NEW YORK, November 18, 2007For unknown reasons a protein called amyloid beta aggregates into toxic plaques in the brain, killing neurons. These plaques are one of the hallmarks of Alzheimers disease. Now two new animal studies show for the first time that the deadly transformation of amyloid beta into plaques can be prevented through an interaction between amyloid beta and another protein called cystatin C.
Although much work needs to be done, these new findings may open the door to new treatments for Alzheimers disease that mimic the effects of cystatin C, says Efrat Levy, Ph.D., Associate Professor in the Departments of Psychiatry and Pharmacology at New York University School of Medicine, and the lead author of the study. We are really excited by these findings because recent studies show that cystatin C is protective against a variety of insults that cause cell death in the brain. Our potential therapeutic approach focuses on keeping amyloid beta in a water soluble form, preventing its accumulation in the brain, and thus slowing, halting, or reversing disease progression, says Dr. Levy, who is also Director of the Laboratory of Molecular Pathology of Cerebral Amyloidosis at the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, New York.
With support from the Alzheimers Association, Dr. Levys laboratory has already begun studies to develop a drug that will mimic the ability of cystatin C to bind to a non-pathological form of amyloid beta and thereby prevent its accumulation into plaques in the brain.
Alzheimers is estimated to affect 5 million Americans and there are no medicines that can delay or prevent the disease. Many laboratories worldwide are pursuing ways to prevent the clumping of amyloid beta as possible therapies for the disease. It isnt known whether the protein actually causes Alzheimers, but amyloid beta is one of the proteins implicated in the disease process.
The two studies appear in
|Contact: Pam McDonnell|
New York University Medical Center and School of Medicine