FDA Approves First Generic Aricept to Treat Dementia Related to Alzheimer’s Disease

The U.S. Food and Drug Administration approved the first generic versions of Aricept (donepezil hydrochloride) orally disintegrating tablet s on Dec. 11. Donepezil hydrochloride is indicated for the treatment of dementia related to Alzheimer’s disease.

Although other generic versions of donepezil hydrochloride are already available, the orally disintegrating tablets dissolve on the tongue, without having to be swallowed whole. This may make it easier to take the medication for older or disabled patients who have difficulty swallowing.

“Generics offer greater access to health care for all Americans,” said Gary Buehler, director of the FDA’s Office of Generic Drugs. “Health care professionals and consumers can be assured that FDA-approved generic drugs have met the same rigorous standards as the brand-name drug and are the same as the branded in dosage form, safety, strength, route of administration, quality, performance characteristics and intended use.”

Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks of daily living. In most people with Alzheimer’s disease, symptoms first appear after age 60. Alzheimer’s disease is the most common cause of dementia among older people, but it is not a normal part of aging.

Dementia refers to a decline in cognitive function that interferes with daily life and activities. Alzheimer’s disease starts in a region of the brain that affects recent memory, then gradually spreads to other parts of the brain.

The generic donepezil hydrochloride orally disintegrating tablets, manufactured by Mutual Pharmaceutical of Philadelphia, have been approved in 5 milligram and 10 mg strengths.

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Public Seminar for Alzheimer’s Caregivers Co-Hosted by Emory

A group of experts will gather in Atlanta on Thursday, Nov. 5 to discuss caring for a person with Alzheimer’s disease. Presenters at the evening seminar, "Practical Strategies: Caring for a Loved One with Alzheimer’s,” will cover topics including managing daily life, planning future decisions, handling crises, dealing with family and caring for yourself. Members of the public are invited to attend and participate in a Q&A session with panelists.

The seminar is sponsored by the Emory University Alzheimer’s Disease Research Center, the Georgia chapter of the Alzheimer’s Association and the Fulton County Human Services Department, Office of Aging

The event will be held from 5:30 p.m. to 7:30 p.m. at the Helene Mills Senior Center located at 515 John Wesley Dobbs Ave., Atlanta, Ga., 30312. Admission and parking are free. Beverages and light snacks will be provided. For more information, please call (404) 523-3353.

Presenters/Topics Include:

Dr. Angela Ashley
Director, Grady Memory Assessment Clinic
Assistant Professor, Emory University School of Medicine

Shileah Cantey
Diversity Outreach Coordinator, Alzheimer's Association

Dr. Adriana Hermida
Assistant Professor, Emory University School of Medicine

Miles Hurley
Elder Care Law Attorney

Moderator: Dr. Ken Hepburn
Emory University School of Nursing
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Avian Influenza Strain Primes Brain for Parkinson's Disease

/PRNewswire/ -- At least one strain of the H5N1 avian influenza virus leaves survivors at significantly increased risk for Parkinson's disease and possibly other neurological problems later in life, according to new research from St. Jude Children's Research Hospital.

In the August 10 online early edition of the Proceedings of the National Academy of Sciences, researchers reported that mice which survived infection with an H5N1 flu strain were more likely than uninfected mice to develop brain changes associated with neurological disorders like Parkinson's and Alzheimer's diseases. Parkinson's and Alzheimer's involve loss of brain cells crucial to a variety of tasks, including movement, memory and intellectual functioning. The study revealed the H5N1 flu strain caused a 17 percent loss of the same neurons lost in Parkinson's as well as accumulation in certain brain cells of a protein implicated in both diseases.

"This avian flu strain does not directly cause Parkinson's disease, but it does make you more susceptible," said Richard Smeyne, Ph.D., associate member in St. Jude Developmental Neurobiology. Smeyne is the paper's senior author.

"Around age 40, people start to get a decline in brain cells. Most people die before they lose enough neurons to get Parkinson's. But we believe this H5N1 infection changes the curve. It makes the brain more sensitive to another hit, possibly involving other environmental toxins," Smeyne explained.

