Alzheimer's Club

Mouse 8P205-4 appeared to be an unremarkable rodent as it scampered around its glass cage in the research laboratory.

But there was something going on deep in the brain of 8P205-4 that made it different from most other mice.

"This is a very important mouse," scientist Karen Duff said as she picked up the animal by its tail and allowed it to run up the arm of her white lab coat one morning this month.

Mouse 8P205-4 has Alzheimer's disease.

Duff, a molecular biologist at the Nathan Kline Institute for Psychiatric Research in Orangeburg, has spent the past decade perfecting a method of breeding mice with specific genetic mutations known to lead to Alzheimer's.

The genetically engineered mice allow her and other researchers nationwide to study what happens in the brain when Alzheimer's disease strikes.

"We're trying to replicate the pattern of Alzheimer's disease," she said.

In July, her discoveries earned her an $8 million grant from the National Institute of Neurological Disorders and Stroke for her Alzheimer's research.

Next week, Duff, who also is an associate professor of psychiatry at New York University School of Medicine, will receive the prestigious Potamkin award from the American Academy of Neurology. She will share the $100,000 prize with two other researchers.

"Their work has revolutionized the way we conduct Alzheimer research and drug discovery," John H. Growdon, a Harvard University scientist who helped select the winners, said in a statement released by the Minnesota-based association. "The work of these three individuals warrants recognition in that it will have a direct effect on developing treatments and finding a cure for Alzheimer disease."

Duff and other researchers hope that the genetically engineered rodent and others like it can help shed light on the changes that occur in the human brain leading to Alzheimer's.

Understanding those changes in mice can help find new treatments for the disease in the estimated 4 million people nationwide who develop the disorder, which is marked by progressive loss of memory and cognitive function. The number of people afflicted with the disease is expected to rise to 14 million by 2040 as baby boomers age, according to figures from the national Alzheimer's Association.

Stony Point residents Dennis and Nancy Murphy are among the millions of families nationwide who are learning to live with the ravages of the disease.

Four years ago, when Dennis Murphy was 61, he was diagnosed with the early stages of Alzheimer's.

But because of research like the kind Duff is doing, Murphy is still able to lead a satisfying life. He takes several newly discovered medications that appear to be halting the progression of the disease.

"He drives, he gardens, he sees friends and family," Nancy Murphy said. "We're lucky he had early diagnosis and got early treatment to stave it off."

Scientists have long suspected that two abnormal microscopic proteins in the brain are responsible for the memory loss and deterioration in cognitive functioning that signals Alzheimer's disease. One protein is known as amyloid plaque, which accumulates outside the brain's nerve cells. The second are called "tangles," which are twisted strands of protein that form inside cells.

Mouse 8P205-4 was bred to have a form of Alzheimer's disease caused by a buildup of amyloid plaque in the brain.

Duff has devised a series of experiments to test the cognitive function of that mouse and others.

In one experiment, the mouse is put into a shallow pool of water. The pool has several "arms" or corners equipped with a platform above the water. As part of the experiment, the mice are given clues — a light or a bright color — to help them find the correct arm with the platform.

Mice without Alzheimer's disease are able to find the platform easily and remember where it is.

But mice that are bred to have the disorder are unable to find it.

"They swim around the pool, and they don't know where they are going," Duff said. "It's like a person with Alzheimer's, who can't remember how to get home."

Other experiments with the mice are leading to new insights into the development and treatment of Alzheimer's.

Duff, along with researchers at the Mayo Clinic, are experimenting to see if lithium can reduce brain "tangles" that also lead to dementia.

Lithium helped remove the tangles from some of her genetically engineered mice, Duff said. Researchers are now experimenting to see if doses of lithium can reverse dementia in people. "The initial data is good," she said. "It looks very promising."

Source: Jane Lerner. Orangeburg researchers tackle Alzheimer's disease. The Journal News (28 March 2006) [FullText]

MIAMI, FL - Clinicians who assess patients with Alzheimer's disease are failing to recognize their symptoms of anxiety, mistaking them instead for agitation, researchers said in a presentation here at the 26th Annual Conference of the Anxiety Disorders Association of America (ADAA).

"Anxiety in Alzheimer's disease right now is not being picked up and current assessment tools may be mistaking anxiety for agitation," said presenter Maria S. Almeida, MD, resident psychiatrist, University of Nebraska Medical Center, Omaha, Nebraska.

Tools being used to assess patients with Alzheimer's disease focus on a very limited set of anxious behaviors, she said. "We suggest looking at anxiety in different ways," Dr. Almeida said during the meeting's New Research poster session.

Anxiety in Alzheimer's disease patients can be provoked in ways that are unique to the disease. Earlier research by Gene D. Cohen, MD, PhD, Professor of Psychiatry and Director, Center on Aging, Health & Humanities at George Washington University in Washington, DC, suggests that anxiety in this population has the following precipitants:

· challenging situations or performance demands;
· changes in the patient's environment;
· lack of engagement with people or the environment;
· settings that lack structure.

