptors trigger the release of neurotransmitters involved in memory, so activating the right receptors might lessen Alzheimer's memory loss.

"One reason people smoke is they feel their thinking may be a little better, with increased attention and focus," McIntosh says, noting that pharmaceutical companies "would like to mimic that positive benefit without all the downsides of cigarette smoke."

Other nicotinic receptors influence "the release of serotonin and norepinephrine, two neurotransmitters strongly implicated in mood disorders" such as depression, so a drug to activate those receptors might treat depression, he adds.

Schizophrenics tend to smoke heavily because something in cigarette smoke "seems to help them filter out irrelevant stimuli. They can focus better," McIntosh says. So a drug aimed at certain nicotinic receptors might treat schizophrenia.

New Neurotoxin is a Key for Designing New Medicines

McIntosh says the new toxin itself is unlikely to become a drug because it blocks rather than stimulates nicotinic receptors. But because it can act on some types of nicotinic receptors and not others ・like a key that opens some locks but not others ・it has great potential as a tool for precisely identifying the shape and structure of the receptor "locks," thus making it easier to design new medicines or "keys" to fit those receptors and trigger them to release desired neurotransmitters.

In the new study, about 70 compounds from numerous cone snail species were screened in collaboration with Taylor's lab at the University of California, San Diego.

Taylor uses "acetylcholine binding protein" as a model for nicotinic receptors. In other words, cone snail toxin "keys" that fit into nicotinic receptor "locks" also fit into highly similar "locks" made of this binding protein. So the binding protein was used as a way to find toxins that also would fit into nicotinic receptors. The new OmIA toxin was most interesting because it tightly fits some nicotinic receptors but not others. A drug that tightly fits desired receptors but not others is less likely to have undesirable side effects.

Unlike nicotinic receptors, the binding protein can be grown in crystal form, allowing Taylor's team to use X-ray crystallography to make detailed microscopic pictures of how the toxin fit into the binding protein. Meanwhile, Han in South Korea used nuclear magnetic resonance to make pictures showing the structure of the new toxin.

Together, the images provide a highly detailed picture of how the cone snail toxin fits into the binding protein, and thus how it also would fit into a nicotinic receptor.

"By putting the two together, you can get a high-resolution picture of the binding site," says McIntosh. "That allows for rational drug development. It allows you to design compounds that will bind to the same [nicotinic receptor] site, and it allows you to begin to understand how to bind to one receptor subtype and not another" to trigger the release of whatever neurotransmitter is needed to treat or prevent a particular disease.

"It is the picture of the binding site and the ability to distinguish one type of nicotinic receptor from another that makes the toxin so valuable," he adds.

How the Study was Performed

The snails from which the new toxin was obtained were collected by divers in Olivera's native Philippines. Venomous snails use a dart-like tooth to zap fish, snails and other prey, injecting them with an immobilizing toxin. Venom from the collected snails was extracted at a lab in the Philippines, and then sent to Utah.

Once the screening process identified OmIA as promising, McIntosh and colleagues purified the toxin ・one of perhaps 200 components in Conus omaria venom. They determined its chemical structure and then synthesized more of the toxin, since they had only a small amount of the natural version.

Next, the synthetic toxin was tested to see how well it acted as a "key" to fit into the "locks" represented both by binding proteins (from freshwater snails and a sea slug) and by actual nicotinic receptors, which came from rat cells but were grown in frog eggs. That allowed the researcher to grow various subtypes of the nicotinic receptors and see how well the toxin fit them.

Taylor and Han provided pictures of the physical structures of the binding protein "locks" and toxin "key," and then "used computer simulation to dock the two structures together," says McIntosh. "That generates a picture of the binding site ・the points of contact between the toxin and the binding protein."

The site is the place a new drug would be designed to fit.

"The whole idea is to make the model of the nicotinic receptor so predictive that you can then really speed up the development of drugs," McIntosh says. "If you have an accurate model of the receptor, you can plug in a model of your drugs and do a lot of 'virtual screening.' Rather than synthesizing a million compounds and having all but one be duds, you can synthesize a few thousand compounds based on the model and come up with a better drug with less time and resources."


###
The Center for Peptide Neuropharmacology studies neurotransmitters and receptors that enable rapid information transfer in the brain. The Brain Institute includes more than 100 University of Utah scientists unlocking mysteries of the human brain via interdisciplinary collaboration. The institute supports scientists in turning research advances into technologies and treatments for brain disorders. See http://brain.utah.edu

University of Utah Public Relations
201 Presidents Circle, Room 308
Salt Lake City, Utah 84112-9017
(801) 581-6773
fax: 585-3350
www.unews.utah.edu

1195.Myriad Genetics Closes Enrollment In US Phase 3 Clinical Trial Of Flurizan For Alzheimer's Disease - Quick Facts

Tuesday, August 22, 2006; Posted: 06:45 AM

(RTTNews) - Myriad Genetics, Inc (MYGN | charts | news | PowerRating) revealed completion of enrollment in its US Phase 3 clinical trial of Flurizan for patients with Alzheimer's disease.