Smeyne noted the work involved a single strain of the H5N1 flu virus, the A/Vietnam/1203/04 strain. The threat posed by other viruses, including the current H1N1 pandemic flu virus, is still being studied.

Early indications are that the H1N1 pandemic strain carries a low neurologic risk, said Richard Webby, Ph.D., director of the World Health Organization Collaborating Center for Studies on the Ecology of Influenza in Animals and Birds, which is based at St. Jude. Webby, who is also an associate member of the St. Jude Department of Infectious Diseases, was not involved in the H5N1 study led by Smeyne.

This study also supports the theory that a hit-and-run mechanism is at work in Parkinson's disease. The investigators believe the H5N1 infection sparks an immune response that persists long after the initial threat is gone, setting patients up for further devastating losses from a second hit, possibly from another infection, drug or environmental toxin. In this case, researchers believe the flu virus is the first hit that sets up development of Parkinson's at a later time.

An estimated 4.1 million Americans, including 1 to 2 percent age 55 and older, have Parkinson's. Many suspect both genetic and environmental factors play a role in its development. The disease is linked to the death of dopamine-secreting cells in an area of the midbrain known as the substantia nigra pars compacta (SNpc). Dopamine is a neurotransmitter responsible for stimulating the motor neurons that control movement. Parkinson's is usually diagnosed after individuals lose 70 to 80 percent of the dopamine-producing cells. Treatment is available, but there is no cure.

Flu is primarily a respiratory disease, but indirect evidence dating back to 1385 links it to neurological problems, including the brain inflammation known as encephalitis. The association between flu and brain disorders like Parkinson's was strengthened by an outbreak of encephalitic lethargic, also known as von Economo's encephalopathy, following the 1918 Spanish flu pandemic. Some of those patients developed Parkinson's symptoms.

St. Jude researchers launched this study nearly three years ago in response to the threat posed by avian flu. Smeyne said there was concern about possible long-term neurological risks facing H5N1 survivors.

Previous studies had isolated H5N1 in the nervous system. But this is the first to show the path the virus takes to enter the brain as well as the aftermath of the infection. Smeyne said the virus' path from the stomach through the nervous system and into the brain is reminiscent of how Parkinson's unfolds.

In this study, mice were infected with an H5N1 flu strain isolated in 2004 from a patient in Vietnam. Robert Webster, Ph.D., said the strain remains the most virulent of the avian flu viruses. Webster, a co-author of the study, holds the Rose Marie Thomas Chair in Infectious Diseases at St. Jude.

About two-thirds of the mice developed flu symptoms, primarily weight loss. After three weeks there was no evidence of H5N1 in the nervous systems of the mice that survived.

But the inflammation the infection triggered within the brain continued for months. It was similar to inflammation associated with inherited forms of Parkinson's. Although the tremor and movement problems disappeared as flu symptoms eased, investigators reported that 60 days later mice had lost roughly 17 percent of dopamine-producing cells in SNpc, a structure found in the midbrain.

Researchers also found evidence that the avian flu infection led to over-production of a protein found in the brain cells of individuals with both Alzheimer's and Parkinson's diseases. The protein, alpha-synuclein, collected in H5N1-infected cells throughout the brain, including the midbrain where key dopamine-producing cells are located. There was little protein accumulation in the brain cells of uninfected mice.

The study marks the first time scientists were able to naturally trigger the protein build-up in an experimental Parkinson's system. "The virus activates this protein," Smeyne explained.

Other authors in this paper include Haeman Jang, David Boltz and Yun Jiao (St. Jude); and Katharine Sturm-Ramirez and Kennie Shephard (formerly of St. Jude).

This work was supported in part by the National Institute of Allergy and Infectious Diseases, National Parkinson's Foundation, Michael J. Fox Foundation, National Institutes of Health and ALSAC.

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Emory and HBO Host Alzheimer's Disease Documentary Screening May 2

The Emory University Alzheimer's Disease Research Center in partnership with HBO and the Alzheimer's Association of Georgia will premiere the HBO documentary film, "MOMENTUM IN SCIENCE" on Saturday, May 2, for a gathering of medical professionals and families who have loved ones living with Alzheimer's disease.