To determine whether the currently used assessment tool -- the Neuropsychiatric Inventory (NPI) -- is relevant to Dr. Cohen's model of anxiety, Dr. Almeida and her colleagues analysed the anxiety subsection of the inventory. The NPI is often used for assessment of psychopathology in patients with dementia and other neuropsychiatric disorders.

Their analysis found that the NPI emphasized the somatic and cognitive components of Alzheimer's disease, but did not adequately assess the behavioral aspects of anxiety associated with the disease.

"The NPI has a screening question for anxiety, and if the answer to that question is a no, then we tend not to go ahead and ask further questions, and so we end up missing the real signs and symptoms of anxiety in Alzheimer's," she said.

"What we recommend is -- irrespective of the answer to that screener question, whether it be yes or no -- to go ahead and ask other questions, and perhaps we will enhance our ability to pick up on the anxiety component," she added. "If we understand it better, then maybe we could treat it better."

[Presentation title: Lack of Recognition of Anxiety in Alzheimer's Disease.]

Source: Fran Lowry. Anxiety in Alzheimer's Disease Patients is Not Being Recognized: Presented at ADAA. Peer Review Media Bar (28 March 2006) [FullText]

Scientific researchers have discovered that a drug used to treat Alzheimer's disease, a neurodegenerative affection clinically characterized by progressive deterioration of neural and other daily living activities, can actually improve the condition of patients suffering from a severe form of dementia.

Generically known as donepezil, the drug is called Aricept and is marketed by Pfizer and Japan's Eisai Co. Ltd.

Swedish researchers at the Karolinska Institute claim that it can improve language, memory and understanding in patients with a severe form of dementia, Swedish researchers said on Thursday.

A test has been run on about 200 elderly patients and it seems that they showed improvements – they began to function better, do daily tasks and were less reliant on nursing care; their speech, memory and communication skills also improved.

"We got impressive results", affirmed Professor Bengt Winblad, who led the 6-month study. "We now have a drug that will improve the intellectual capacity of the elderly with severe Alzheimer's disease", he added.

However, a week ago, Eisai announced that 11 patients suffering from a different form of dementia had died while taking Aricept during a clinical trial. Patients in that study suffered from vascular dementia, which is caused by a stroke or diseased blood vessels and is the second most common form of dementia after Alzheimer's disease. Nearly 650 patients in the trial were given the drug. There were no deaths among the 326 people who received a placebo, according to Reuters.

Even if the drug does considerably improve the condition of the patients suffering from Alzheimer's, Winblad insisted on the fact that the drug is not a cure for the illness.

Source: PlayFuls.com (24 March 2006) [FullText]

Zinc may be a familiar dietary supplement to millions of health-conscious people, but it remains a mystery metal to scientists who study zinc's role in Alzheimer's disease, stroke and other health problems. They are just beginning to fathom how the body keeps levels of zinc under the precise control that spells the difference between health and disease.

Researchers now have developed a biochemical metal detector to help crack the mystery. It is a biosensor that has yielded the first measurements of the tiny amounts of zinc ordinarily present inside living cells.

The study appears in the current issue of ACS Chemical Biology, the newest of 34 journals published by the American Chemical Society, the world's largest scientific organization.

It was conducted by Rebecca A. Bozym and Richard B. Thompson, Ph.D. of the department of biochemistry and molecular biology, University of Maryland School of Medicine, Baltimore, and Andrea K. Stoddard and Carol A. Fierke, Ph.D. of the Department of Chemistry, University of Michigan, Ann Arbor.

The question of how much zinc is available in a cell has emerged at the forefront of chemical biology, Amy R. Barrios, Ph.D., of the University of Southern California, Los Angeles, wrote in an accompanying Point of View in ACS Chemical Biology.

Barrios described the new research as a critical step forward, and predicted many more exciting breakthroughs in measuring levels of metals in human cells.

Just 2-3 grams of zinc (the weight of a penny coin) exist in the entire human body. The metal is a key building block in enzymes and other substances involved in functioning of the nervous system, the immune response, and the reproductive system.

We believe this new technique can help us understand how zinc is involved in plaque formation in Alzheimer's disease, how prolonged seizures or stroke kill brain cells, and how the cell normally allocates zinc to different proteins, said Thompson.

Thompson explained that almost all zinc inside cells is incorporated into proteins, where it plays many vital roles, such as helping to read the genetic code of DNA.

We know that if there is much zinc in the cell that is not attached to protein or otherwise encapsulated "so-called free zinc" the cell is stressed or may be undergoing programmed cell death. This has been observed in animal models of epilepsy and stroke.

In the past, scientists could only measure the relatively high levels of zinc in sick cells. The new sensing technology can measure very low free zinc concentrations in healthy cells.

The technique uses a special protein molecule that has been re-engineered to report when zinc becomes stuck to it as a change in luminescence that can be seen in the microscope. This protein (originally found in blood cells) is very selective, recognizing tiny levels of free zinc even in the presence of the million-fold higher levels of other metals present in cells, such as calcium or magnesium.