The company stated that the US Phase 3 trial is designed with an 18-month study period, however an interim review of the data after 12 months has the potential to halt the trial early if exceptional results are achieved.

Myriad noted that Flurizan is not an NSAID and does not inhibit COX1 or COX2 enzymes and with a safety database consisting of over 600 patient-years of exposure data, Myriad has not seen gastrointestinal toxicity attributable to Flurizan.

Copyright(c) 2006 RealTimeTraders.com, Inc. All Rights Reserved

1196.Alzheimer's Caregivers Report More Stress, Higher Costs And A Greater Commitment Of Time, According To New MetLife Mature Market Institute Study
22.08.2006 13:39:00 http://www.finanzen.net/index.asp


The cost of care and the related stress for those whocare for someone with Alzheimer's disease increases substantially overthose who care for someone with another disabling condition, accordingto a new study by the MetLife Mature Market Institute(R) (MMI). Thestudy reports that the dollar value of family caregiving forAlzheimer's caregivers is 41% higher than for others and thatAlzheimer's caregivers indicate that caregiving has caused theirhealth to worsen 45% more often than other caregivers. Additionally,Alzheimer's caregiving requires a greater commitment of time, andspouses of Alzheimer's caregivers more often report having left theirjobs to provide care.
"The MetLife Study of Alzheimer's Disease: The CaregivingExperience" studied more than 400 people whose care recipients wereover the age of 65 and had long-term care insurance policies fromwhich they were receiving benefits. It found the following:
-- Amount and Type of Caregiving Assistance

Caregivers for those with Alzheimer's disease or other
dementias provided an average of 47 hours of care per week,
compared to 33 hours by caregivers for physically impaired
individuals. Those with Alzheimer's disease (AD) or another
dementia needed additional help with personal care tasks
called Activities of Daily Living (ADLs), more help with
activities such as transportation, cooking and shopping called
Instrumental Activities of Daily Living (IADLs) and more hours
of companionship care, including supervision for safety.

-- Caregiver Stress

Compared to peers caring for people with purely physical
impairments, caregivers of persons with dementia experienced
more stress on all measures.

-- Disruption for Working Caregivers

Spouses of individuals with Alzheimer's disease or another
dementia were at the highest risk of quitting work due to
caregiving responsibilities --10.6% left their jobs to provide
care, compared to 4% of the other caregiving spouses.

-- Costs of Care

Caring in the community for someone with dementia costs 31%
more overall than caring for a person with serious physical
ailments. For an individual with Alzheimer's disease or a
related disorder, the total average cost of services annually,
considering paid and unpaid care, was $77,447, compared to
$59,088 for a person with serious physical problems. The
dollar value of family caregiving is 41% higher for those
caring for a family member with dementia than for other
caregivers with the major difference being in the category of
companionship care (23% of the dollar value of family care for
AD versus 17% for other caregivers). This is consistent with
concerns for safety that family members of those with
Alzheimer's disease have.

-- Caregiver Health

Individuals caring for a family member with dementia were 45%
more likely to indicate that caregiving has caused their
health to worsen.

"Caring for a family member with Alzheimer's disease exacts anenormous toll," said Sandra Timmermann, Ed.D., director of the MetLifeMature Market Institute. "Of the approximately 4.5 million Americanswith AD or a similar disorder, more than two-thirds live at home caredfor by family and friends. That number is expected to triple by 2050to 13.2 million. With these increasing numbers of individuals in needof long-term care, family caregivers will become an even more criticalcomponent of the long-term care delivery system in the years ahead.Having supports such as long-term care insurance and communityservices is important to allow caregivers to continue to care fortheir loved ones without neglecting their own needs. We know thatworkplace flexibility can ease the burden tremendously."

Claimants from eight long-term care insurance companies(representing 80% of the market) were included in the study and 92% ofidentified primary family caregivers for these claimants responded toquestions about their experience during a telephone interview with atrained clinician. Forty-two percent of the respondents (178) werecaring for an individual with AD or another dementia while 58% (245)cared for someone with serious physical problems. In both groups, justmore than 50% of caregivers were spouses.