"MOMENTUM IN SCIENCE," is part of an HBO Films' Documentary series called THE ALZHEIMER'S PROJECT.

The ALZHEIMER'S PROJECT, executive produced by Maria Shriver, is a multi-part, multi-platform series that brings new understanding and hope for millions of people affected by Alzheimer's disease.

The screening will be held from 9 a.m. to1 p.m. at the Emory Conference
Center located at 1615 Clifton Rd. in Atlanta. It will be followed by a panel
discussion and Q & A with leading Alzheimer's disease researchers, including:
*Allan Levey, MD, PhD – Professor and Chair, Department of Neurology, Emory
University
*James Lah, MD, PhD – Associate Professor and Vice Chair, Department of
Neurology, Emory University
*Felicia Goldstein, PhD – Director of Neuropsychology, Emory University
*Larry Tune, MD – Professor of Psychiatry and Neurology, Emory University
*Angela Ashley, MD – Assistant Professor of Neurology, Emory University
*Ginny Helms – Vice President of Programs and Services, Alzheimer's Association of Georgia
*Monica W. Parker, MD – Assistant Professor of Medicine, Emory University
*Kenneth Hepburn, PhD – Professor and Associate Dean for Research, Nell
Hodgson Woodruff School of Nursing, Emory University
*Carolyn Clevenger, DNP – Assistant Professor of Nursing, Nell Hodgson
Woodruff School of Nursing, Emory University
*Suzette Binford, Executive Director, Alzheimer's Association of Georgia

THE ALZHEIMER'S PROJECT is a presentation of HBO Documentary Films and the National Institute on Aging of the National Institutes of Health in association with the Alzheimer's Association®, Fidelity® Charitable Gift Fund and Geoffrey Beene Gives Back® Alzheimer's Initiative. The series of four films will debut on HBO on May 10, 11 and 12.
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Study Suggests Blood Test for Alzheimer’s Possible

Researchers have revealed a direct relationship between two specific antibodies and the severity of Alzheimer’s disease symptoms, raising hopes that a diagnostic blood test for the devastating disorder is within reach.

Researchers from the University of Georgia, the Charlie Norwood VA Medical Center in Augusta and the Medical College of Georgia compared antibody levels in blood samples from 118 older adults with the participant’s level of dementia. The team, whose results appear in the current edition of Journal of Gerontology: Medical Sciences, found that the concentration of two specific proteins that are involved in the immune response increases as the severity of dementia increases.

“We found a strong and consistent relationship between two particular antibodies and the level of impairment,” said study co-author L. Stephen Miller, professor and director of clinical psychology training in the UGA Franklin College of Arts and Sciences. “The finding brings us closer to our ultimate goal of developing a blood test that can diagnose Alzheimer’s disease or potentially identify if someone is at higher risk for the disease.”

Miller’s co-authors include Jennifer S. Wilson, a former undergraduate student in the UGA Honors program who is now pursing graduate studies at Emory University; Shyamala Mruthinti, research pharmacologist at the VA Medical Center and adjunct professor at MCG; and Jerry Buccafusco, director of the MCG Alzheimer’s Research Center. The team focused on antibodies that the body creates in response to two proteins that are associated with Alzheimer’s disease. One protein, known as amyloid-beta, forms the plaques that are evident in the brains of people with Alzheimer’s upon autopsy. The other protein, known as RAGE, is involved in the normal aging process but is expressed at higher levels in the brains of people with Alzheimer’s.

In a previous study that compared a group of people with Alzheimer’s disease to a healthy control group, Mruthinti and her colleagues found that anti-amyloid beta and anti-RAGE antibodies are significantly higher in the group with Alzheimer’s. The team’s latest study expands on that finding to reveal a direct relationship between severity of Alzheimer’s disease and levels of the two antibodies in the blood.

“Alzheimer’s is an inflammatory disease of the brain, and these two antibodies give us a way to measure that inflammation,” Mruthinti said. “Using them as an early diagnostic marker may allow us to start drug treatment early, when it’s most effective, to increase the patient’s quality of life.”