Because proper zinc levels are so important in health and disease, scientists have been seeking ways of measuring zinc inside and outside of cells for more than a decade.

This is an important discovery, said Sarah B. Tegen, Ph.D., managing editor of ACS Chemical Biology. We need to know how the body controls levels of zinc inside cells. Too much zinc can kill nerve cells. With too little, nerve cells will not work properly.

Now we have a metal detector, technology that can measure tiny amounts of zinc in living cells. Understanding how zinc is stored and released in different cells throughout the body may help us understand some of the nerve damage that occurs during a stroke and other nerve injuries.

Source: www.acs.org, news-medical.net (23 March 2006) [FullText]

WEDNESDAY, 22 March 2006 (HealthDay News) - New research finds that a natural enzyme may help prevent Alzheimer's disease onset.

Scientists had already known that the enzyme, called Pin1, blocks the formation of tangle-like lesions (tau tangles) common to the brains of people with Alzheimer's.

This new study, conducted in animals and led by researchers at Harvard Medical School and Beth Israel Deaconess Medical Center (BIDMC), found that Pin1 also helps protect against the development of amyloid peptide plaques, another kind of brain lesion that's characteristic of Alzheimer's.

The findings, published in the March 23 issue of Nature, provide further evidence that Pin1 plays a crucial role in guarding people against age-related neurodegeneration. The study also provides the first evidence of a direct link between amyloid peptide plaques and tau tangles.

"Throughout the years, intensive studies have been done to find out the causes of these two major lesions, but the exact relationship between the two has remained controversial and elusive," study senior author Dr. Kun Ping Lu, an investigator in the division of cancer cell biology at BIDMC and an associate professor of medicine at Harvard Medical School, said in a prepared statement.

"Coupled with recent independent studies showing that genetic changes in the human Pin1 gene are associated with reduced Pin1 protein levels as well as an increased risk of Alzheimer's disease, these new results suggest that lack of sufficient Pin1 enzyme may be a key culprit in the onset of Alzheimer's disease," Lu said.

Source: Enzyme Slows Alzheimer's Disease. Forbes.com (22 March 2006) [FullText]

Stigma and Denial Delay Diagnosis of Alzheimer's Disease by More Than Two Years on Average, According to New Nationwide Survey

'Serious and Unnecessary Setback' Can Rob Caregivers and People with Alzheimer's Disease of Support Services and Treatment'

NEW YORK - Concern about stigma and denial of symptoms can delay a diagnosis of Alzheimer's disease by more than two years (28.7 months) on average after symptoms appear, according to a new survey from the Alzheimer's Foundation of America (AFA). When people with Alzheimer's disease are concerned about stigma, a diagnosis of Alzheimer's disease occurred on average 3.5 years (40.1 months) after symptoms appear. When caregivers are concerned about stigma, delay of diagnosis is even more severe, averaging 6 years (71.4 months). The survey was conducted by Harris Interactive(R) on behalf of AFA, a national nonprofit organization providing care and services to individuals with Alzheimer's disease and related dementias, and their families.

"Any delay in diagnosis is a setback for people with Alzheimer's disease and their caregivers -- and a delay of two years or more is a serious and unnecessary setback," said Eric J. Hall, chief executive officer of the Alzheimer's Foundation of America. "While facing Alzheimer's disease is never easy, getting a diagnosis is an essential step to managing and treating the disease. Living with this in silence can isolate people with Alzheimer's disease and their caregivers, leaving them without critical support, resources, and proper treatment. We encourage everyone touched by Alzheimer's disease to reach out for support -- help is out there."

FAMILIES FEEL ABANDONED, STRUGGLE WITH CARING FOR LOVED ONES ON THEIR OWN

Survey results also reveal a distinct generation gap between caregivers of parents and caregivers of spouses with Alzheimer's disease. Caregivers of parents are significantly more likely than caregivers of spouses to say they now have less time for themselves (74% vs. 56%) and have felt abandoned by family (34% vs. 14%). Caregivers of spouses confide in significantly fewer sources of support than caregivers of parents (2.7 vs. 3.3 on average), and are significantly less likely to say they would like more help (52% vs. 77%).

In addition, caregivers of spouses (33%) are significantly more likely than caregivers of parents (12%) to indicate that their own denial was an obstacle to diagnosis.

Many sibling relationships suffer under the stress of caring for a parent with Alzheimer's disease and the division of caregiving responsibilities. More than half of caregivers of parents, with siblings (60%), report that they are the only one of their siblings responsible for their parent's care. Many of these respondents report that relationships with siblings deteriorated after a parent was diagnosed (86% of siblings were somewhat or very close prior to diagnosis vs. 75% post-diagnosis).

MORE EDUCATION, SUPPORT NEEDED

Sixty-nine percent of caregivers surveyed report that they want more help from family and friends. Caregivers indicate that more help in certain areas could ease the caregiving strain, most notably assistance with day-to-day caregiving activities (20%), more financial support (16%), more emotional support (15%) and more time for themselves (13%). Caregivers of parents are significantly more likely than caregivers of spouses to feel comfortable talking about the condition with all of the people in their life (80% vs. 64%). Caregivers overall are most likely to confide in friends (58%), physicians/healthcare professionals (41%), children (38%), spouses (35%), and siblings (33%).