The MetLife Mature Market Institute is the company's informationand policy resource center on issues related to aging, retirement,long-term care and the mature market. The Institute, staffed bygerontologists, provides research, training and education,consultation and information to support Metropolitan Life InsuranceCompany, its corporate customers and business partners. MetLife, asubsidiary of MetLife, Inc. (NYSE: MET), is a leading provider ofinsurance and other financial services to individuals andinstitutional customers.

LifePlans, Inc., which conducted the analysis for the MetLifeMature Market Institute, is a risk management and consulting firm thatprovides data analysis and information to the long-term care insuranceindustry. The firm works with insurers, the Federal Government,industry groups and other organizations to conduct research that helpsthese groups monitor their business, understand industry trends,perform effective advocacy, and modify their strategic direction.

The entire report, The MetLife Study of Alzheimer's Disease: TheCaregiving Experience, can be found at: www.maturemarketinstitute.comunder "What's New."

1197.Ablynx Completes ?40 Million (~US$50 Million) Series C Financing ? One of the Two Largest Private Placements in European Biotech This Year
http://www.engelpub.com/
GHENT, Belgium, Aug. 23, 2006 ? Ablynx, the pioneer in the discovery and development of Nanobodies?, a novel class of antibody-derived therapeutic proteins, has announced the successful closing of its series C financing round raising ?40 million (~US$50 million). The international syndicate of investors was led by new investor KBC (Belgium), Belgium’s leading bank for private and public equities. SR One (USA and UK), the venture capital arm of GSK, one of the world’s leading research-based pharmaceutical and healthcare companies was the second new investor. All existing financial investors participated in the round - Abingworth Management (UK), Alta Partners (USA), Biotech Fund Flanders (Belgium), Gilde Healthcare Partners (The Netherlands), GIMV (Belgium) and Sofinnova Partners (France). In addition, VIB (Belgium) also participated to a significant degree. This brings the total capital raised by Ablynx since its inception in 2002 to date to ?70 million (~US$87.5 million).

Combined with its existing cash, Ablynx will now be able to fund operations through to at least mid-2008, allowing the Company to further develop its product pipeline based on its proprietary Nanobody? technology and to rapidly increase its headcount which is currently just over seventy. Ablynx is developing a portfolio of Nanobody?-based therapeutic programs in a number of major disease areas, including inflammation, thrombosis, oncology and Alzheimer’s disease. Three of these programs are in preclinical development, and Ablynx is on track to submit its first regulatory filing before the end of this year and anticipates to initiate phase I studies in early 2007.

Ablynx’ strategy is to build a diverse and broad portfolio of therapeutic Nanobodies? based on strategic partnerships as well as on its own internal discovery pipeline. It has ongoing research collaborations and significant, multi-target partnerships with several major pharmaceutical companies, including Novartis, Centocor (J&J), Kirin Breweries and P&G Pharmaceuticals.

Commenting on the financing, Dr. Edwin Moses, Chairman and CEO said:

“We are delighted to have received such strong financial support from top class international investors with a broad range of capabilities and resources. The Company is now in an excellent financial position to rapidly expand its operations and aggressively develop its product pipeline.”

Ruth Devenyns, Senior Investment Manager at KBC Private Equity joining the Ablynx Board, commented:

“Ablynx’ Nanobody? technology has the opportunity to revolutionize the biologics landscape. We are excited to have led the investment and we are looking forward to working with Ablynx’ existing premier investment syndicate and the strong and experienced international management team to take the Company forward to its next stage of development. We believe that Ablynx’ impressive development is another indicator of the growing strength and critical mass of biotech in the Benelux.”

Denis Lucquin, Managing Partner at Sofinnova Partners, said:

“The existing investors were all extremely confident about the future of Ablynx and were cautious about allowing new investors to become involved. However, in KBC and SR One we have found organisations which provide a lot more than just cash and we are delighted that they are joining this exciting endeavour.”

? ends ?

Contacts:

Media relations for Ablynx:
Sue Charles, CEO

Northbank Communications

t : +44 (0)20 7886 8152

m: +44 (0)7968 726585

e: ablynx@northbankcommunications.com

At Ablynx:

Dr. Edwin Moses, Chairman and CEO

Ablynx NV

t : +32 (0)9 241 11 51

m: +44 (0)777 1954193 / +32 (0)473 39 50 68

e: edwin.moses@ablynx.com

NOTES

About Ablynx

Ablynx is a biopharmaceutical company engaged in the discovery and development of Nanobodies?, a novel class of therapeutic proteins based on single-domain antibody fragments, for a range of serious and life-threatening human diseases. Ablynx is developing a portfolio of Nanobody? based therapeutic programs in a number of major disease areas, including inflammation, thrombosis, oncology and Alzheimer’s disease. Already Ablynx has generated Nanobodies? against more than twenty different disease targets. The company and its collaborators have obtained positive in vivo efficacy data from animal studies in five major therapeutic programs in four disease areas. Importantly, Ablynx has shown the absence of any detectable immunogenicity for its Nanobody? development candidates in advanced primate studies. Today, three of these programs are in advanced preclinical development, and Ablynx expects to have progressed two of those into clinical trials by 2007.

