Abstract
Current research in molecular genetics and molecular cell biology has disclosed that Alzheimer's disease (AD) is composed of a number of etiologically heterogenous disorders. In dominantly inherited early onset AD, the missense mutations found in the genes encoding amyloid precursor protein (APP), presenilin‐1, and/or presenilin‐2, are all known to increase the production and secretion of Aβ1–42(43). The abnormal deposition of Aβ1–42 is currently considered to play a key role in triggering a pathological array of symptoms in AD. Investigation of the molecular mechanism causing dominant AD provides a powerful model to understand the etiology of sporadic late‐onset AD, whose mechanism remains unknown.
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