beta-amyloid protein aggregation: its implication in the physiopathology of Alzheimer's disease

beta -Amyloid protein (A beta), a 39-42 residue peptide resulting from the proteolytic processing of a membrane-bound beta -amyloid precursor protein (APP), is one of the major components of the fibrillar deposits observed in Alzheimer patients. A beta fibril formation is a complex process which inv olves changes in A beta conformation and self-association to form cross-bet a pleated sheets, protofibrils, and fibrils. Since the aggregation of solub le A beta peptide into fibrils is viewed as a critical event in the physiop athology of Alzheimer's disease (AD), preventing, altering, or reversing fi bril formation may thus be of therapeutic value. This review will focus on the current state of knowledge of A beta fibril formation, with special emp hasis on physiological and exogenous inhibitors which may have a therapeuti c potential. (C) 2001 Editions scientifiques et medicales Elsevier SAS.