Ablynx has ongoing research collaborations and significant, multi-target partnerships with several major pharmaceutical companies, including Novartis, Centocor (J&J), Kirin Breweries and P&G Pharma. Ablynx is building a diverse and broad portfolio of therapeutic Nanobodies? based on these collaborative deals as well as on its own internal discovery pipeline.

Nanobody?-based therapeutics represent a major commercial opportunity as they combine the beneficial features of conventional antibodies, with desirable properties of small-molecule drugs. Because they are derived from naturally-occurring heavy-chain antibodies, Nanobodies? have unparalleled stability and can be administered in a variety of ways (injected, orally, in sprays or creams), thus overcoming the delivery issues associated with full-sized antibodies, that can only be delivered by injection. In addition, because of their unique structure they can also address therapeutic opportunities that are beyond the reach of conventional antibodies or their fragments, for example targeting epitopes such as receptor clefts, enzyme active sites and viral canyon sites. Nanobodies? are manufactured in micro-organisms which also presents a significant cost advantage in comparison to production methods for conventional antibodies.

Ablynx holds the dominant patent position in the field of Nanobodies?. It has exclusive and worldwide rights to more than forty families of granted patents and pending patent applications, including the patents covering the basic structure, composition, preparation and uses of Nanobodies? (the ‘Hamers patents’) which have been granted in major territories including the US, Europe and Japan. All products, including therapeutics, that contain Nanobodies? are covered by these patents.

Headquartered in Ghent, Belgium, Ablynx has raised over ?70 million (over US$87,5 million) from a strong investor consortium including Abingworth Management (UK), Alta Partners (USA), Biotech Fund Flanders (Belgium), Gilde Investment Management (The Netherlands), GIMV (Belgium), KBC (Belgium), Sofinnova Partners (France), and SR One (USA). Basic nanobody patents were contributed by its founding institutions VIB and VUB (Vrije Universiteit Brussel).

For further information please visit the website at www.ablynx.com

About Abingworth Management (UK and USA) - www.abingworth.com

A long-established venture capital firm, Abingworth specializes in unquoted and life science biomedical companies. With offices in London, Cambridge (UK), Menlo Park and Boston (USA), Abingworth is active on both sides of the Atlantic and, in the past fifteen years, has backed more than 80 developing life science/medical businesses. The majority of these have gone on to public offerings or have merged or been acquired by leading companies in the industry. Abingworth has funds under management of over US$700 million.

Stephen Bunting, Managing Director, t: +44 207 7534 1500, e:bunting@abingworth.co.uk

About Alta Partners (USA) ? www.altapartners.com

Alta Partners is a San Francisco-based venture capital firm focused on life sciences investing. Founded in 1996, the firm currently manages US$1.5 billion in committed capital through seven venture funds. Alta invests in biopharmaceutical and medical technology companies across the development continuum, from company formation to later-stage opportunities, and has funded more than 110 life sciences companies to date.

Ekaterina (Katya) Smirnyagina, Venture Partner, t:+33 685802191, +1 415 362 4022,

e: ekaterina@altapartners.com

About Gilde Healthcare Partners (The Netherlands) ? www.gilde.nl

Gilde Investment Management is a leading global private equity investor with more than ?2 billion under management. Since Gilde’s inception in 1982 investments have been made in over 200 companies.

Gilde Healthcare Partners is managing two funds with a total capitalization exceeding ?200 million (US$250 million). The Funds focus on unquoted European start-ups across the healthcare sector including therapeutics, diagnostics, medical devices and enabling technologies. The healthcare funds are managed by experienced industry professionals with a balanced mix of operational and venture capital expertise. The team actively assists scientific entrepreneurs in the development of their ideas into successful companies. Gilde has the experience and resources to assist companies at any stage of development and take them beyond a public listing.

Pieter van der Meer, General Partner, t: +31 302192554, e: vandermeer@gilde.nl

About GIMV and Biotech Fund Flanders (Belgium) ? www.gimv.com

GIMV is a Belgian investment company. It was established in 1980, and since 1997, it has been quoted on Euronext Brussels. Its purpose is to invest in the equity of unlisted companies (private equity).

GIMV operates in three areas. GIMV’s venture capital is invested primarily in ICT and Life Sciences. In more traditional industries it also undertakes management buy-outs (MBOs) and it provides growth capital (Corporate Investment). The portfolio maintains a balance among start-up companies, fast growth companies and major enterprises. In this way, GIMV positions itself as a player on the international market.

