Abstract
A hallmark of Alzheimer's disease is the deposition of amyloid plaques within neural tissue. Indeed, it has been widely suggested that neural damage caused by plaque deposition is the physiological basis for the pathogenesis of Alzheimer's disease. A variety of molecular-biological studies have shown that these amyloid plaques principally comprise a 40–42 amino-acid peptide known as Aβ, which is itself a proteolytic cleavage product of a ∼770 amino-acid transmembrane protein known as Aβ precursor protein (APP). Thus, generation of Aβ from APP is considered to be a crucial requirement for the development of Alzheimer's disease.
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