Lack of knowledge about the disease is a barrier to diagnosis for two in five caregivers surveyed (40%), suggesting that more education is needed. While the majority (92%) of caregivers report that they are aware of medications that may slow the progression of symptoms, only half (51%) of caregivers surveyed are aware of the opportunity for combination therapy.

"If you notice memory problems or any other possible warning signs, such as agitation, restlessness, disorientation, or difficulty performing regular tasks, make an appointment with your doctor," said Beth Safirstein, M.D., co- president/medical director and practicing physician at the MD Clinical/MD Clinical Trials Foundation, Inc., Hallandale Beach, FL. "Diagnosis and treatment are essential because there are treatments available, including combination therapy, that have shown to potentially help maintain a person's ability to think clearly and perform everyday tasks for a longer period of time than if left untreated."

CAREGIVERS EMERGE STRONGER, MORE COMPASSIONATE

Remarkably, many caregivers who mentioned fear of stigma and/or denial as a reason for delay in diagnosis appear to have largely overcome their fear and are more likely than those who did not struggle with stigma and denial to say they are extremely or very knowledgeable about Alzheimer's disease (72% vs. 59%).

Moreover, the majority of caregivers surveyed report finding new, positive qualities in themselves during the process of caregiving: roughly two-thirds (64%) of caregivers report they have become a more compassionate person since caring for a loved one with Alzheimer's. Additionally, 76 percent of caregivers state they have learned that they are stronger than they thought since caring for someone with the disease.

Source: Alzheimer's Foundation of America, PRNewswire (21 March 2006) [FullText]

CALAIS - Terry Rohe understands what a mind-robbing disease Alzheimer's is.

The former senior correspondent for ABC's "Good Morning America" was diagnosed with the disease several years ago.

But that hasn't stopped her or her message. Rohe has accepted the challenges of the disease as she has taken on every other assignment in her life: with grace, vigor and a heart-stopping smile.

The irony of her situation - 24 years ago Rohe did a five-part series on the disease for a Boston television station.

At the time, she said, she knew nothing about Alzheimer's.

Now, Rohe, 81, is doing her own continuing series as she lectures and talks about the disease.

Rohe was one of two guest speakers Wednesday at the Washington County Community College's and St. Croix Valley Healthy Community's "Step-up to Nutrition and Health Conference."

Alzheimer's, according to the Alzheimer's Association, is a progressive brain disorder that eventually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily living activities.

In this country alone, it is anticipated there will be a 44 percent increase in the disease by 2025.

"According to U.S. Census data, the size of the older population will double over the next 25 years, growing to 70 million by 2030 when the youngest of the post-World War II baby boomers will be more than 65 years old," the Alzheimer's Association said in its fact sheet. "Because age is a known risk factor for Alzheimer's, the United States could realize a 70 percent increase in the prevalence of Alzheimer's disease, with an estimated 7.7 million people affected."

Right now there is no known cure.

But Rohe isn't giving up.

First she found a good doctor near her home in Hancock County, then she created a scrapbook titled "KAAB - Keep Alzheimer's At Bay." She shared the scrapbook Wednesday night.

For Rohe, the key to battling Alzheimer's begins with a good diet, plenty of exercise, lots of music and volumes of laughter.

Rohe and her musician husband, Robert, 90, a bassist for the Bangor Symphony Orchestra then entertained the group with a variation on the words of a musical selection sung to the theme "Darling we are Growing Older."

Rohe who spoke the words to the song, at the end of it turned to her husband and said, "So darling, when silver threads knock out the gold and you can't remember what you've been told, just remember KAAB, and it will head off Alzheimer's to some degree."

Katherine Musgrave, 87, premier dietitian and professor emeritus at the University of Maine, talked about good nutrition and eating right as senior citizens. Musgrave's message - "a proper diet" leads to a "better life."

That diet includes eating plenty of grains, vegetables, milk, fruit, meat, beans and fish.

A fact sheet she handed out recommended that seniors consume a variety of nutrient-dense foods and beverages within and among the basic food groups and limit the intake of saturated and trans fats, cholesterol, added sugars, salt and alcohol.

Then it was off to the nearby gymnasium, which had been turned into a four-star restaurant for the night and included mood lighting and soft music.

There, the more than 50 people feasted on a nine-course meal prepared by students in the Culinary Arts Program at the college. Student chef Lorie Haag and sous chef Randy Taylor designed the meal that included braised beef Napoleon sauced two ways.

It was tops in flavor and presentation with its cracked peppercorn noodle sheets that blanketed a savory braised beef in a bordelaise sauce topped by a layer of sauteed button mushrooms. It was followed by one of three desserts that included cream puff Marsala with raspberry coulis.

The students received a warm round of applause from the audience for their culinary feast.