Biotech Fund Flanders is a venture fund focused on investments in life science projects in Flanders. The fund, which is sponsored by the Flemish government and managed by GIMV, has ?25 million to make commitments in both Flemish companies and foreign companies that intend to start activities in Flanders.

Frank Bulens, Executive Investment Manager, t: +32 3 290 2156, e: FrankB@gimv.be

About KBC Private Equity (Belgium) and KBC Private Equity Fund Biotech (Belgium) ? www.kbcpe.be and www.kbcam.be/biotech

KBC Private Equity, the private equity company of the KBC Group, provides development capital to and finances buy-outs of medium-sized companies for amounts between ?2 million and ?50 million. KBC Private Equity operates primarily in Belgium and in Central Europe, KBC Group’s home markets.

KBC Private Equity can take both majority and minority stakes in companies and contributes financial resources in the form of equity finance and/or mezzanine finance. Boasting an experienced team of 25 people, KBC Private Equity has more than 60 active direct investments in portfolio with a market value in excess of ?400 million.

As an active shareholder with a long-term perspective, it is involved in taking strategic decisions and providing support to management in the further development of their company. As part of KBC Group, KBC Private Equity can rely on the Group’s extensive network and knowledge.

KBC Private Equity Fund Biotech NV (‘Biotech NV’) is a Privak, i.e. a closed-end Belgian investment company. Biotech invests both in listed and private biotech companies around the world. It is listed on Euronext Brussels and jointly managed by KBC Private Equity and KBC Asset Management.

Ruth Devenyns, Senior Investment Manager, t: +32 2 429 96 94,

e: ruth.devenyns@kbcpe.be

About Sofinnova Partners (France) ? www.sofinnova.fr

Founded in Paris in 1972, Sofinnova Partners is one of Europe's leading independent venture capital firms. With ?900 million under management, Sofinnova Partners invests in start-ups and early-stage companies in information technology and life sciences. Its investment strategy consists of investing early in teams and projects with high potential, most often acting as lead or co-lead investor. Sofinnova Partners also benefits from a long-established relationship with its sister company in San Francisco, Sofinnova Ventures. Sofinnova Partners’ teams consist of 10 professionals who bring valuable market insight and technical expertise to portfolio companies.

Denis Lucquin, Managing Partner: +33 1 53054103, e: DLucquin@sofinnova.fr

About SR One (USA) ? www.srone.com

SR One is GlaxoSmithKline’s independent corporate healthcare venture capital fund. Based in West Conshohocken, PA, and London, U.K., SR One invests globally in emerging biotechnology companies that are engaged in drug discovery, development and delivery with the potential to yield dramatic patient benefits. Since its founding in 1985, SR One has invested over $400 million in more than 120 emerging biotechnology companies. For more information on SR One, its staff and portfolio companies, please visit www.srone.com.

Adrian Rawcliffe, Managing Partner, SR One, t: +1 610 567 1006, e: ad.g.rawcliffe@gsk.com

About VIB (Belgium) - www.vib.be

VIB (the Flanders Interuniversity Institute for Biotechnology) is a research institution performing cutting edge research in the fields of molecular medicine, plant system biology and structural biology. VIB implements technology transfer to translate its research results into products for the benefit of society. VIB currently manages a portfolio exceeding 150 patent families, collaborates with dozens of companies worldwide and establishes start-up companies such as Devgen, CropDesign, Ablynx, Peakadilly and Solucel. VIB also exploits multiple bio-incubators and was catalyst in the establishment of the biotech cluster FlandersBio. VIB is also actively involved in science communication.

Rudy Dekeyser, Vice General Director and Director Technology Transfer, t: +32 9 2446611, e: Rudy.Dekeyser@vib.be

1198.Even when the mind forgets, the heart always remembers
August 24, 2006
http://www.thevictoriaadvocate.com/
Since 1998 Homewood Residence at Victoria Retirement Community has been a leading provider of Independent Living and Assisted Care for seniors in Victoria County and beyond.

Today the scope of our services expands to include The Arbors, a newly constructed on-campus community dedicated to the care and well being of residents with Alzheimer's disease and other forms of dementia.

But The Arbors is so much more than merely a comfortable, caring place to live. From carpeting to lighting, to layout and floor plans; everything has been designed with the special needs of our residents in mind.

Accommodations and common areas Private apartments are just the right size: Large enough to provide a sense of personal space but small enough so as not to be overwhelming.

Hallways form an indoor loop, allowing residents to explore safely and confidently, without the fear of disorientation or the anxiety of confinement.