While optimistic about their findings, the researchers caution that it could still be years before a diagnostic test based on their work is clinically available. The study found that the relationship between the two antibodies and Alzheimer’s severity persists even after controlling for patient age and total antibody levels. To further test the strength of the relationship, the researchers are now working with a sample that controls for other factors that have the potential to influence levels of the two antibodies, such as diabetes and heart disease. Buccafusco and his colleagues are also working to decrease the cost and time involved in the test.

“We’re in the process of trying to reduce the test to a one-day procedure, whereas right now it takes three to four days,” Buccafusco said. “But even now, our test is orders of magnitude cheaper than having people come in every few months to get a functional MRI or PET scan to try to discern brain plaques.”

The team is targeting the two proteins themselves as a possible treatment for Alzheimer’s disease. Mruthinti explains that, individually, amyloid-beta and RAGE proteins don’t provoke an immune response. The trouble begins when the two bind and the immune system attacks, resulting in constant state of inflammation that damages the brain. The researchers recently developed a way to measure levels of amyloid beta-RAGE complex, and preliminary data using transgenic mice that express Alzheimer’s symptoms suggest that an antigen they created to boost the body’s natural immune response to the complex can reduce the formation of the brain plaques.

“The amyloid beta-RAGE complex cuts off the connections between neurons,” Mruthinti explained, “but our hope is that we can protect those connections by preventing those plaques from forming.”

The research was funded by a Merit Review Award from the Veterans Administration to principal investigator Mruthinti and by the Medical College of Georgia Alzheimer’s Research Center.

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Alzheimer's Gene Slows Brain's Ability to Export Toxic Protein

PRNewswire-USNewswire/ -- The only known genetic risk factor for Alzheimer's disease slows down the brain's ability to export a toxic protein known as amyloid-beta that is central to the damage the disease causes, scientists have found.

The research, published Nov. 13 by the Journal of Clinical Investigation, provides new clues into the workings of a protein known as apolipoprotein E4, or ApoE4. People who carry two copies of the gene have roughly eight to 10 times the risk of getting Alzheimer's disease than people who do not.

The new results mark a step toward resolving a longstanding question that scientists have had about exactly how ApoE4 increases a person's risk for the disease. The findings point to differences in the way that amyloid-beta is removed from the brain depending on which ApoE protein is involved.

Scientists found that when ApoE4 is present, the brain is less efficient at ridding itself of the toxic material, because a molecule that is much slower at removing the substance becomes much more involved.

The new results are in line with a body of research amassed over the last 15 years by the leader of the team, Berislav Zlokovic, M.D., Ph.D., of the University of Rochester Medical Center, that blood circulation plays a key role in the disease. His team has identified much of the molecular machinery that allows amyloid-beta to sidestep the body's safeguards and enter the brain, and he has discovered molecules that falter when the toxic protein accumulates in the brain.

"Our latest findings help explain one of the major risk factors for Alzheimer's disease," said Zlokovic. "ApoE4 changes the brain's ability to rid itself of amyloid-beta. It's becoming more and more apparent that the brain's ability to clear out amyloid-beta, through the vascular system and across the blood-brain barrier, is central to the development of Alzheimer's disease."

In the latest work the Rochester team, working with colleagues at Washington University School of Medicine in St. Louis, found that a molecule known as very low-density lipoprotein receptor, or VLDLR, is an active - but slow - player in the removal of amyloid-beta from the brain. That step is crucial: Once amyloid-beta gets out of the brain and into the body, it can be eliminated easily.

"It's as if you have a pile of trash building up in the brain, and you need to move the trash away before it becomes toxic," said Rashid Deane, Ph.D., one of the authors of the paper and research professor of Neurosurgery at the University of Rochester Medical Center.

"We've known that the brain uses a molecule called LRP1, which is extremely efficient and acts like a fast ferry to remove amyloid-beta. Now we've found that there is another molecule involved, which works much more slowly, and it's especially active when amyloid is coupled to ApoE4," Deane added.

The team showed that speedy LRP1 is central to removing amyloid-beta when ApoE2 or ApoE3 is involved, with the slower VLDLR picking up some of the slack. But when the form of the gene that puts people at risk, ApoE4, is involved, VLDLR nearly alone is responsible for hauling the amyloid-beta away.