Source: Former ABC reporter battles Alzheimer's: Rohe speaks out against disease at WCCC nutrition event. Bangor Daily News (17 March 2006) [FullText]

Kotti TJ, Ramirez DM, Pfeiffer BE, Huber KM, Russell DW.
Brain cholesterol turnover required for geranylgeraniol production and learning in mice
Proc Natl Acad Sci U S A (7 March 2006) 103(10): 3869-74
Department of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.

Abstract: The mevalonate pathway produces cholesterol and nonsterol isoprenoids, such as geranylgeraniol. In the brain, a fraction of cholesterol is metabolized in neurons by the enzyme cholesterol 24-hydroxylase, and this depletion activates the mevalonate pathway. Brains from mice lacking 24-hydroxylase excrete cholesterol more slowly, and the tissue compensates by suppressing the mevalonate pathway. Here we report that this suppression causes a defect in learning. 24-Hydroxylase knockout mice exhibit severe deficiencies in spatial, associative, and motor learning, and in hippocampal long-term potentiation (LTP). Acute treatment of wild-type hippocampal slices with an inhibitor of the mevalonate pathway (a statin) also impairs LTP. The effects of statin treatment and genetic elimination of 24-hydroxylase on LTP are reversed by a 20-min treatment with geranylgeraniol but not by cholesterol. We conclude that cholesterol turnover in brain activates the mevalonate pathway and that a constant production of geranylgeraniol in a small subset of neurons is required for LTP and learning.

[PubMed Abstract] [AlzForum Comments]

Also see: Neurobiology of Lipids

Alzheimer's is the most common form of dementia, a group of conditions that all gradually destroy brain cells and lead to decline in mental function.

"You have to imagine that the family member of yours has a broken brain," said Lynda Markut, director of consultation and training/dementia care specialist at Family Alliance, Inc. in Woodstock. "When you think: 'How could they do that?' You have to remember their brains are not working properly. They are really trying to use every little bit of reserve capacity they can."

Dementia is a term for a syndrome that covers a variety of symptoms, with Alzheimer's at the most severe extreme. Vascular dementia, another common form, results from reduced blood flow to the brain's nerve cells. In some cases, Alzheimer's disease and vascular dementia can occur together in a condition called "mixed dementia." Other causes of dementia include Creutzfeldt-Jakob disease and Parkinson's disease.

"Dementia is brain failure," Markut said, "and with every type of dementia, there will be different symptoms."

With Alzheimer's disease there is some short-term memory loss, trouble learning and recalling information recently presented. Other symptoms include difficulty naming items, forgetting the order of things, an inability to recognize everyday objects and difficulty in making a plan and following it.

They know what a pen is used for, Markut said, but they may not be able to name it. They may slip their socks over their shoes.

"They get up on the morning and know they have to go to the store," Markut said. "Then they sit down, put a pen in their hand and forget what they wrote. They can't execute ... With Alzheimer's, if all the cabinet doors are closed, in my mind there is no food in the kitchen."

It is important that things are readily accessible and visible. For example, leaving a light on in the bathroom at night helps an Alzheimer's patient find the toilet. Caregivers also can help out by with reminder notes and by substituting words they can comprehend.

The idea is to communicate, to stimulate their brains.

Staying active stimulates the brain and lessens the risk of depression. Markut said it also seems to have an inhibiting effect on the "tangles" and "plaque" that choke off and kill the brain cells, or neurons. Working the brain creates new pathways, not unlike rerouting electricity around a downed wire.

"The people who have linguistic richness can have tangles, but not as early," Markut said. "The more neuro-pathways in the brain, the more routes you have to get information."

Researchers are not sure what causes Alzheimer's disease. But Markut said evidence suggests a genetic propensity in one's family can contribute to an early onset of the disease.

"I've been in the field for 23 years and I have never seen the diagnosis proceed in the same fashion in any one person," said Markut, who co-wrote "Dementia Caregivers Share Their Stories: A Support Group in a Book" published in May 2005. She said the book, which relays the stories of 28 families, helps people they are not alone.

"They fight care. They fight people coming in to give them a bath, because they don't understand the limitations the illness has imposed on them," Markut said. "It is not just physically draining, it is emotionally draining ... You never feel like you are doing anything right, because the person keeps changing."

Source: Kurt Begalka. Dementia illnesses require individual care. Sun City Herald (9 Mar 2006) [FullText]

Nymox (NASDAQ: NYMX) Has Global Patent Rights for Statin Drugs for the Treatment and Prevention of Alzheimer's Disease (Benjamin Wolozin, Inventor)

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. Statins are a class of cholesterol-lowering drugs that are the biggest-selling prescription pills in pharmaceutical history with estimated 2004 global sales of up to $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. alone.

The potential for statin drugs to treat or reduce the risk of Alzheimer's disease (AD) has been bolstered by several 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: 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 of statin drugs to help in the treatment and prevention of AD was the subject of a recent article in Chemistry & Industry (Issue 2, 2006). The potential of statin drugs for AD has also been featured in a cover story in Newsweek, as well as in the New York Times, Fortune, Los Angeles Times, and The Wall Street Journal.

