Relationships in the early onset of dementia

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The early stages when a spouse or an adult child becomes a caregiver for someone with Alzheimer's disease or another type of progressive dementia is fraught with a tug-of-war of emotions from resentment to protectiveness, according to a new study from the Mandel School of Applied Social Sciences at Case Western Reserve University.

"Little has been known about what happens in the everyday lives and in relationships in very early stages of the caregiving," said Kathryn Betts Adams, assistant professor of social work.

Adams examined the changing dynamics of familial relationships in the early onset of dementia. Her findings appear in the article, "The Transition to Caregiving: The Experience of Family Members Embarking on the Dementia Caregiving Career," in the November issue of the Journal of Gerontological Social Work.
She got a glimpse into the lives of these families through interviews with the spouses and children of individuals with dementia, through a study funded by the National Institute on Aging. Adams pointed out that many families are reluctant to see help until a crisis arises and forces the family to seek services. It can take some families up to two years before asking for that outside help. "At work in this early stage," Adam said, "there seems to be a strong desire to keep things as they were, to stick with familiar routines as much as possible, and to manage without resorting to obtaining extra help."

The role of caregiver begins when at least one daily task needs to be done for the care recipient. That can be a reminder to take a shower or to do a simple task the individual always performed. Adams reported that many family members began to take on more responsibilities - many they have not done before such as wives balancing checkbooks that once were husbands' responsibility and husbands taking on housekeeping tasks like doing dishes and laundry. She found that the early stage of caregiving is marked by many struggles with negotiating care and decision-making and that taking over responsibilities is not a smooth process for many caregivers.

Throughout the interviews, family members reported experiencing frustration, resentment, grief and loss of intimacy while at the same time increasing protectiveness and tenderness towards the person experiencing the dementia. The spouses also began to mourn the loss of their intimacy with their partners as roles shifted from a marital to caregiving. This information will enable social workers to help families transition and understand that what they are experiencing is normal for those individuals thrust into the caretaker role, said Adams. She added that social workers can also find ways to help individuals diagnosed with cognitive impairment to find ways to lead as normal a life as possible.

Statins May Be Good For Alzheimer's Disease

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November is National Alzheimer's Disease Awareness Month and also the 100th anniversary of the first report of Dr. Alois Alzheimer characterizing the hallmarks of the disease. Alzheimer's disease is the leading cause of dementia in the elderly, afflicting an estimated 4.5 million people in the U.S. and 15 million worldwide.
Statins are well-known, widely available cholesterol-lowering drugs with a well-established track record of safety and may offer a relatively straightforward regulatory path to a new treatment for Alzheimer’s disease. Statins are the biggest-selling prescription pills in pharmaceutical history with estimated 2004 global sales of $26 billion. Further trials are needed to advance these findings according to the editorial.
A newly published editorial in Expert Opinion on Investigational Drugs has concluded that statins, the widely used cholesterol drugs, “probably strike at the heart of the sporadic Alzheimer’s disease-inducing mechanism” (Expert Opin. Investig. Drugs (Dec. 2006) 15(12):1479-1485). The editorial, “Can statins put the brakes on Alzheimer’s disease?”, reviews current research into the potential benefits that statins may offer for the prevention or treatment of Alzheimer’s disease and concludes that statins can affect Alzheimer’s disease (AD) in at least two ways: by reducing cerebrovascular damage and by inhibiting some of the biochemical pathways believed to be implicated in the disease process.
This is more good news for Nymox Pharmaceutical Corporation (NASDAQ:NYMX), the company which holds U.S. and global patent rights for the use of statin drugs for the prevention and treatment of AD, including for patients at risk for AD because of vascular-related risk factors or disease.

Alzheimer's First Scan

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Researcher Stephen Carter of the School of Psychological Sciences is investigating the transition from mild cognitive impairment (MCI) to early AD, as MCI is often considered a precursor of Alzheimer's.

He will examine the physiological factors and mental processes at work during this transition, and hopes to determine whether reduced consumption of glucose in the brain is more closely linked to cognitive impairment than the deposition of the protein amyloid, which many believe to be the cause of AD.

The high-tech scans will also allow him to assess whether changes in connectivity between the part of the brain responsible for memory - the medial temporal lobe - and associated areas correlate with these types of cognitive dysfunction.

He said, "It is of significant clinical importance to be able to detect the early changes associated with Alzheimer's Disease and thereby enable more accurate diagnosis, as by the time dementia is currently diagnosed significant and irreversible brain damage has typically already taken place.

"Early detection could identify possible candidates for future clinical drug trials before large-scale global damage has occurred, which is essential for beneficial effects.

"Combining our new-breed, high-resolution PET scanner with MRI scanning in a single research environment allows us to compare the brain functions of MCI and probable AD patients in a unique way. Our machine also allows us to accurately measure amyloid deposition, which is not possible with standard PET scanners."

Co-supervisor Professor Alistair Burns of the University's Division of Psychiatry said: "This research is particularly timely given the recent decision by the National Institute for Clinical Excellence (NICE) not to make the drug Aricept available to patients with early Alzheimer's Disease. This could result in the first judicial review against NICE which I hope will overturn this decision, and the earlier we're able to diagnose the disease the quicker we'll be able to take action against the irreversible damage it brings."

The Centre's Director Professor Karl Herholz said: "We're thrilled to be carrying out this first patient brain scan, as it represents the whole essence of the WMIC; bridging the gap between advances in the lab and their application to help patients.

"With this series of experiments we hope that a convergent approach that investigates the multiple aspects of physiology and cognition at play in AD can be developed, which will enable early accurate diagnosis and distinguish MCI patients who will progress to full AD from those who will not."

Link between diabetes and Alzheimer's disease

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What's the evidence that diabetes could be a factor in the development of Alzheimer's disease? If so, what can you do to decrease the risk?
Here are now 17.5 million people with diabetes in North America and 5.5 million suffering from Alzheimer's disease. It's estimated that by 2050 the number of diabetes patients will reach 32 million and 18 million will have Alzheimer's.These huge numbers make you wonder if the diseases share a connection.