"It's like having a choice between a fast ferry and a slow ferry," said Deane. "For reasons we don't yet understand, when ApoE4 is involved, the slow ferry is used almost exclusively. This means that the amyloid-beta isn't removed as quickly as it otherwise would, potentially giving it a chance to accumulate, like we see in the brains of patients with Alzheimer's disease."

The team found that LRP1 is able to export amyloid from the brain about 20 times faster than VLDLR. Consequently, in mice with the more efficient versions of the ApoE protein, ApoE2 and ApoE3, amyloid is cleared out of the brain at a rate about twice or three times as fast as it is in mice with the ApoE4 protein. Amyloid deposits accumulate in the brains of mice with the ApoE4 protein in much higher amounts, about 10 to 15 times as much as in the brains of mice with either ApoE2 or ApoE3.

Not only do the ApoE proteins help determine how quickly amyloid-beta is removed from the brain; the proteins actually couple with amyloid-beta in the brain to form sticky complexes. This gunk gathers around cells and is much more difficult to remove from the brain than free-floating amyloid-beta. Companies are trying to develop drugs that would break up the relationship, freeing amyloid-beta and making it easier to remove from the brain.

The work described in the paper published in the Journal of Clinical Investigation was funded by a Senator Jacob Javits Award from the National Institute of Neurological Disorders and Stroke, and by the National Institute on Aging.

In addition to Zlokovic and Deane, other Rochester authors of the paper include instructor Abhay Sagare, Ph.D., who performed much of the research; technicians Katie Hamm, Margaret Parisi, and Steven Lane; and neuroscientist David Holtzman and graduate student Mary Beth Finn at Washington University School of Medicine.

Zlokovic is a founder of a company, Socratech, which is seeking to commercialize his team's discoveries about how amyloid-beta collects in the brain and how it might be removed more efficiently. He is also the Dean's Professor of Neurosurgery and Neurology and director of the Center for Neurodegenerative and Vascular Brain Disorders.

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Breakthrough Mapping of Alzheimer's Genome Helps ID Four New Suspect Genes

PRNewswire-USNewswire/ -- Four novel genes that may significantly increase the risk of the most common form of late-onset Alzheimer's have been identified by researchers at Massachusetts General Hospital and Harvard Medical School, as reported in the November 7th issue of American Journal of Human Genetics. The findings, part of a larger "Alzheimer's Genome Project" (AGP) established three years ago to identify the full set of Alzheimer's disease genetic risk factors, may lead to more aggressive therapeutic interventions to slow, stop or even reverse the effects of the disease. These new therapies would differ from current treatments that only address the symptoms of the disease.

Dr. Rudolph Tanzi, chairman of the Cure Alzheimer's Fund Research Consortium and the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School, completed the largest family-based genome-wide association screen conducted to date. More than 400 families affected by Alzheimer's disease were screened to determine genetic variants associated with the inheritance of Alzheimer's. The four genes discovered in the family study are described in the article.

Technological advances are improving the understanding of the genetic mechanism that governs Alzheimer's disease and are making it feasible to identify the complete set of genes influencing risk for Alzheimer's disease, Dr. Tanzi said.

In addition to the genome-wide association screen, Dr. Tanzi and Dr. Lars Bertram of Harvard Medical School have been analyzing Alzheimer's genetics literature to determine which of the hundreds of proposed Alzheimer's candidate genes are genuine disease genetic risk factors. These summarized findings, implicating 30 gene candidates, are updated regularly at http://alzgene.org/ (a public Web site sponsored by the Cure Alzheimer's Fund). Tanzi and Bertram highlighted 10 of the most interesting of these genes in the current issue of Nature Reviews Neuroscience. Ultimately, the goal is to combine the results of the Alzheimer's family-based genome-wide association screen with the bioinformatics results of AlzGene.org.

The combined efforts of the family-based genome-wide association screen and AlzGene.org studies have led to the identification of 70 genes containing variants that either confer risk for, or protect against, Alzheimer's, making up the most comprehensive genetic map of the disease.