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.

Source: Statin Drug Potential for Alzheimer's Disease Gains Ground with Recent Studies. CCNMatthews (8 March 2006) [FullText]

Ecublens & Lausanne, Switzerland (8 March 2006) -- AC Immune, a Swiss Biotech Company developing innovative therapies against Alzheimer's Disease, today announced that it has identified lead drug candidates for clinical development for both active and passive immunotherapies. Both therapeutic approaches have shown significant improvement of the memory function in animal studies.

AC Immune's proprietary therapeutic approach against Alzheimer's Disease has resulted in the development of a vaccine as well as a passive immunotherapy with a selected monoclonal antibody which was highly active in animal models for Alzheimer's Disease. Both treatments significantly improved the memory capacity. The results also provided proof of AC Immune's key technology for active and passive immunization. Both therapies build on antibodies generated by AC Immune's SupraAntigen(TM) Technology. They are conformation-specific and have induced the anticipated transition from the insoluble to the soluble form of the plaque forming beta amyloid protein. This event directly correlated with the observed memory improvement.

"The highly significant functional improvement of memory function in Alzheimer's Disease animal models gives us a solid basis for the clinical development program in front of us," said Andrea Pfeifer, CEO of AC Immune.

AC Immune also hired additional key staff with Dr. Andeas Muhs as Chief Scientific Officer (CSO) and Dr. Wolfgang Frostl as Head of Chemistry and Dr. Maria Pihlgren as Head of Biology. Dr. Muhs has long-term experience in pre-clinical development of Biotech Products and has moved several projects from research to clinical programs. Dr. Frostl combines 28 years of medicinal chemistry experience in the pharmaceutical industry with specialization in drugs for the Central Nervous System (CNS). Dr. Pihlgren is an expert in Immunotherapy and worked several years at the WHO Collaboration Center for Vaccinology.

AC Immune now has a total staff of 13 coming from eight different nations.

"AC Immune's SupraAntigen(TM) technology has proven potential for conformation-specific immunotherapy of Alzheimer's Disease and opens possibilities for the treatment of other conformational diseases," said Andreas Muhs.

"AC Immune's product development progress positions the company well for potentially contributing to a disease-modifying therapy against Alzheimer's. With the recent financing of CHF 21 million, the new Laboratory location close to the EPFL and the important recruitment of specialized staff, the company is well prepared to bring therapeutic solutions and create shareholder and social value," commented Martin Velasco, Chairman of the Board of AC Immune.

AC Immune was founded in 2003 in Basel and is located in the Science Park on the Campus of the Swiss Federal Institute of Technology in Lausanne (EPFL).

Contact: Dr. Andrea Pfeifer, CEO, AC Immune Phone: +(41)-21-693-91-22 andrea.pfeifer@acimmune.com , www.acimmune.com

Source: PRNewsWire (8 March 2006) [FullText]

TOLEDO, Ohio -- According to a recent study, Alzheimer's disease advances more quickly in highly educated people. But before you quit school and abandon your college education, studies also show that the more years of higher education, the later the disease may appear.

Alzheimer's disease is a form of dementia that affects the brain mostly in areas of thought, memory and language. Dr. Nikolaos Scarmeas of Colombia University Medical Center in New York, studied 312 people diagnosed with Alzheimer's, with different levels of education, for five years, testing their brain functions. His results concluded that all patients showed a decline of 9 percent overall, but each additional year of education saw a 0.3 percent additional deterioration.

The theory of "cognitive reserve" explains his findings. It states that people with higher brain skills and functions are able to delay illness, because of more brain cells or more efficient brain systems. However, as the diseases accumulate in the brain, the brain eventually succumbs to the diseases, which quickly take over, and progress faster than normal.

Scientists do not know what causes the disease or how to cure it. About 12 million people throughout the world currently suffer from Alzheimer's disease.

Source: Jessica Schwind. The Owens Outlook (Owens Community College) U-Wire (March 8, 2006) [FullText]

ROCHESTER, N.Y. - Jim Ruppert, a former school counselor and family therapist, was diagnosed with Alzheimer's four years ago. He is 58 and has a form of the disease that strikes early in life.

But the common concept of Alzheimer's is not one of somebody who is as vital and talkative as Jim Ruppert. What's going on here?

“I think,” he explains, “the public thinks about people in the hospital bed or, you know, getting lost, which they do in advanced-stage. I'm still in the first stages of the disease.”

But already, just to function around the house, Ruppert, with the help of his wife, Vicky, continually writes notes and makes voice recordings to try to remember the smallest details of life.

“I can go from one end of the house and decide something I need at the other end of the house,” he says, “and unless I repeat it in my head or out loud, I forget.”

And after awhile the forgetting is apparent even in conversation.

Is he glad to know the diagnosis?

“You really don't have a choice with the disease, just in terms of, you know, forgetting 50 times a day what you're doing,” Ruppert says. “Sometimes it gets really frustrating. And ... I forgot your question. I didn't get around to answering it.”