Researchers in Chicago studied 842 older Catholic nuns, priests and brothers who had diabetes. None had any sign of Alzheimer's disease at the start, but nine years later 151 had developed this disease.
Another study published in the Archives of Neurology in 2004 claimed that those with Type 2 diabetes had a 65% greater chance of developing Alzheimer's disease. But how does Type 2 diabetes increase this risk?
Dr. Gregory Cole, a researcher at the University of California, says that excess weight causes not only diabetes, but also insulin resistance in which cells do not respond to the hormone insulin.
Insulin normally transports sugar (glucose) into cells where it's used as energy. But when insulin resistance occurs, cells fail to get sufficient sugar. And brain cells starved of sugar may either malfunction or die, setting the stage for Alzheimer's disease.
Cole suggests the entire process may be kicked off by too much fat in the diet. In one experiment Cole fed rats a high-fat diet causing insulin resistance. This in turn resulted in a buildup of poisonous protein called beta amyloid.
Beta amyloid clumps together, damaging brain cells and the connections between them. This is believed to play a major role in memory loss.
We also know that diabetes results in atherosclerosis, a narrowing of arteries which results in a decrease of oxygenated blood to organs. This is why so many diabetics die from heart attack, blindness, kidney failure and gangrene of the legs. Without oxygen we die. And brain cells are even more dependant on an adequate supply of oxygen.
Undoubtedly other factors play a role in the development of Alzheimer's disease. But this research shows again what we so often see in medicine, one problem leading to another often bigger one. In this case it's a huge one.
A report from the World Health Organization shows that 75% of Americans over the age of 50 have insulin resistance. Not surprising, since obesity is so rampant in the U.S. where every meal is super-size.

PREVENT IT

1. If you're overweight, take it seriously and lose pounds. Even a modest loss of 10 pounds can either improve or prevent insulin resistance.
2. Build activity into your life by walking, running or biking. Exercise helps insulin to be more efficient.
3. Concentrate on a low-fat diet that contains whole grains, fruits and vegetables and fish (fish contains healthy omega-3 fatty acids, a fat that may help to lower the risk of Alzheimer's).

You don't know you're gaining weight if you don't have a scale!

Dementia Care

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"Caring for a loved one with dementia presents a number of challenges that can seriously compromise the caregiver's quality of life," said Dr. Louis Burgio, Distinguished Research Professor at the Center for Mental Health and Aging at The University of Alabama and principal investigator at one of the five study sites. "For the millions of Americans who care for a loved one at home, an intervention that can improve their quality of life and lessen the burden of caregiving can make meaningful differences in their ability to better care both for themselves and their loved ones," he said.

The findings are significant, according to the researchers, because not only is caring for a loved one with dementia stressful, but the experience can contribute to the development of psychiatric and physical illnesses and increased risk for death among the caregivers.
The researchers found that, overall, the intervention was effective across racial and ethnic groups, with the most significant improvements among Hispanic and white caregivers. In African-Americans, the intervention was effective among spouse-caregivers, but relatively ineffective among caregivers who were caring for a relative other than their husband or wife.

The study enrolled 642 people who were caring for a relative with Alzheimer's disease or a related disorder at sites in Birmingham and Tuscaloosa, Ala.; Memphis, Tenn.; Miami; Palo Alto, Calif.; and Philadelphia. Hispanics, whites and African-Americans were evenly represented. The more than 200 participants in each ethnic group were randomized to receive either the intervention or an approach used for controlled comparison.

Hispanic and white participants saw the greatest benefit. African-American spouse-caregivers also saw improvement in the problem areas as a result of the intervention, while African-Americans caring for a non-spousal relative did not see any benefit.
In the intervention group, Hispanics had the greatest improvement in reduction of caregiver depressive symptoms and problem behaviors of the recipient. Whites saw the most impact in the area of social support, and African-American spouse-caregivers had the most positive outcome in reducing the caregiver burden and improving self-care.
At the six-month follow-up, the rate of clinical depression was significantly lower among participants who received the intervention from those in the control group. Caregivers also reported that the intervention helped them feel more confident and able to deal with caring for their loved one, improved the care-recipient's quality of life and helped them keep the recipient at home.

"Medicine doesn't work in the same way across all races and ethnicities, or even from person-to-person," said Burgio, the researcher in The University of Alabama's College of Arts and Sciences. "Health professionals need to identify caregivers whose quality of life has been compromised and help them to get the help they need, for their sake and the sake of their loved ones."

The study intervention was developed based on findings from the first phase of this study, Resources for Enhancing Alzheimer's Caregiver Health (REACH) I, in which multiple caregiver interventions were studied to identify which were the most promising.

An Explanation Memory And Cognitive Decline In Alzheimer's Disease

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A discovery on how neural circuitry develops to aid proper cerebral cortex activity may help explain the memory and cognitive decline seen in Alzheimer's disease patients - a discovery that could point toward potential treatments, according to UC Irvine scientists.

The study uncovers how cholinergic neuronal circuits, which help the cerebral cortex process information more efficiently, rely on neurotrophin-3, a chemical that stimulates nerve growth. The scientists have determined the circuits need this chemical in order to recognize and reach their target nerve cells in the brain.

Richard Robertson, professor of anatomy and neurobiology, and other researchers from UCI's School of Medicine found that cholinergic nerve fibers grow toward sources of neurotrophin-3 during early development. In experiments with mice, without neurotrophin-3 to direct growth, the developing cholinergic nerve fibers appeared to not recognize their normal target cells in the brain. Because of this, the axon nerve fibers aided by these circuits grew irregularly and missed their specific target neural cells.

This finding, according to Robertson, has significant implications for neurodegenerative diseases like Alzheimer's. Cholinergic neuronal circuits play a key role in the proper information processing by the cerebral cortex and other areas of the brain. The cerebral cortex is the part of the brain that determines intelligence, personality, and planning and organization, and these actions are compromised by neurodegenerative diseases.

"Studies on the brains of Alzheimer's patients have shown a marked decline in these cholinergic circuits. Our work demonstrates that neurotrophin-3 is essential to maintain the connections to cerebral cortex neurons," Robertson said. "This study shows that a neurotrophin-3 therapy may be able to induce nerve fibers to regrow in the cerebral cortex, which would be beneficial to people with Alzheimer's."

Study results appear in the Dec. 1 issue of the journal Neuroscience.

In further studies on this subject, supported by a recently awarded three-year grant from the Alzheimer's Association, Robertson and his colleagues are testing the respective roles of nerve growth factor and neurotrophin-3 in a laboratory model of Alzheimer's disease. Laboratory rats with experimental damage to forebrain cholinergic circuits will be treated with either nerve growth factor or neurotrophin-3, or a combination of both, to determine their ability to produce anatomical, molecular and behavioral recovery.

Yeast Model As Alzheimer's Test

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A U.S. scientist has developed a research tool that might provide a means of treating the earliest stage of Alzheimer`s disease.
Alzheimer`s disease is characterized by the formation of plaques in the brain largely composed of fibers made from a peptide called beta-amyloid, or A-beta. While earlier research suggested A-beta fiber caused Alzheimer`s, recent research points at much smaller aggregates of the peptide as the culprit.

'We`ve developed a yeast model system in which A-beta small aggregate formation can be detected,' said University of Illinois-Chicago Professor Susan Liebman. 'The system employs a fusion of the human A-beta peptide to a functional yeast protein, called a reporter protein, which is only active in allowing cells to grow on test media if the fusion does not form aggregates.' "One promising, emerging approach for treatment of Alzheimer's disease is to prevent these smaller aggregates from forming," said Liebman. "Disruption of these small aggregates rather than the larger fibers seems prudent since inhibition of A-beta fiber formation might cause the smaller aggregate species to accumulate, and since inhibiting smaller aggregate formation should also prevent the initial formation of the fibers."