A living room with fireplace provides a feeling of home, additional warmth and a sense of security. Scrapbooks are strategically placed in small seating areas in an effort to promote conversation.

Dining We've designed a "safe" kitchen where residents can enjoy the sights, sounds and aromas of meal preparation. They may also actively participate by "lending a helping hand," thus providing a sense of purpose and an opportunity for social interaction.

Life Stations Imagine a desk set up for business, a workbench with tools, a laundry basket with clothes for folding, or a potting bench to use for gardening. We've created these activity areas known as "Life Stations" so that residents may participate in meaningful activities that they once enjoyed. Or for those who enjoyed the simple pleasures of being outdoors, a covered porch, secured outdoor walking paths and gardens have all been designed for that purpose. Those with "green thumbs" may also maintain their contact with nature by planting, hoeing, raking or weeding fresh flowers and homegrown vegetables and herbs.

Daily routine Each and every day is structured to give residents a sense of routine and predictability. A calendar of activities sets aside time for personal tasks such as grooming and dressing, and activities that help stimulate intellectual, physical, spiritual, purposeful and social interaction.

There are also occasions for family participation. Volunteering, creating personal memory scrapbooks, parties, family meetings and personal service plans are just a few of the ways we encourage family members to stay involved and maintain a growing and nurturing relationship with their loved one.

Next steps If someone in your family is affected by Alzheimer's disease or some other form of dementia, it is time to get acquainted with the numerous resources at your disposal.

? Join a support group, like the one facilitated by The Arbors.

? Familiarize yourself with professional resources.

? Make an appointment to tour The Arbors to learn more about our scope of services.

? Become a Future's List Depositor. This fully refundable deposit will keep your informed of upcoming events, research opportunities and allow you to interact with our community and caregivers before there is an urgent need.
? Establish your priority Wait List deposit. You will be contacted when an opening becomes available.
? The Arbors will open in September 2006. Please contact Homewood marketing director Kelly Reeder at 361-582-2100 for more information. The executive director is Sharon Andress, and the Arbors program coordinator is Deborah Maraggia, LVN. Homewood Residence hosts The Alzheimer's Support Group Meeting for Families and Caregivers the third Thursday of each month, 2:30-3:30 at Homewood Residence at Victoria.

Posted on Thu, Aug. 24, 2006
1199.Lessons in living　Montessori-based method eases symptoms of Alzheimer's
By JAN JARVIS
STAR-TELEGRAM STAFF WRITER
http://www.dfw.com/mld/dfw/
ARLINGTON -- At 89, Lester Atherton has golden brown hair that is thick and barely streaked with silver. His voice is strong and his concentration steady.

For 25 years he was a Realtor in Florida, a dedicated family man who raised two daughters with Grace, his wife of 63 years. After he retired he was active, working as a bailiff well into his 70s.

It's different now that Atherton has Alzheimer's disease.

Matching dominoes or working puzzles is the focus of his days. Simple tasks repeated over and over allow him to experience success, pleasure and independence. It's an approach borrowed from the Montessori Method, which was developed in 1907 by Maria Montessori and was originally used primarily to reach children then considered unteachable.

Most days Pam Stalewski can no longer carry on a conversation with Atherton. Her father rambles constantly about things she cannot understand. But there's comfort in seeing his face lost in concentration as he matches a pile of dominoes.

"He loves being busy," Stalewski says. "He was like that even before he had Alzheimer's."

The Montessori Method encourages children to learn by exploring, practicing and training themselves. At Arden Courts, an Alzheimer's assisted-living center in north Arlington, that approach is being used to improve the lives of people with dementia.

The Myers Research Institute in Ohio began applying Montessori principles at assisted-living facilities in 1995. The concept has begun catching on at centers around the country in recent years.

The sorting, manipulating and categorizing that is a staple of Montessori preschool classrooms works well in Alzheimer's facilities where puzzles, memory games and everyday items are used to improve motor skills, stimulate senses and reach out to people with dementia.

The goal of a Montessori-based education is to create independent members of society who care about themselves, others and the environment, said Megan Malone, lead trainer at the Meyers Research Institute at Menorah Park Center for Senior Living.

"The mission of the Montessori school is identical to the goals of a long-term care facility," she said. "It's just a different age group."

Everyday activities

Children, Montessori experts contend, love to learn and do their work, not so much to complete the job but for the sake of the activity itself. It's the same with people who have dementia. Their activities must be based on things they have enjoyed doing all of their lives, but with a little twist, Malone said.

A former piano teacher, for example, might enjoy categorizing musicians or sorting sheet music. A woman who took pride in being a wonderful hostess may find just as much pleasure in greeting people at the door. Someone who once had beautiful penmanship might derive satisfaction from signing Christmas cards.