"This project is the most complete and comprehensive search for the genes that cause Alzheimer's disease published to date," Tanzi said. "Our hope is to use this new information to not only better diagnose and someday predict risk for Alzheimer's but to also learn from these genes the biological causes of Alzheimer's. The knowledge gained from understanding the Alzheimer's-associated defects in these genes will almost certainly accelerate the development of novel therapeutics and hopefully lead to a potential cure for this devastating disease."

The current understanding of the causes and pathological progression of Alzheimer's disease have been made possible by studies of four Alzheimer's genes discovered between 1987 and 1995, three of which were co-discovered by Tanzi. Since these genes account for only 30 percent of the genetic basis of Alzheimer's disease, three years ago Cure Alzheimer's Fund initiated the Alzheimer's Genome Project aimed at determining the remaining 70 percent of the genetic basis of Alzheimer's disease. Taking advantage of major technological and analytical breakthroughs in human genetic studies, the project was able to reach this milestone with a limited budget, led by a contribution of $3 million from Cure Alzheimer's Fund.

"We are on the cusp of a rare 'science moment' that could alter the way we diagnose, treat and prevent Alzheimer's disease," said Tanzi. "Ultimately, the combined results of the family-based genome-wide screen and AlzGene.org will allow for the reliable prediction of Alzheimer's disease while also guiding the development of therapies."

Alzheimer's disease is the most common cause of dementia in the elderly and a burgeoning unmet medical need that only will worsen as individuals continue to live longer. The Alzheimer's Association estimates that as many as 5.2 million Americans are living with Alzheimer's disease, including between 200,000 and 500,000 people under age 65 with young-onset Alzheimer's disease or other dementias. Experts predict that, by 2010, nearly a half million new cases of Alzheimer's disease will occur each year; and by 2050, nearly a million new cases will occur annually.

Cure Alzheimer's Fund has no endowment and passes funds raised directly to selected research as determined by the Cure Alzheimer's Research Consortium. The Foundation has no financial or intellectual property interest in the research funded, and will make known the results of all funded research as soon as possible. At a time when the federal government investment for Alzheimer's research and education is decreasing, Cure Alzheimer's Fund has raised more than $10 million, investing all of it directly into research.

Cure Alzheimer's Fund(TM) is a 501c3 public charity established to fund targeted research with the highest probability of slowing, stopping or reversing Alzheimer's disease. For more information, please visit http://www.curealzfund.org/.

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Alzheimer's Passes Diabetes As Sixth Leading Cause Of Death In U.S.

(SPM Wire) Alzheimer's disease is now the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention (CDC) National Center for Health Statistics.

The CDC estimates that 72,914 Americans died of Alzheimer's disease in 2006. With an unprecedented historic population shift of 78 million aging baby boomers in the country and this disease poised to strike 10 million boomers -- it is clear this escalating epidemic must be addressed now.

Today, as many as 5.2 million Americans are living with Alzheimer's disease. The Alzheimer's Association's "2008 Alzheimer's Disease Facts and Figures" report revealed one out of eight baby boomers will develop this disease that currently has no effective disease-modifying treatments to halt or delay its progression.

Experts predict by 2010, there will be almost a half million new cases of Alzheimer's disease each year; and by 2050, there will be almost a million new cases each year.

"The CDC's announcement that Alzheimer's disease jumped from the seventh to the sixth leading cause of death should serve as a wake-up call to the nation," said William Thies, PhD, vice president of Medical and Scientific Relations at the Alzheimer's Association. "The fact that there are no effective treatments for Alzheimer's has allowed the disease to pass diabetes. It is vitally important that we increase Alzheimer's research funding to slow or stop the progression of this devastating disease."

Researchers are closing the gap in developing accurate ways to diagnose and treat Alzheimer's.

Although there are several promising drugs currently in Phase III clinical trials, many feel that insufficient research funds are committed to research focused on Alzheimer's disease treatment and prevention. This situation is further compounded by the fact that for the past five years the NIH budget has been essentially flat, stresses the Alzheimer's Association, which continues to push for the acceleration of research.