Liebman said the yeast model system can be used to develop a high throughput assay to screen small molecules to find those that inhibit the A-beta dependent aggregation. Once that is perfected, animal and human trials would follow.

The findings were reported in BMC Biology. It was the journal's most viewed article this past month. UIC graduate student Sviatoslav Bagriantsev worked on the project in Liebman's laboratory and co-authored the paper.

Insight Into Alzheimer's Disease

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Tesseur and Wyss-Coray hypothesized that by protecting neurons, TGF-beta may help prevent Alzheimer's disease. If the TGF-beta pathway is turned off, the brain becomes more susceptible to a toxic buildup of proteins. "We tried to see what happens if we block neurons from getting this beneficial signal," said Wyss-Coray.

To investigate that hypothesis, the researchers genetically engineered mice with a defect similar to the one they found in the brains of Alzheimer's patients: These mice had brain cells that could no longer respond to TGF-beta's salutary signal. The mutation did not directly affect the TGF-beta protein, which is found throughout the body. Instead, it blocked brain cells' ability to detect and respond to the molecule. This way, the TGF-beta pathway was active everywhere else besides the neurons of the mice. Unable to receive the beneficial TGF-beta signal, the rodents with the broken pathway showed signs of Alzheimer's disease. Brain cells died as the mice grew older, and the cells failed to make connections to other brain cells, a defining trait of the cells.

The results were even more striking when the researchers blocked the TGF-beta pathway in mice that were already susceptible to an Alzheimer's-like disease. These mice had a rare version of a human gene that causes people to develop Alzheimer's in their 40s and 50s, said Wyss-Coray. Blocking TGF-beta in these mice caused the animals to display signs of Alzheimer's disease that researchers had until then failed to recreate. The brains of the mice had more dead cells and a protein buildup characteristic of the disease in humans.

"Our study offers the possibility that if you have a reduction in this pathway, then you can accelerate the pathology," said Wyss-Coray. The flip side is that activating the TGF-beta pathway may offer a treatment for Alzheimer's, he said. In the past, researchers have tried using molecules that work like TGF-beta to provide protection against Alzheimer's, but they had trouble getting them into the brain, said Wyss-Coray. Those proteins, or the cells used to carry them, are too large to enter the brain through the bloodstream.

To sidestep that problem, Wyss-Coray is working with chemists to identify small molecules - drugs - that can boost the TGF-beta pathway in neurons. Because of TGF-beta's many roles in the body, Wyss-Coray will also be searching for molecules that act only on brain cells. He will test whether these drugs can ameliorate the Alzheimer's-like disease he created in mice. Wyss-Coray said that for now the strategy is "wishful thinking," but based on the results of this study, it's worth trying.

Reduced oxygen flow leads to AD

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Scientists have proved that illnesses which reduce blood flow, including strokes and heart attacks, are likely to lead the sufferer developing Alzheimer's disease (AD).

The theory has been circulated round medical circles for a long time, but this is the first instance which has provided a concrete molecular explanation.
Led by Mr Weihong Song, the team of scientists came from University of British Columbia in Vancouver, Canada. Mr Song explained how the theory had been proven:
"If you have less oxygen, you turn up this gene and obviously generate more beta-amyloid [protein]. If you have a higher level of beta-amyloid, you form more plaque. If you have this plaque, then you will have dementia."
Beta-amyloid collects in knots in the brains of people with AD and it is this action which is thought to cause brain damage.
The link between low oxygen and plaque formation is thought to be a gene called BACE 1 and in studies with mice, this gene's activity increased when it was denied a regular supply of oxygen.
Rebecca Wood, chief executive of the Alzheimer's Research Trust, told the BBC: "We hope that research in this area could suggest new methods to prevent and treat dementia in the future, particularly for those individuals who have suffered head trauma or a stroke."
Professor Clive Ballard, director of research at the Alzheimer's Society, added that regular exercise could aid prevention of dementia because it provides the brain with a regular supply of fresh blood.

Metals In Alzheimer's Disease

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Alzheimer's disease (AD) is a devastating condition and its causes are still largely unknown. Various metals have been implicated as possible contributors to the development of AD. In a special double issue of the Journal of Alzheimer's Disease published in November 2006, guest editors Andrei C. Miu and Oana Benga have brought together 14 insightful articles that explore the roles that metals play in the biochemistry and physiology of AD. The articles cover six major categories: Comprehensive historical reviews, methodological perspectives, a topical review, integrative genetic and epigenetic reports, a review of risk factors and a "benchmark to clinical" review:
- the four-decades-old controversy about aluminum neurotoxicity, examining data on the possible cellular mechanisms underlying aluminum neurotoxicity and potential neuroprotective strategies against aluminum toxicity.
- how metal ions such as zinc and copper can potentiate Alzheimer's disease by participating in the aggregation of normal cellular proteins and in the generation of reactive oxygen species.
- how aluminum and copper can initiate or propagate an inflammatory response in the aging brain.
- metals found in plaque cores in AD brains and concludes that aluminum and iron could cause oxidative damage but copper and zinc likely do not.
- history of aluminum's hypothetical role in AD and several lines of evidence for involvement of aluminum as a secondary aggravating factor or risk factor and argue that further studies are warranted.
- the methodologies that have been used to identify Alzheimer- and dementia-related targets for exogenous toxins.
- recent approaches to locate and identify iron compounds in neurodegenerative tissue. In addition to complementary techniques that allow them to quantify and identify iron compounds using magnetometry, extraction and electron microscopy, they utilize a powerful combined mapping/characterization approach with synchrotron X-rays.
- the movement of metals across the blood-brain barrier and a number of transporters are described that could mediate metal transport into and out of the brain.
- model of amyloid-beta induced heme-deficiency that could account for neurodegeneration in AD patients.
- how presenelins can trigger a cascade of processes that lead to amyloid-beta production, leading to AD.
- the apoE4 isoform of apolipoprotein E and the nucleation, growth and reversibility of amyloid-beta deposition in mice should shed new light on this genetic risk factor for AD.
- the possible role of macronutrients and the basic elements of carbohydrates, proteins, and fat in the development of AD.
- the role of aluminum and metals such as copper and zinc in AD, as well as on metal chelator therapy as a potential treatment for AD. The effects of aluminum, copper and zinc chelating agents on amyloid-beta plaques are reviewed.

Healthy diets, antioxidant supplements, and the prevention of nutritional deficiencies or exposure to foods and water with high content of metals could be considered the first line of defense against the development and progression of cognitive decline.

