Alzheimer's Association Announces 1999 Zenith Research Awards

Alzheimer's Association
Friday, 1 October 1999

The Alzheimer's Association announced today that eight researchers from around the country have been selected to receive grants of $200,000 each over two years from the Association's 1999 Zenith Fellows Award Program.

"The Zenith Awards are an especially exciting part of the Association's grantmaking program because they are significant financial awards to senior scientists doing the most aggressive, innovative work," said William Thies, the Association's vice president of medical and scientific affairs. "These are the kinds of groundbreaking projects that open new doors and serve as the catalyst for important new developments in Alzheimer research."

The Zenith awards are funded by generous donations from the Alzheimer's Association Zenith Fellows, a group of individuals and organizations who have made a substantial personal commitment to the advancement of Alzheimer's disease research.

"It is absolutely crucial that we provide scientists with the resources they need to help us create a world without Alzheimer's disease," Thies said. "About four million Americans currently have Alzheimer's and unless a cure or prevention is found, that number could grow to 14 million in just the next 50 years."

Alzheimer's Association 1999 Zenith Award Recipients

Gregg G. Gundersen, Ph.D.
Columbia University, New York, N.Y.
"Novel Microtubule Targeting Function of Tau Protein"

Gundersen is investigating the function of tau protein, a principal component of neurofibrillary tangles that are one of the pathological hallmarks of Alzheimer's disease. Gundersen's research will explore how tau changes during the Alzheimer's disease process. In understanding this change, Gundersen's research may lead to interventions that could prevent the development of neurofibrillary tangles and potentially halt the progression of Alzheimer's disease.

John Hardy, Ph. D.
Mayo Clinic, Jacksonville, Fla.
"Genetic Resolution of Presenilin as a Therapeutic Target"

Hardy is investigating the role of presenilin genes, genes associated with early-onset Alzheimer's disease. Hardy's research will determine whether these genes stimulate the metabolism of amyloid precusor protein (APP) — a protein that is abnormally processed and converted to beta amyloid plaques, a pathological hallmark in people with Alzheimer's disease. Results from this research may enable scientists to develop a therapy aimed at stimulating or inhibiting the function of presenilins in order to halt the Alzheimer's disease process.

John Maggio, Ph.D.
University of Cincinnati, Cincinnati, Ohio
"In Vivo Measurement of Amyloid-Beta Deposition"

Maggio's research focuses on the use of noninvasive imaging to monitor the accumulation of beta amyloid plaques in the brain, a defining pathological feature of Alzheimer's disease. Currently, Alzheimer's is diagnosed through a process of elimination to rule out other diseases, and probable diagnosis is obtained only after symptoms appear. Maggio plans to develop a radioactive molecule that can be absorbed by beta amyloid plaques in the brain.

This development may enable researchers to use noninvasive, gamma camera imaging to monitor the development of amyloid plaques throughout the Alzheimer disease process and potentially diagnose Alzheimer's before outward symptoms are present. The same technology could significantly facilitate clinical trials of experimental therapeutic agents now under development.

Lennart Mucke, Ph.D.
University of California, San Francisco, CA
"Regulated Transgenic Models to Test Novel Treatment Strategies for Alzheimer's Disease"

Mucke is studying novel Alzheimer's disease treatment strategies in transgenic mice models — mice that have been genetically altered to develop Alzheimer's disease pathology. Mucke's research will determine whether decreasing apoE4, a protein associated with late-onset Alzheimer's disease, in brains of mice for different periods of time can improve cognitive function and diminish neurodegeneration. The results of these studies could provide important guidance in the development of apoE-targeted drug treatments.

Mark Smith, Ph.D.
Case Western Reserve University, Cleveland, Ohio
"Cell Cycle Dysfunction in Alzheimer's Disease"

Based on his groundbreaking findings that neurons in people with Alzheimer's disease share characteristics with cells that are dividing, Smith is studying the causes and consequences of such biochemical abnormalities. Smith's research will lead to a greater understanding of the changes in Alzheimer's disease as well as provide a model system that could potentially be used to screen therapeutic agents.

Keith Thulborn, M.D., Ph.D.
University of Pittsburgh
"Functional Magnetic Resonance Imaging (FMRI) of Cognitive Changes in Normal Elderly Subjects and Patients with Probable Alzheimer's disease (pAD)"

Thulborn's research will involve the use of functional magnetic resonance imaging (fMRI), a noninvasive imaging device that measures the brain's function through changes in blood flow and metabolism. Thulborn will compare changes in the brain's cognitive function of healthy elderly people to people diagnosed with probable Alzheimer's disease. Results from this research may show fMRI is a tool that could be useful in diagnosing Alzheimer's before symptoms are present. Thulborn's work also may serve to design and monitor interventions for this devastating disease.

Thomas Wisniewski, M.D.
New York University, New York, NY
"Amyloid Beta and Apolipoprotein E Interactions in Vitro and in Vivo"

Wisniewski's research will focus on the interaction between apoE, a protein whose main function is to transport cholesterol, and beta amyloid, a protein abnormally processed by nerve cells in the brains of people with Alzheimer's disease. Wisniewski will determine apoE's role in influencing the formation of neurofibrillary tangles, one of the pathological hallmarks of Alzheimer's, as well as its ability to clear beta amyloid from the brain.

Bruce A. Yankner, M.D., Ph.D.
Harvard Medical School, Boston, Mass.
"Regulation of Amyloid b Protein Metabolism and Toxicity by Apolipoproteins and Dietary Cholesterol"

Yankner is studying the relationship between dietary cholesterol and the development of beta amyloid plaques, a defining pathological feature in the brains of people with Alzheimer's disease. Yankner's research is based on a working hypothesis that the level of apoE — a protein whose main function is to transport cholesterol — is a major determinant of beta amyloid levels in the brain and can be regulated by dietary cholesterol. If Yankner's research shows that the risk of Alzheimer's disease associated with an apoE4 gene, a gene associated with late-onset Alzheimer's, can be reduced by diet, then early apoE genetic testing may be beneficial.

Alzheimer's disease is a progressive, degenerative disease that usually manifests itself with subtle symptoms of memory loss and forgetfulness. These early symptoms are often dismissed as normal signs of aging. As the disease takes its toll, it eventually causes people to lose their ability to think and function independently.

The Alzheimer's Association was established in 1980, a time when little biomedical research was done on Alzheimer's disease, few physicians could diagnose it, and most Americans had never heard of it. The Association created its own research program in 1982 specifically to encourage Alzheimer's disease research. That year, it awarded seven grants totaling $78,000.

For more information, or to contact Alzheimer's Association, see their website at: www.alz.org

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