The CDC also reported that while deaths from Alzheimer's disease were on the rise, other chronic conditions were on the decline. Between 2005 and 2006, the largest decline in age-adjusted death rates occurred for influenza/pneumonia (12.8 percent), and also included chronic lower respiratory diseases (6.5 percent), stroke (6.4 percent), heart disease (5.5 percent) diabetes (5.3 percent), hypertension (5 percent), chronic liver disease (3.3 percent) and cancer (1.6 percent).

The Alzheimer's Association is the leading voluntary health organization in Alzheimer care, support and research. For more information, visit www.alz.org.

Emory Begins Testing New Alzheimer's Disease Vaccine

Doctors at Emory University will begin testing a vaccine designed to slow the accumulation of amyloid plaques in the brains of patients with Alzheimer's disease.

Alzheimer's affects more than 4.5 million Americans and is marked by gradual nerve cell death and a progressive loss of memory and mental functioning. All of the medications now available aim to improve the functioning of the nerve cells that remain alive.

Several still-experimental vaccines or immunotherapies take a different approach. They target beta-amyloid, a naturally occurring protein that clumps together and forms plaques in the brains of Alzheimer's patients. The clumps appear to damage brain cells.

The study's main purpose is to evaluate the vaccine's safety, possible side effects and how well it stimulates the immune system.

"This is an exciting time for those who treat and care for people with Alzheimer's," says Allan Levey, MD, the principal investigator for the study and chairman of the Department of Neurology at Emory University School of Medicine. "By harnessing the patient's own immune system, it may be possible to change the course of the disease, rather than simply treat its symptoms."

Previous research on mice genetically engineered to develop an Alzheimer's-like condition has found that vaccination with beta-amyloid at birth protects them from plaque formation and mental decline. Older mice also showed some benefit from vaccination.

"Experiments in mice and still-limited evidence from human trials suggest that antibodies against the beta-amyloid protein can aid in clearing its buildup from the brain," Dr. Levey says.

An earlier clinical trial of a beta-amyloid vaccine in humans was halted in 2002 because a small fraction -- six percent -- of the participating patients developed meningoencephalitis, an inflammation of the brain and the tissue surrounding it.

The new vaccine, developed by the pharmaceutical firm Merck, uses a smaller piece of the beta-amyloid protein. The smaller piece is expected to stimulate antibody production but avoid activating T cells, which are the shock troops in an inflammatory response. This trial is the first time this vaccine will be used in people.

Despite the unacceptable safety profile of the previous vaccine, patients who developed antibodies against amyloid protein -- about 20 percent of those participating -- did appear to benefit.

As a group, "antibody responders" showed improvement on a set of tests designed to measure memory, decision-making and verbal ability, but not on other tests often used on patients with Alzheimer's, according to a 2005 study published in the journal Neurology.

Some antibody responders also showed reductions in the level of another protein called tau in their cerebrospinal fluid. Tau tends to build up inside neurons in Alzheimer's disease and scientists believe its presence in cerebrospinal fluid is related to cell death.

Other companies are testing related medications called passive immunotherapies, where a vaccine is replaced with pre-made antibodies either from human donors or engineered to resemble human antibodies. Emory researchers anticipate they will participate in these clinical trials later in 2008.

In the current study, sponsored by Merck, men and women ages 55 and older with mild to moderate Alzheimer's disease are eligible to participate. Several other medical centers across the United States and Sweden are also taking part.

The patient must have a reliable caregiver, who will attend all visits and answer questions about him or her. In addition, a patient must not live in a nursing home or facility, have another neurological disorder, have a history of stroke, drug or alcohol abuse, or have received blood donations or blood derived-products in the last six months.

"It is important for patients and caregivers to recognize that this is an experimental vaccine and some previous trials did fail," says Dr. Levey. "We can proceed only with a sense of balance and respect for patient safety."

Patients will receive three intramuscular injections of the vaccine or a placebo over the course of six months.

They will be monitored by magnetic resonance imaging (MRI) before each dose of vaccine to guard against indications of inflammation or other side effects. The study is expected to last for a total of four years.

For more information, call the Emory Alzheimer's Disease Research Center at 404-728-6950.
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