Senile plaques in natural course of Alzheimer disease

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A recent report describes regression-stage senile plaques in the natural course of Alzheimer disease.
"Resolution process of cerebroparenchymal amyloid beta-protein (Abeta) deposition has become of increasing interest in the light of recent advance in the Abeta vaccination therapy for Alzheimer disease (AD). However, the neuropathological features of degraded and disappearing senile plaque remain poorly characterized, especially in the natural course of the disease," scientists in Japan report.

"To clarify the natural removal processes of Abeta burden in the brain with AD, we devised a triple-step staining method: Bodian for dystrophic neurites, anti-glial fibrillary acidic protein for astrocytes, and anti-Abeta," said Takashi Oide at Musashi Hospital and collaborators in Japan. "We thus examined 24 autopsied AD brains. A novel form of senile plaques, termed 'remnant plaques', was identified."

Oide and associates stated, "Remnant plaques were characterized by mesh-like astroglial fibrils within the entire plaque part, Abeta deposit debris exhibiting weak Abeta immunoreactivity, and only a few slender dystrophic neurites. In remnant plaques, amyloid burden was apparently decreased. The density of remnant plaques increased significantly with disease duration. Dual-labeling immunohistochemistry revealed many Abeta-immunoreactive granules in astrocytes and a modest number in microglia, both of which accumulated in senile plaques."

"We consider amyloid deposits of diffuse and neuritic plaques to be shredded by astrocytic processes from the marginal zone of plaques, and to gradually disintegrate into smaller compartments," stated the investigators."

They concluded, "Cerebroparenchymal Abeta deposits undergo degradation. After a long-standing resolution process, diffuse and neuritic plaques may finally proceed to remnant plaques. Astrocytes are actively engaged in the natural Abeta clearance mechanism in advanced stage AD brains, which may provide clues for developing new therapeutic strategies for AD."

Oide and coauthors published their study in Neuropathology and Applied Neurobiology (Regression stage senile plaques in the natural course of Alzheimer's disease. Neuropathol Appl Neurobiol, 2006;32(5):539-556).

Alzheimer's Drug Restriction

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After the National Institute for Clinical Excellence (NICE), UK, recommended restricting the use of Alzheimer's drug, Aricept (donepezil), Eisai and Pfizer, the makers, say they plan to apply for a judicial review regarding NICE's decision. Eisai and Pfizer claim the process used by NICE for this guidance was not fair. They say it is illegal and irrational.
Eisai and Pfizer say NICE should use a more accurate and cost effective model and data.
NICE had decided that National Health Service (NHS) patients who have just* been diagnosed with Alzheimer's disease should not receive prescribed Aricept. In the UK anyone receiving an NHS prescription pays just £6.50 ($12) for the one-month-course - NHS patients over 65 get their prescriptions free. If a patient has to buy the drug privately it will cost £2.50 ($4.80) per day.

Alzheimer's support groups throughout England and Wales are pleased NICE will be challenged. They state that NICE's decision has serious consequences for thousands of people throughout the country. The Alzheimer's Society is organizing a series of protest marches.
Here is a quote from the Alzheimer's Society:
"What sort of society have we become when the health of hundreds of thousands are sold to save just £2.50 a day? This blatant cost cutting will rob people of priceless time early in the disease and later clinicians will have no choice but to use dangerous sedatives that increase the risk of heart disease and stroke. This is victimisation of the most vulnerable in society and today is an opportunity for people to take a stand."

Alzheimer's test developed

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Amyloid beta protein accumulates in the brain in Alzheimer's disease but whether the body produces too much or cannot break it down is unclear.
But by labelling the protein with a carbon isotope, doctors can measure the rate of turnover, a report in Nature Medicine suggests.
Experts said the test could help improve diagnosis and treatment.
Doctors are already able to measure amounts of amyloid beta protein - or abeta - in the cerebrospinal fluid but that doesn't indicate why the build-up is occurring.
By working out whether the body is producing too much or is unable to break it down, researchers develop drugs too accurately target the right process.

Furthermore, the test may also prove useful in the diagnosis of Alzheimer's prior to the onset of clinical symptoms.
The team at the Washington School of Medicine gave eight healthy volunteers an intravenous infusion which contained an amino acid - Leucine - that had carbon molecules with one extra neutron.
They then took samples of cerebral spinal fluid - the fluid that surrounds the brain - over a period of 36 hours.
The body uses amino acids to form proteins so the researchers were able to measure how the carbon isotope was taken up in the production of amyloid beta protein and then how long it took to break the labelled proteins down.

Dimebon(TM) for Alzheimer's

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"Given the safety and significant efficacy data generated in our recently completed Phase 2 trial in Alzheimer's disease, we believe that aggressive development of Dimebon is clearly merited," said David Hung, M.D., president and chief executive officer of Medivation. "We, therefore, are pleased to announce a comprehensive clinical development program that we believe puts us on-track to apply for marketing approval in Alzheimer's disease in 2010. "

To support these target submission dates, Medivation intends to conduct global Phase 3 development programs in Alzheimer's disease and Huntington's disease beginning in 2008. For 2007, Dimebon development will focus on completing efficacy studies in both Alzheimer's diseases, and preparing for global Phase 3 studies. Key Dimebon development activities in 2007 include:

-- Completing Alzheimer's disease one-year Phase 2 efficacy trial (Russia);

-- Conducting Phase 1 clinical trial (U.S.);

-- Conducting Alzheimer's disease Phase 2 dose finding clinical trial (U.S.);

-- Manufacturing Dimebon for use in global Phase 3 clinical trials.

"Because of Dimebon's long history of commercial use in Russia, we had the unusual opportunity to proceed directly to a large efficacy study with the same duration of treatment and clinical endpoints used by the U.S. Food and Drug Administration (FDA) to approve drugs for mild to moderate Alzheimer's disease," explained Lynn Seely, M.D., chief medical officer of Medivation. "Taking this approach provided us with risk-reducing data on the safety and efficacy of Dimebon in Alzheimer's patients sooner than would have been possible under a more traditional drug development pathway. Moving forward, we will complete standard regulatory requirements before starting Phase 3 in Alzheimer's disease."

Lower Dementia Risk And Higher Level Of Fatty Acid

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Individuals who have higher levels of a fatty acid known as docosahexaenoic acid (DHA) in their blood may have a significantly lower risk of developing dementia and Alzheimer's disease, according to a report in the November issue of Archives of Neurology, one of the JAMA/Archives journals.
Ernst J. Schaefer, M.D., Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, and colleagues studied the association between DHA levels and dementia in the blood of 899 men and women who were part of the population-based Framingham Heart Study. The participants of an average age of 76 years provided blood samples and underwent neuropsychological testing, and were followed for an average of nine years. A subgroup of 488 also filled out a questionnaire assessing their diet, including information about fish consumption. None of the participants had dementia at the beginning of the study; and they were given a mental examination every two years to screen for its development.

