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Research in our laboratory focuses on the biochemistry and biophysics of amyloid plaques and their relationship to sporadic and familial forms of Alzheimer’s disease. Plaques are a principal pathological feature of Alzheimer’s disease and appear as abnormal accumulations of fibrous or thread-like structures within the brain. These plaques are assembled by the misfolding and aggregation of the amyloid-beta (Abeta) protein. We have been studying its properties with an emphasis on the factors responsible for the transition from the normal to diseased fibrous state, the ability of aggregated Abeta‚ to kill nerve cells in culture, and the mechanism by which this is accomplished. Considerable advances have been made in this area and we are expanding our efforts to look for modulators of plaque formation as well as the cellular receptors which we feel are responsible for amyloid’s “killer” action. Our ultimate goal is to understand the events that culminate in these abnormal and detrimental proteins and the development of drugs capable of controlling these processes. These investigations are relevant to both the sporadic and familial forms of Alzheimer’s disease which exhibit identical amyloid pathology but differ only in their rate of progression.
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