Ruppert and his wife traveled for much of their lives and they want to squeeze in as much more as they can in the time remaining.

What do they fear most?

“Being in a nursing home,” Jim Ruppert says, “not being able to tell somebody that I need to go to the bathroom. Not being able to put on my own clothes.”

“I don't really look at it as far as fear is concerned,” says Vicky Ruppert. “I will do whatever I have to and I will keep Jim at home as long as I can.”

But they both know they will be lucky if he can stay at home another two years.

Source: Robert Bazell. Living with Alzheimer's disease: A first-hand account of what it's like to lose your memory. NBC News (7 March 2006) [FullText]

The world's leading physicians and scientists in the fields of Alzheimer's disease treatment and dementia research will participate in the 9th International Geneva/Springfield Symposium on the Advances in Alzheimer Therapy. The conference will be held April 19-22 at the International Conference Center in Geneva, Switzerland. They will highlight the latest discoveries in the treatment of dementia and results of the most recent clinical trials using drug, cellular and gene therapies.

More than 100 sessions will be presented by 125 speakers during the four-day symposium. Nearly 800 specialists are expected to attend the international gathering.

Included in those presentations will be historical data reflecting the progress of the treatment of Alzheimer's disease with cholinesterase inhibitors over the past 20 years; the results of three large clinical trials utilizing cholinesterase inhibitors in at-risk patients; and recommendations for usage of vaccination against beta-amyloid aggregation, the accumulation of toxins in the brain that destroys nerves which can lead to Alzheimer's disease.

Dr. Paul Coleman, neuroscientist at the Center for Aging and Developmental Biology in Rochester, New York, will give the keynote address entitled The Impact of Science on Future Alzheimer Disease Diagnosis.

The symposium was established by Dr. Ezio Giacobini, Ph.D., professor of rehabilitation and geriatrics at the University of Geneva Medical School in Switzerland and professor emeritus of the Southern Illinois University School of Medicine in Springfield, Ill., USA. Giacobini organized this year's conference with Dr. Jean-Pierre Michel, professor and chair of rehabilitation and geriatrics at the University of Geneva Medical School in Switzerland.

Featured speakers and their topics at the ninth annual symposium include:

Dr. Kaj Blennow, Department of Clinical Neuroscience, Sahlgren's University Hospital, Molndal, Sweden: Use of CFS Biomarkers in Early Diagnosis and Monitoring of Treatment;
Karen Duff, Ph.D. , Nathan Kline Institute, Orangeburg, New York: Impact of Kinase Modulation on Pathogenesis in Mouse Models of Neurodegenerative Diseases;
Dr. Nick Fox, Dementia Research Group, Institute of Neurology, London, England: Immunotherapy of Alzheimer Disease: MR Imaging of Changes in Brain Morphology;
Stephen L. Minger, Ph.D., Wolfson Center for Age-Related Disease, London, England: Stem Cell Therapy of Alzheimer Disease: Which Way to Go?;
Dr. Roger Nitsch, Division of Psychiatric Research, University of Zurich, Zurich, Switzerland: The Immunotherapy of Alzheimer Disease;
Dr. Agneta Nordberg, Ph.D., Division of Molecular Neuropharmacology, Karolinska Institute, Stockholm, Sweden: Amyloid Imaging in MCI Patients;
Dr. Lon Schneider, Department of Psychiatry, Neurology & Gerontology, Keck School of Medicine, University of California Los Angeles: Treatment of Behavioral Symptoms in Alzheimer Disease;
Rudy Tanzi, Ph.D. , Genetics & Aging Research, Massachusetts General Hospital, Charlestown: Identifying the Genetics Causes of Alzheimer Disease;
Dr. Anders Wimo, Ph.D., Karolinska Institute, Stockholm, Sweden: Cholinesterase Inhibitors for Alzheimer Disease Therapy: Are They Worth the Price?;
Dr. Bengt Winblad, Ph.D., Karolinska Institute, Stockholm, Sweden: Treatment Strategies in Severe Dementia.

The International Geneva/Springfield Symposium on the Advances in Alzheimer Therapy was first held in 1988 in Springfield, Illinois. The conference is held biennially. Information about the conference, including a complete list of speakers, is posted online at: www.siumed.edu/cme/alzheimer/media.

Southern Illinois University Carbondale, 1010 S. Elizabeth St. MC6519, Carbondale, IL 62901-6519, United States, news.siu.edu

Source: Medical News Today (5 March 2006) [FullText]

Frank LaFerla, a professor of neurobiology at the University of California, Irvine (UCI) and also the senior author in the research said that the experimental drug AF267B is effective against both forms of brain lesions found in Alzheimer's disease in mice. This compound (AF267B) curbs both the amyloid protein plaques that collect in Alzheimer's-affected brains, as well as another lesion, the tangles of protein called tau. In mice that have been genetically designed to mimic Alzheimer's disease AF267B also appears to reverse cognitive declines. Researchers said that the mice appeared to gain renewed powers of memory and learning after treatment. The findings of the study were reported in the journal Neuron. AF267B is a perfect drug for the Alzheimer's disease. It has the disease-modifying capacity that treats the symptoms and also reverses the cognitive declines. Frank LaFerla said that AF267B is an M1 agonist. It acts by stimulating the muscarinic receptor which is present on the surface of nerve cells. In the Alzheimer's disease there is a selective loss of neurons which produce the neurotransmitter acetylcholine. He said that by stimulating the M1 receptor one can boost the acetylcholine activity and AF267B does the stimulation. It was developed by the famous Alzheimer's researcher and study co-author Abraham Fisher, of the Israel Institute for Biological Research, in Ness-Ziona, Israel.