Through the nine-year study period, 99 out of 899 participants developed dementia, including 71 with Alzheimer's disease. After controlling for other known risk factors for dementia, including age and homocysteine levels, and dividing the study population into fourths (quartiles) based on levels of DHA, the researchers found that men and women in the quartile with the highest DHA levels had a 47 percent lower risk of developing dementia and 39 percent lower risk of developing Alzheimer's disease than the other three quartiles with lower DHA levels. Among the participants who completed the dietary questionnaire, those in the top quartile of blood DHA levels reported that they ate an average of .18 grams of DHA a day and an average of three fish servings a week. Participants in the other quartiles ate substantially less fish. DHA levels in the blood vary by the degree to which the liver converts alpha-linolenic acid, an essential fatty acid, to DHA and also by the amount of DHA in the diet. "In our study, the correlation between [blood] DHA content and fish intake was significant, indicating that fish intake is an important source of dietary DHA," the authors write.

"In the future, it will also be important to determine whether combined dietary supplementation with DHA can decrease further mental deterioration in patients with established dementia," they conclude.

Remnant plaques plaques in Alzheimer disease

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"Resolution process of cerebroparenchymal amyloid beta-protein (Abeta) deposition has become of increasing interest in the light of recent advance in the Abeta vaccination therapy for Alzheimer disease (AD). However, the neuropathological features of degraded and disappearing senile plaque remain poorly characterized, especially in the natural course of the disease," scientists in Japan report.

"To clarify the natural removal processes of Abeta burden in the brain with AD, we devised a triple-step staining method: Bodian for dystrophic neurites, anti-glial fibrillary acidic protein for astrocytes, and anti-Abeta," said Takashi Oide at Musashi Hospital and collaborators in Japan. "We thus examined 24 autopsied AD brains. A novel form of senile plaques, termed 'remnant plaques', was identified." Oide and associates stated, "Remnant plaques were characterized by mesh-like astroglial fibrils within the entire plaque part, Abeta deposit debris exhibiting weak Abeta immunoreactivity, and only a few slender dystrophic neurites. In remnant plaques, amyloid burden was apparently decreased. The density of remnant plaques increased significantly with disease duration. Dual-labeling immunohistochemistry revealed many Abeta-immunoreactive granules in astrocytes and a modest number in microglia, both of which accumulated in senile plaques."

"We consider amyloid deposits of diffuse and neuritic plaques to be shredded by astrocytic processes from the marginal zone of plaques, and to gradually disintegrate into smaller compartments," stated the investigators." They concluded, "Cerebroparenchymal Abeta deposits undergo degradation. After a long-standing resolution process, diffuse and neuritic plaques may finally proceed to remnant plaques. Astrocytes are actively engaged in the natural Abeta clearance mechanism in advanced stage AD brains, which may provide clues for developing new therapeutic strategies for AD."

Possible approach to treating Alzheimer's Disease

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The disease, which progessively damages memory and cognitive functioning, typically occurs when cells in the brain overproduce a protein called amyloid-B, or beta amyloid, and create a damaging plaque material. To stop the development of Alzheimer's disease, scientists must create a medication that inhibits beta amyloid production, increases cells' ability to rid the brain of that protein, or both. That is, they have to turn off the faucet and open one or two chemical "drains" to solve the problem. Stopping beta amyloid over-production cannot be the only potential solution, he said.

"That only represents about 5 percent of all Alzheimer's cases," he said. "And we know that in most cases, the 'faucet' is not turned up. That leads to the other possibility which is that one or more 'drains' are clogged. So you get the same effect but for a different reason." Leissring, two other Scripps Florida scientists, and three Florida Atlantic University undergraduates are performing research on this type of dementia.

For many years, much of Alzheimer's research focused on stopping beta amyloid production. Now, with the University of Chicago/Argonne National Laboratory discovery, scientists are working to activate IDE. The Scripps Florida team is focusing on that approach.

Leissring has studied this angle with his former Brigham and Women's Hospital colleague Dennis Selkoe, a leader in Alzheimer's disease research. The two scientists reviewed and wrote commentary about the Shen and company breakthrough for the online edition of the journal Nature. "Selkoe could win the Nobel Prize for his Alzheimer's research," Leissring said.

"Our group was the first to show that if you increase the drainage system by increasing the amount of these proteases that degrade beta amyloid, we could completely prevent Alzheimer's disease inside an animal model," Leissring said. Proteases start and stop enzymatic activity by cutting the molecular link between amino acids. Scripps scientists are aided by a $10 million Kalypsys research robot that can quickly screen thousands of chemical compounds a day for potential drug uses. Scripps is the only academic facility with such a device, he said. The institution, however, needs more funds to keep its laboratories running. "I was over budget the day I walked into the lab. Currently government funding is at record lows. It's just tragic because there are so many new opportunities that have emerged in the last five to 10 years. We really should be accelerating," he said.

Coffee the cure?

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Those cups of coffee you drink every day could be staving off your chance of getting Alzheimer’s.
A recent study at Byrd Alzheimer’s Institute, Tampa, Fla., suggests daily caffeine consumption can reduce the risk of degenerative brain diseases such as Alzheimer’s and Parkinson’s.
“We think it might protect against Alzheimer’s,” said Dr. Gary W. Arendash, the leading researcher for the long-term study that used mice bred with the abnormal protein, beta-amyloid, that is believed to cause Alzheimer’s. Beta-amyloid molecules, formed by two enzymes, accumulate and create plaque within the brain. This causes dysfunction and death of brain cells that control learning and memory.
Alzheimer-stricken mice that consumed caffeine-spiked drinking water performed much better, including finding their way through a maze, than the Alzheimer-stricken mice without caffeine. Arendash said the mice without caffeine seemed lost and confused.
“Caffeine gets into the brain quickly,” Arendash said. The advantage of caffeine, since it decreases the levels of enzymes in the beta-amyloid protein, is it is readily available and fights disease unlike any other drug on the market today.

“Caffeine is the most widely-used psychoactive drug in the world,” Arendash said. “It is not addictive in the sense of heroin or alcohol. People who have been taking caffeine, if they stop cold turkey, they will have caffeine withdrawal. You can gradually get off it.”
However, Arendash cautioned people who have a sensitivity to caffeine to avoid it or take lower dosages. Caffeine may cause hypertension and high blood pressure, although Arendash disputed this theories.
In pregnant women, he said caffeine can cause low birth weight and spontaneous abortion, but no birth effects are known to be associated with caffeine. In older adults, caffeine may counteract their medication.
Note that caffeine is a diuretic, so drink plenty of water and take extra calcium. Consultant your physician before starting any caffeine regimen.
“We have so few things we can recommend people can do to fight Alzheimer’s,” Arendash said. “You need to strongly consider (caffeine) if Alzheimer’s runs in your family. Anything that can reduce the risk, this is very important. It can slow down the progression.”

