Contact: Deborah Miller
Lourdes Torres
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For Immediate Release
NYU School of Medicine Researchers Receive $11.4 Million for Alzheimer's Research
New York, NY - January 31, 2000 -- NYU School of Medicine researchers have received more than $11 million from the National Institute on Aging to study amyloid beta, a protein associated with Alzheimer's disease. Ralph Nixon, M.D., Ph.D., Professor of Psychiatry, and Sam Gandy, M.D., Ph.D., Professor of Psychiatry, each received funding to lead large collaborative studies.
Deposits of amyloid beta are one of the pathologic hallmarks of Alzheimer's disease. The memory robbing disease, which is estimated to affect some four million people in the United States, is the most common form of dementia to strike people over the age of 65. Amyloid beta hasn't yet been determined definitively to cause the disease, but based on increasing evidence from many laboratories, most researchers believe that it is the most directly implicated.
Amyloid is the general term used to describe proteins that form so-called beta-sheets, which fold in a particular way to form deposits in the brain. The new NYU studies, which involve more than 25 investigators from five institutions, will advance the understanding of Alzheimer's and may lead to new treatments for the most common form of dementia to strike people over age 65.
Dr. Nixon received a $7.7 million grant to elucidate how amyloid beta is processed in the compartments of nerve cells called endosomes and lysosomes. Part of this work will involve the creation of new animal models to clarify how aberrant protein processing contributes to Alzheimer's.
Dr. Gandy received $3.7 million to clarify the biochemical role of certain chaperone compounds, called apolipoproteins, in the metabolism of amyloid beta and to identify the tissues that produce the protein.
Over the past 14 years, Drs. Nixon and Gandy have distinguished themselves as leading Alzheimer's investigators. Dr. Gandy's research, for example, has elucidated the two pathways that generate amyloid. One pathway generates a soluble, innocuous form of amyloid, while the other generates an insoluble, "bad" form that aggregates into plaques.
"Everyone normally generates amyloid beta throughout the body and the brain," says Dr. Gandy. "However, not everyone forms amyloid beta deposits and Alzheimer's disease. We will be investigating how apolipoproteins and other compounds influence the deposition of amyloid. By finding out how apolipoproteins influence the production of amyloid beta plaques, we may be able to find a novel therapy for this disease," says Dr. Gandy, who also is an investigator in the Center for Dementia Research at the Nathan S. Kline Institute in Orangeburg, N.Y., an affiliate of NYU School of Medicine.
Dr. Nixon's research has identified the compartments within nerve cells that exhibit the first telltale signs of Alzheimer's disease. His group found, for example, that endosomes within nerve cells from the brains of Alzheimer's patients were up to 32 times larger than normal, suggesting an enormous increase in activity. All cells possess endocytic pathways, a sort of relay station for proteins. Endosomes play a vital role in processing proteins in the cell's internal and external environment. Dr. Nixon believes that the activation of endocytic pathways in cells promotes the generation of amyloid beta in Alzheimer's disease.
"Some of the early signs of disease that we have found may be used as markers to screen for disease and as targets for early treatment," says Dr. Nixon, who is also Director of the Center for Dementia Research at the Nathan S. Kline Institute.
Dr. Nixon's five-year collaborative study involves 17 researchers at NYU School of Medicine and the Nathan Kline Institute. Among the investigators are: Karen Duff, Ph.D., Associate Professor of Psychiatry; Thomas Wisniewski, M.D., Associate Professor of Neurology and Pathology; Blas Frangione, M.D. Ph.D., Professor of Pathology; Mony de Leon, Ed.D., Professor of Psychiatry; Anne Cataldo, Ph.D., Associate Professor of Psychiatry; and Joseph Helpern, Ph.D., Research Professor of Psychiatry and Radiology and Paul Mathews, Ph.D., Assistant Professor of Psychiatry
Dr. Gandy's four-year collaborative study involves more than 10 investigators from five institutions. Dr. Gandy's group will determine how the genetic variant of apolipoprotein most often associated with Alzheimer's disease regulates amyloid deposition. Dr. Jorge Ghiso, Associate Professor of Pathology at NYU School of Medicine, will lead a group investigating how different forms of apolipoprotein contribute to the soluble amyloid found in body fluids and to the toxic form of amyloid found in deposits in the brain. Dr. Michelle E.Ehrlich, Associate Professor of Psychiatry and Cell Biology at NYU School of Medicine, will lead a group establishing animal models that can be used to study the role of apolipoproteins and amyloid deposition.
Dr. Joseph Buxbaum, Associate Professor of Pathology at Mount Sinai School of Medicine, and Dr. Rong Wang, an Assistant Professor at The Rockefeller University, will provide measurements of amyloid protein using state-of-the-art assays. Finally, Dr. Charles C. Ouimet, Professor of Neuroscience and Psychology at Florida State University, will analyze amyloid deposits in the brain using sophisticated staining techniques. Another major collaborator is Dr. David Holtzman, Associate Professor of Neurology, Molecular Biology and Pharmacology at Washington University School of Medicine in St. Louis, who is an expert in the biochemistry and transgenesis of apolipoprotein-amyloid interactions.
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