Researchers have discovered that such activities can help Alzheimer's patients cope with "sundowning," or the agitation that escalates as the day comes to an end. Although some researchers associate the behavior with being overly tired, Noreen Gray of HCA Manor Care said she believes that people with dementia start to worry more about where they will sleep as night approaches.

"Imagine how you would feel if you thought you were going to Cancun, but when you got off the plane you're in Russia," Gray said. "That's what it's like to have Alzheimer's."

Meyers Research Institute studies have shown that Montessori-based activities can ease some of that stress.

"People are smiling and laughing as a result of the activities," Malone said. "There's a decrease in sleeping through activities and exhibiting anxiety."

The activities room at Arden Courts is filled with the materials of everyday life. There are socks to sort and flowers to water. People with dementia often find satisfaction in such repetition of movement, researchers say.

Residents are capable of doing things, but their tasks need to have a purpose, said Gray, who is director of lifestyle programming for HCR Manor Care, a long-term care provider with more than 50 Alzheimer's facilities nationwide, including Arden Courts.

"That's what Montessori does," she said. "It gives them a job, and that gives them a sense of self-worth."

"Polishing and organizing silverware can be very comforting to a person with dementia," Gray said. "Some people like to sweep. I don't care if the porch is swept 20 times a day if that is what gives them comfort."

The orderliness that is a hallmark of Montessori classrooms also works perfectly in an Alzheimer's facility, said Karen Brenner, a longtime Montessori educator, writer and consultant with Creative Care Alternatives in the Chicago area.

"A Montessori classroom is well-ordered, clean and neat; everything has its place," said Brenner, who trains caregivers nationwide. "That's the way a nursing home should be as well.

"You can't have a messy environment when you have a person with memory disorders; it becomes a real burden to them."

At Arden Courts, signs are used as step-by-step guides to everyday activities.

"In people with dementia, their start button is missing," Gray said. "When they read a sign that tells them to sit down and match the socks, it turns on their start button."

Other tools taken from the Montessori preschool classroom are used to help adults with dementia work more independently. Laminated templates, such as the outline of a plate or fork, make it easier to set the table. Trays provide boundaries and help small children focus, Gray said.

"It's the same thing with older adults who have a limited attention span," she said.

One recent afternoon at Arden Courts, Jeanne Edwards, Emma Martin and other residents laughed all the way through a memory game that involved finishing famous phrases.

"Better late than ..." Vyki Baker, an activities services assistant, read aloud as she held up a card with the words on it.

"Never," Edwards answered immediately.

"How many of you know someone who's never on time?" Baker asked.

"Just work for a doctor and you'll see what it means," said Edwards, who worked in a dentist's office for years.

The game is not only fun, it's a conversation starter and a way to connect, Baker said.

"They have no short-term memory," Baker said. "All of this is long-term."

Alzheimer's patients, Gray said, are like time travelers who are living in the 1940s and 1950s.

They love big-band music and Tony Bennett. Black-and-white photos and old movies.

Their ability to name things and recognize faces tends to go. But their "muscle memory," or procedural memory -- the kind filled with learned actions such as riding a bike -- remains intact.

"Montessori calls on that kind of memory to do the same movement over and over again," Brenner said.

It's why people with dementia can often read well, Malone said. They may need larger type and short sentences, but they often enjoy books, especially historical novels or biographies.

Better days

For the past decade, Florence Marcucci has watched Alzheimer's gradually rob her mother of her memory and judgment. Pearl Azzolin lived alone in Chicago and bowled for fun until she was 90.

But she eventually stopped cooking and caring for herself. At times, she would go out in 10-degree weather wearing only a sweater, Marcucci said. Azzolin would talk about her daughter as Florence sat beside her.

"It's just a really awful disease," Marcucci said. "She's not here, but she's not gone either."

Now 96, Azzolin rarely speaks to anyone.

Some days are better than others. Since she moved to Arden Courts two years ago, Azzolin has developed a sweet tooth and seems to find comfort in walking, said her daughter, who visits her mother daily for strolls around the building.

"One thing about Alzheimer's is you can't take it personally," Marcucci said.

Stalewski said that as her father's disease progressed, the once sweet and gentle man became moody and unpredictable. Sometimes her father would run outdoors and hide from her. Other times he would stick his favorite pillow in the kitchen drawer.

When he moved to Arden Courts in April, Stalewski didn't know what to expect. But he is clearly happier, she said, because he has things to do.

When the staff learned that Atherton loved to garden, they gave him the job of planting and watering bedding plants.

"He can walk forever and not realize he can't get out," she said. "And he has a friend here; she doesn't talk, but he talks to her while they walk."