The study’s results were published in the online version of the medical journal, Neuroscience.

Promise for Alzheimer's
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Scientists may soon be launching another assault on Alzheimer's disease.

Researchers from Merck have identified a gene important in production of the sticky protein that clogs the brains of Alzheimer's patients.
"If we can block the action of this gene, we could have a potential therapeutic," said Dr. David Stone, lead scientist of the research conducted over three years at Merck's laboratories in Seattle.

The protein, called amyloid beta, is believed to be a major factor in Alzheimer's. It binds to brain cells, killing them and impairing memory, reason and the ability to move and speak. The gene found by Stone and his colleagues is important in the way cells use an enzyme to cut a larger protein to form amyloid beta. The scientists aren't exactly sure how the gene works. But when they stopped its action in human cells in the laboratory, they found it reduced production of the toxic amyloid beta by about half.

The gene is believed active in the form of Alzheimer's disease that begins later in life, after age 65. Most of the genetic research has been on a form that affects younger people.

Researchers are especially enthusiastic about the discovery because the gene is on a chromosome previously linked to Alzheimer's, though no one knew why. And it is active in parts of the brain known to be susceptible to the disease. "It's an excellent candidate gene (for a drug) at this point," said Stone, who is now based at Merck's West Point, Pa., laboratories. The research is reported in this week's online edition of the Proceedings of the National Academy of Sciences.

About 4.5 million people in the U.S. have Alzheimer's disease. But researchers believe that as the population ages, that could grow to 16 million by 2050. Just last week, the 100th anniversary of the identification of the disease by Alios Alzheimer was observed in Tubingen, Germany. Scientists from around the world gathered to discuss both the earliest and latest findings about the disease.

Drugs now approved to treat the disease slow symptoms, but they typically are effective for only a few years. Another drug, made by Eli Lilly, is now being tested in humans. It is designed to stop production of an enzyme important in amyloid beta production. Stone said the Merck team is now observing how amyloid beta production is affected in mice when the gene is removed. He said it is difficult to know when a drug could be developed and when testing it could begin in humans. If all goes well, it would be at least five to seven years before a new drug could be on the market.

The Seattle researchers screened more than 15,000 genes before finding the one they're pinning their hopes on: Leucine Rich Repeat Transmembrane 3. They used a technique that actually blocked the gene's activity to learn its function. Stone said the gene appears to be active only in the brain, so a drug acting on the gene is not likely to affect any other part of the body, he said. Dr. Gerard Schellenberg, a geneticist at the Veterans Affairs medical center in Seattle, said the Merck-discovered gene may well have promise as a drug target.

Brain electric stimulation and memory

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Stimulating the brain with gentle electric currents boosts memory, German scientists said.

When they applied several currents that mimic natural slow oscillating brain waves in sleep they enhanced the memory. "It leads to improved memory retention," said Jan Born, a neuroscientist at the University of Luebeck.

The scientists, believe brain stimulation could help people with memory problems and Alzheimer's disease. "This is an alternative way to intensify or to improve sleep and its memory function," Born told Reuters.

He and his team asked the students to learn a list of paired words in a standard memory test before they fell asleep. The researchers stimulated their brain while they slept. After they woke up, the students had to recall the words they had memorized. If the currents were applied to the scalp during deep sleep, the first few hours of nocturnal sleep, the students recalled a greater number of words than if they had been given a sham brain stimulation. "It is an eight percent increase overall. This is a striking increase," he added.

The students did not feel any sensation from the currents to the frontal cortex of the brain or any adverse side effects. The currents forced the brain more into the deep slow-wave sleep to improve the memory function, according to the scientists.

Memory function in the medical students was already very good before they received the brain stimulation but the currents managed to improve it. "There is growing evidence that you can very effectively manipulate brain function by different types of electrical simulation," Born said.

He believes the natural slow oscillations and those induced by the electrical currents affect the hippocampus area of the brain which plays a part in memory. "The slow oscillations during slow-wave sleep trigger a kind of replay of these memories in the hippocampus," he added.

The hippocampus is one of the first regions of the brain that is damaged in patients with Alzheimer's disease, a degenerative illness that robs people of their memory and cognitive ability.

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Diabetes and Alzheimer's

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Diabetes — a strong risk factor for dementias like Alzheimer's — also becomes more common with age. Type 2 diabetes, which is by far the most common form of the disease, often occurs in people who weigh too much and exercise too little — a group that includes a large proportion of baby boomers. If you already have diabetes, controlling your blood sugar with diet and medication, if needed, appears to decrease your risk of Alzheimer's.

How diabetes accelerates dementia
Your body changes the food you eat into glucose, the sugar that fuels all your cells. People who have type 1 diabetes don't produce enough insulin, a hormone that makes it possible for glucose to enter your cells. People with type 2 diabetes produce enough insulin, but their cells resist the hormone's action and fail to take up enough glucose.

Scientists have identified several ways:

High blood sugar and blood vessel damage
When your blood sugar is too high, it damages your blood vessels. This damage may first become evident in the tiny vessels of your eyes and feet, but it can also affect your brain. Small-vessel damage in the brain often contributes to vascular dementia.
While vascular dementia and Alzheimer's disease are separate types of dementia, they often occur together. Some scientists have suggested that vascular dementia may deplete a person's cognitive reserve, making Alzheimer's symptoms appear earlier.

Insulin in the brain
Before full-blown type 2 diabetes develops, your body becomes less responsive to insulin. The result is elevated blood sugar, a condition sometimes referred to as prediabetes. Your body compensates by producing more insulin.
A modest increase in insulin makes more glucose available to brain cells, resulting in improved memory. But if you're insulin resistant and the level of insulin in your bloodstream remains high, the brain takes measures to slow the transport of insulin across the blood-brain barrier. That reduces the amount of insulin in the brain, making less glucose available to nourish brain cells.
Researchers have found that some people with Alzheimer's experience improved memory when they use a nasal spray containing insulin. The nasal spray bypasses the bloodstream to deliver the insulin directly to the brain.

Insulin, amyloid and inflammation
Excessive insulin in the bloodstream may trigger increased production of beta-amyloid, a segment of a protein the body normally makes. In Alzheimer's disease, beta-amyloid builds up in the brain, forming clumps, or amyloid plaques. Excess insulin may also be responsible for brain cells' failure to clear beta-amyloid.
This whole process appears to be worsened by inflammation, another side effect of high levels of insulin in the blood.

Reduce your risk

You can counter insulin resistance through modest weight loss and exercise.

You can cut your risk in half
by
losing 5 percent of your body weight

— 10 pounds for a 200-pound person —

by
exercising - 30 minutes most days of the week -

In addition to reducing your risk of diabetes and Alzheimer's, these lifestyle changes can also help protect you from heart attacks and strokes.