Source: MedIndia.com (2 March 2006) [FullText]

New York City (1 March 2006) -- The Institute for the Study of Aging (ISOA), a biomedical venture philanthropy founded by the Estee Lauder family, and Elan Pharmaceuticals, Inc., a neuroscience-based biotechnology company, are pleased to announce the winners of their new research award program, Novel Approaches to Drug Discovery for Alzheimer's Disease. Four recipients were selected from a highly competitive pool of 45 scientists from 12 countries.

The award-winners are Steven S. Schreiber, PhD, Professor of Neurology and Anatomy and Neurobiology at the University of California Irvine School of Medicine; Greg R. J. Thatcher, PhD, Professor of Medicinal Chemistry at the University of Illinois at Chicago; Nicholas Webster, PhD, Professor in Residence at University of California, San Diego; and Berislav Zlokovic, PhD, Professor and Associate Chair of Neurosurgery at the University of Rochester Medical Center. They were chosen by an independent scientific review panel of 10 experts chaired by ISOA Executive Director Howard Fillit, MD, a leading geriatrician and neuroscientist.

According to Dr. Fillit, "These awardees are conducting innovative research in Alzheimer's drug discovery. Their programs were recognized as most promising to advance the discovery of effective disease-modifying drugs for Alzheimer's. Thanks to our collaboration with Elan, we are delighted to present grant awards of $130,000 each to support their work."

The scientists received their awards at a recent luncheon held in New York City. Mr. Leonard Lauder, ISOA Co-Chairperson and Chairman of the Estee Lauder Companies Inc., and Mr. Kelly Martin, Elan President and CEO, welcomed an audience of over 40 distinguished guests to celebrate the inauguration of the first annual ISOA/Elan Alzheimer's Disease Drug Discovery Awards and to recognize the recipients. During the luncheon, Mr. Lauder and Mr. Martin both commented on the importance of this program and the ongoing need to accelerate the discovery of effective drugs to conquer one of the most devastating diseases of the 21st Century. This disease affects 1 out of 3 people over the age of 80.

Mr. Martin stated, "Elan is proud to be working with the ISOA to enable more scientists to pursue original, breakthrough research in the fight against Alzheimer's disease. We look forward to expanding on our alliance in the years to come. Working together, we have a greater chance of finding a solution to this debilitating disease, which not only affects patients but also their families and loved ones."

For more information regarding this unique public charity-corporate alliance research program, contact Howard Fillit, MD, at 212-935-2402 or hfillit@aging-institute.org.

About the Institute for the Study of Aging (ISOA)
The Institute for the Study of Aging (ISOA) is a biomedical venture philanthropy whose sole mission is to accelerate the discovery and development of new drugs to prevent, treat and cure Alzheimer's disease and related dementias. Since its founding as a private foundation by the Lauder family in 1998, ISOA has awarded $24 million for 143 research programs and conferences at leading academic institutions and biotechnology companies worldwide. In 2004, the Lauder family established a public charity, the Alzheimer's Drug Discovery Foundation, to enable individuals, foundations and corporations to partner with the Institute in an effort to raise additional funds and award more grants. For more information, visit http://www.aging-institute.org/, or call Howard Fillit, MD (Executive Director) or Suzanne Grossberg (Director of Development) at 212 935 2402.

About Elan Pharmaceuticals, Inc.
Elan Pharmaceuticals, Inc is a wholly owned subsidiary of Elan Corporation, plc (NYSE: ELN). Elan is a neuroscience-based biotechnology company. We are committed to making a difference in the lives of patients and their families by dedicating ourselves to bringing innovations in science to fill significant unmet medical needs that continue to exist around the world. We continue to be dedicated to developing treatment alternatives for patients suffering from Alzheimer's disease. Currently our research programs include four approaches to modifying or halting the progression of the disease. Two of these programs are in collaboration with Wyeth, focused on immunologic approaches to treating the disease. One of the programs that focuses on halting the progression of the disease through humanized monoclonal antibodies is in Phase II clinical trials. Elan shares trade on the New York, London and Dublin Stock Exchanges. For additional information about the company, please visit http://www.elan.com/, or call Davia Temin at 212 588 8788.

Elan is also involved in the scandals associated with the scientific integrity break by Harvard Professor Dennis Selkoe, serving as Elan Director for many years, and the breach of ethics behind Elans' failed Alzheimer's immunization trial .

Source: Market Wire