Elevation of the levels of β-amyloid (Aβ), a ∼4 kDa secreted polypeptide, is thought to be involved in the pathogenesis of AD because mutations in the Aβ precursor protein (AβPP) or presenilin genes that lead to increased production of Aβ are causative for familial AD [1]-[8]. This evidence concerns the gene APP and Alzheimer disease.