New Screening Tool Detects Early Cognitive Problems

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A screening tool for dementia developed by Saint Louis University geriatricians appears to work better in identifying mild cognitive problems in the elderly than the commonly used Mini Mental Status Examination, according to a new study.
Physicians routinely administer the Mini Mental Status Examination (MMSE) to patients who they believe may have Alzheimer's disease. Both the MMSE and SLU's screening tool --- the Saint Louis University Mental Status Examination (SLUMS) --- indicate to doctors when they should pursue further testing in diagnosing dementia.
"This early detection of mild neurocognitive disorder by the SLUMS offers the opportunity for the clinicians to begin early treatment as it becomes available," says Syed Tariq, M.D., lead author and associate professor of geriatric medicine at Saint Louis University.
John Morley, M.D., director of the division of geriatric medicine at Saint Louis University, created the SLUMS to screen more educated patients and to detect early cognitive problems.
"There are potential treatments available and they slow down the progression of the disease," says Morley, who is a coinvestigator. "The earlier you treat, the better people seem to do. But families go through denial and sometimes miss diagnosing dementia until its symptoms are no longer mild."
The researchers found the new screening tool developed by SLU detects early cognitive problems missed by the MMSE.
"The Mini Mental Status Examination has limitations, especially with regard to its use in more educated patients and as a screen for mild neurocognitive disorder," Tariq says.
It takes a clinician about seven minutes to administer the SLUMS, which supplements the Mini Mental Status Examination by asking patients to perform tasks such as doing simple math computations, naming animals, recalling facts and drawing the hands on a clock.
Both screening tools work at detecting dementia, the research found.
"SLUMS has the advantage in that it can help the clinician identify patients with mild neurocognitive disorder on the initial visit compared to MMSE, which requires a follow up screening," Tariq says.
Saint Louis University researchers used both screening tools to test 705 men who were at least 60 and treated at the Geriatric Research Education Clinical Center, Veterans Administration Hospitals in St. Louis in 2003. They found that while both tools detected dementia, only the SLUMS recognized a group of patients as having mild cognitive problems.
The SLUMS is available at this link:
http://medschool.slu.edu/agingsuccessfully/pdfsurveys/slumsexam_05.pdf

Novel Anti-Amyloidal Alzheimer's Drug Candidate Caprospinol
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Samaritan Pharmaceuticals Inc. and Samaritan Pharma Ireland, Inc. (AMEX:LIV) developers of innovative drugs, announced today it has submitted an Investigational New Drug (IND) application to evaluate its lead compound Caprospinol (SP-233) as a potentially new and novel pharmaceutical treatment for Alzheimer's disease. This is an important first step, to test Caprospinol's future in humans, as a potential memory-saving Alzheimer's drug.


Unlike drugs currently used to treat Alzheimer's that just alleviate symptoms, Caprospinol might potentially be a viable treatment for the disease itself. Preclinical studies have shown that Caprospinol targets and binds to the beta-amyloid protein, washing out beta-amyloid plaque from the brain. Today, the beta-amyloid protein is what most researchers believe is the cause of Alzheimer's disease.

Scientists at Samaritan Laboratories, Georgetown University, led the preclinical studies for Caprospinol, while Samaritan's Drug Development executives amassed the seven thousand pages of data to formulate the IND submitted to the FDA. PharmaPlaz, Ireland, Samaritan's collaborative manufacturing partner, led the chemistry, manufacturing and controls (CMC) section of the submitted IND.

Dr. Greeson, CEO of Samaritan Pharmaceuticals, stated, "The long race to develop a cure, or even a viable treatment, for Alzheimer's disease is quickly turning into a sprint for Samaritan. We at Samaritan are extremely excited to apply to enter the sprint and will do everything possible to remain in the running to find a cure or viable treatment for this horrible disease."

New Alzheimer's drug shows promise

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Neurochem Inc. (NASDAQ: NRMX; TSX: NRM) is pleased to announce that Neurology, a worldwide, leading, peer-reviewed, medical journal in the field of neurology, has published today an online version of a publication on the Phase II clinical trial of tramiprosate (3-amino-1-propanesulfonic acid (3APS); ALZHEMED(TM)) conducted in mild-to-moderate Alzheimer's disease (AD) patients. Tramiprosate (ALZHEMED(TM)) represents a potential new class of disease-modifying agents and is Neurochem's investigational product candidate for the treatment of Alzheimer's disease. The results reported in the paper demonstrate that long-term administration of tramiprosate (ALZHEMED(TM)) is safe, tolerated and reduces the level of amyloid (beta)42 (A(beta)42) in the cerebrospinal fluid (CSF) of AD patients. In addition, mean ADAS-cog(1) and MMSE(2) scores remained near baseline levels in the mild AD group over the 20 months of follow-up.
The only drugs currently available for Alzheimer's patients are those that alleviate symptoms, but a team of scientists led by Paul Aisen, MD, director of the memory disorders program at Georgetown University Medical Center, is testing a new class of drugs that actually target the molecule believed to cause the disease.
Aisen and his colleagues report that a compound called tramiprosate reduced levels of a marker for the progression of Alzheimer's disease in a Phase II clinical trial in the November 1 electronic version of Neurology.
"Everyone wants to figure out how to create an Alzheimer's treatment that attacks the amyloid peptide, which is considered to be the molecular cause of the disease," said Aisen. "This is the most advanced anti-amyloid treatment that exists — it has the potential for slowing down progression of the disease."
Aisen and his team are currently in the midst of Phase III clinical trials on tramiprosate (manufactured by Neurochem, for which Aisen is a scientific advisor, as ALZHEMED™) and hope to have results by early next summer.

TGF-beta Signaling Might Make You Demented

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The physical changes that occur in the brain of patients with Alzheimer's disease (AD), the most common cause of dementia in the elderly, have been well characterized, but the cause(s) of this disease and the development of therapies has remained elusive.
Now, in a study appearing in the November issue of the Journal of Clinical Investigation, researchers from Stanford University have shown that decreased signaling through a receptor known as T-beta-RII -- expression of which is decreased in the neurons of patients with AD -- increases neurodegeneration in mice.
Tony Wyss-Coray and colleagues found that neuron expression of T-beta-RII is decreased at an early stage of disease in the brains of individuals with AD. So they generated mice in which signaling by the molecule that triggers T-beta-RII, TGF-beta, is decreased. Analysis of these mice showed age-dependent neurodegeneration and beta-amyloid peptide accumulation in the brain, as is seen in the brain of patients with AD. The authors therefore suggest that increasing TGF-beta signaling in the brain might reduce neurodegeneration and be of benefit to individuals with AD.
In an accompanying commentary, Pritam Das and Todd Golde from the Mayo Clinic in Jacksonville outline how a decrease in TGF-beta signaling in the brain might promote neurodegeneration and beta-amyloid peptide accumulation, but warn that further studies to determine what causes the decreased expression of T-beta-RII are required.

