Alzheimer's Disease (AD) is a debilitating disease characterized b progressive cognitive and memory deficits. Despite the prevalence of AD in the 65 or older population, there is no treatment available for the patient. There is enough evidence to support the hypothesis that amyloid beta peptide (Abeta), which is toxic to neuronal cells, is the cause of the disease. The long term objective of the proposed project is to understand the mechanism by which neuronal cells become resistant to oxidative stress induced by Abeta toxicity, and to identify genes and proteins that are involved in the phenotypic change. Identification of such proteins and genes is important not only for understanding the mechanism by which Abeta kills the neuronal cells but also for developing potential screening techniques and clinical treatments for AD and possibly for other related diseases. Specifically, two different molecular biological procedures, subtractive hybridization and the differential display technique, will be used to identify genes that may contribute to the resistanc3e in the Abeta resistant cell lines or to the sensitivity in the parental Abeta sensitive cell lines.