All doors at the north Arlington center lead to places where residents can walk freely without getting in harm's way. Indoor porches have been built where residents can sit in rockers; outdoor paved paths loop back into the building.

Keeping Alzheimer's residents engaged is key to reaching those with dementia, Malone said.

"There's still a lot to be done while we're waiting for a cure," she said. "There are still things we can do to keep people with dementia happy and feeling good about where they are."

* * *

4 million

Americans with Alzheimer's disease

2003

When Alzheimer's surpassed diabetes, influenza and pneumonia as a cause of death for people 65 and older

80

Average age of diagnosis

3 percent

Men and women ages 65 to 74 who have the disease; by age 85 the risk reaches nearly 50 percent

SOURCES: Alzheimer's Association; National Institute on Aging

IN THE KNOW

Montessori-based activities

Motor skills such as grasping, scooping and pouring

Examples: Making Christmas ornaments, arranging flowers or cutting cloth.

Sensory activities stimulate and enhance senses

Examples: Smelling jars filled with strong aromas such as garlic and guessing the odor.

Cognitive activities that include recognition and discrimination

Examples: Playing song bingo, in which participants listen to a song and guess what the second verse is.

Activities of daily living using familiar experiences

Examples: Using a plate and utensil template to set the table; dusting, sweeping and folding towels.

SOURCE: Arden Courts Alzheimer's assisted-living center

IN THE KNOW

How to help

What: Memory Walk to benefit the Alzheimer's Association

When: The North Central Texas Chapter Walk begins at 9 a.m. Sept. 9

Where: TCU's Garvey-Rosenthal Soccer Stadium, 3600 W. Berry St. in Fort Worth

Cost: No registration fee, but a goal of $200 in donations is encouraged; to get a T-shirt, participants must raise $50

Details: Teams or individuals can participate.

Information: 817-336-4949 or www.alz.org/northcentraltexas/

Since 1989, Memory Walk has raised more than $200 million nationwide.

SOURCE: Alzheimer's Association

1200.SFU discovery could prevent Alzheimer's
http://www.canada.com/vancouversun/index.html
Nicholas Read, Vancouver Sun
Published: Thursday, August 24, 2006
A Simon Fraser University chemist has discovered what might be a way to prevent the onset of Alzheimer's disease.

David Vocadlo, a Canada Research Chair in chemical glycobiology, has synthesized a sugar-like molecule that helps inhibit the progression of Alzheimer's-like symptoms in mice.

And that, he says, could lead to the development of a similar chemical that would prevent Alzheimer's disease in people.

"It's really cool," he said in an interview Tuesday. "And it's very interesting. It has some real potential that we're excited about. Being a scientist, I'm always reserved about making claims, but it is exciting."

Alzheimer's disease can occur in people when a protein called the tau protein becomes "decorated" with too many phosphate molecules, Vocadlo explained.

Phosphate is a naturally-occurring compound in the body that affixes itself to certain cellular proteins and helps those proteins perform specific functions.

Sugar molecules derived from food sources act in the same way, so that the proper function of cell proteins often depends on the body maintaining a correct balance between the number of phosphates and sugars that attach themselves to these proteins. Too many or too few phosphates and/or sugars may cause the proteins to malfunction and lead to disease.

The tau protein is involved in enabling the proper flow of information between cells in the brain. If the protein is absent or begins to malfunction in some way, that flow is disrupted, and Alzheimer's can occur.

One of the ways this can happen, Vocadlo said, is if too many phosphate molecules become attached to the tau. No one knows what causes this irregularity, known as hyper-phosphorylation, but when it occurs, the tau proteins begin to malfunction and form long filaments which, in turn, form visible tangles in the brain, not unlike tangles of hair.

"The extent of these tangles in the brain has been correlated with the severity of [Alzheimer's] disease progression," Vocadlo says.

What he discovered in his laboratory is that when he introduces his synthesized sugar-like molecule into mice, the occurrence of these tangles diminished.

In other words, by helping to restore the proper balance of phosphates and sugars on the tau protein, he was able to reduce the level of phosphorylation that can lead to Alzheimer's disease-like symptoms in mice.

The chemical is introduced as a white powder which Vocadlo sprinkles on the animals' food.

So far, he says, tests have been limited to mice, and still more tests need to be conducted on animals before the molecule is ready to undergo clinical trials in people.

"We need to test it in the animal model for a long time," Vocadlo says.

But if those tests are successful, clinical trials in people would be the next logical step.

As a scientist, Vocadlo is loath to make any predictions beyond that, but he says if his research continues to proceed as he hopes, his molecule could prove to be an important tool in the fight to prevent Alzheimer's.

"And that's pretty exciting," he added.

nread@png.canwest.com

? The Vancouver Sun 2006