One hundred years after the first diagnosis of Alzheimer's disease (AD) November 3, 1906

3 families spark search for genes tied to Alzheimer's

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Frustrated with the slow progress of research on Alzheimer's disease, three prominent families with local connections have formed a nonprofit foundation designed to find a cure for Alzheimer's within a decade.
Operating quietly for two years, the Cure Alzheimer's Fund raised nearly $3 million and awarded one-third to Harvard geneticist Rudy Tanzi and colleagues at Massachusetts General Hospital.
The philanthropists' approach is controversial because they are focusing on identifying all the genes connected with Alzheimer's, rather than spreading their efforts to other possible causes. The founding families, two of whom live in the Boston area, hope this strategy will more quickly and efficiently result in treatments. Currently, there are only a handful of drugs available, none of which significantly affects the disease's relentless destruction of the mind.
The group is going public with its venture today -- almost 100 years to the day after the disease was identified -- with the goal of eventually raising about $15 million a year from foundations, corporations, and wealthy donors.
The initiative is underway as federal funding for Alzheimer's research -- $652 million last year -- is shrinking, despite the growing number of Americans with the disease.
An estimated 4.5 million people have Alzheimer's now, but without effective prevention measures, that could reach 16 million by 2050 because of the aging of the population. The Alzheimer's Association, the largest private funder of research on the disease, spent nearly $21 million this year on a broad range of projects. The pharmaceutical industry is also working to develop new Alzheimer's drugs.
"We thought we'd do a better job," said Jeffrey Morby, an investment banker spearheading the new fund. "We felt we could move faster since our effort is more of a rifle shot -- to find a cure."
Morby, managing director of Amarna Corp. and a former Cambridge resident, is bankrolling the project for the first few years, along with his wife, venture capitalist Jacqueline Morby, developer Phyllis Rappaport, and venture capitalist Henry McCance . Morby said all of the families "have been touched by Alzheimer's." They also have raised funds from about 425 others.
None of the founders is seeking to profit from the research, said Morby, now of Pennsylvania. And the foundation is requiring that the work it supports be made public so that others can build on the findings. The scientists -- and their universities -- will own any rights to treatments developed. Tanzi, who earlier helped found a company working on Alzheimer's drugs, says the company has no rights to the foundation-funded work.

National Alzheimer's Disease Awareness Month

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The Alzheimer's Foundation of America (AFA) is marking National Alzheimer's Disease Awareness Month this November with three major national initiatives aimed at raising awareness of this devastating brain disorder from educational and emotional vantage points.
National Alzheimer's Disease Awareness Month is especially meaningful this November given that 2006 denotes the 100th anniversary of the discovery of Alzheimer's disease. In 1906, Dr. Alois Alzheimer, a German physician detected the disease's characteristic plaques and tangles during an autopsy of a woman's brain.

Today, an estimated five million Americans have Alzheimer's disease; the incidence is expected to triple by mid-century, in large part due to aging baby boomers.

AFA will mark the start of this commemorative month by unveiling the AFA Quilt to Remember, the nation's first dementia-related quilt that is grand in scale and that will continually grow with ongoing contributions. Patterned after the AIDS Memorial Quilt, it consists of massive panels that creatively memorialize or honor individuals affected by Alzheimer's disease and related dementias.
The AFA Quilt to Remember will be showcased in Central Park in New York City on November 3 and 4, with nearly 100 panels on display. Then, the quilt will tour the country for years to come, including stops in Dallas, Chicago, Los Angeles and other major cities in 2007.
"The AFA Quilt to Remember is a powerful work of art that unleashes a huge outpouring of emotion by families across the country. The panels 'speak' for those who can no longer speak for themselves. They both symbolize loss and celebrate life," said Eric J. Hall, AFA's chief executive officer.

Also on an inspirational front, AFA is sponsoring its annual National Commemorative Candle Lighting on November 9. Alzheimer's organizations, long- term care facilities and other community groups across the United States will be hosting candle lighting ceremonies and lighting "candles of care" to remember those who have passed or are living with the disease, and to honor their caregivers.

Then, on November 14, hundreds of sites from coast to coast will offer free confidential memory screenings as part of AFA's fourth annual National Memory Screening Day. Participating agencies will provide face-to-face screenings and information about Alzheimer's disease, successful aging and local resources.
The screening, which consists of a series of questions and tasks, could indicate whether someone should follow up with a complete medical exam. It is not used to diagnose any illness and does not replace consultation with a qualified professional, the AFA said.

The AFA suggests that anyone concerned about changes in memory or other intellectual functions should get screened. Warning signs include forgetfulness about names and events, asking repetitive questions, loss of verbal or written skills, confusion, and erratic mood swings.
With these national initiatives, Hall said, "Our goal is to wake America's consciousness about Alzheimer's disease and related illnesses, and to let people know that real lives are touched by this heartbreaking disease every day. We need to step up the nation's focus on education and care, while we await a cure."

New Treatments For Alzheimer's Disease

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Scientists at the University of Liverpool have created a new chemical compound that could be developed into a drug treatment for Alzheimer's disease.

The research team has used a family of long chain sugars called Heparan Sulphates (HS), found on nearly every cell of the body, to produce a new compound that can prevent the formation of clumps of small proteins that form in the brain. These clumps or 'plaques' disrupt the normal function of cells leading to progressive memory loss which is characteristic of Alzheimer's disease.

The clumps are formed from a small protein fragment called Amyloid-beta (A-beta) peptide released from its 'parent' protein - amyloid precursor protein (APP). This process requires the action of an enzyme called beta-secetase (BACE), which is critical in clipping up the APP to form the smaller A-beta fragments.

Professor Jerry Turnbull and Dr Ed Yates, from the University's School of Biological Sciences, have discovered that the HS sugars may play a key role in limiting the development of Alzheimer's disease. The sugars stick to the BACE enzyme and reduce its ability to 'clip' the A-beta peptide, thus controlling the amount of A-beta peptide available to form damaging plaques in brain tissue.

Professor Turnbull said: "We have developed a new class of compounds called 'engineered heparins' that could possibly be developed into drugs to stop A-beta peptides in the brain from forming and for the first time treat the underlying cause of Alzheimer's. The compound, based on the blood thinning drug, heparin, has modified chemical structures designed to optimise their desired activities and reduce potential side effects.

"The compounds work by blocking the beta-secretase enzyme, responsible for snipping proteins into smaller fragments. Despite its central importance to the disease, there are currently no drug treatments which target this enzyme because it has proved difficult to find inhibitors using traditional drug discovery approaches. The new compounds, based on the body's natural substances, may provide a novel route to effective treatments for this debilitating disease."