A key feature of AD development is enhanced proteolytic cleavage of the amyloid precursor protein (APP) by the aspartyl protease, beta-site APP-cleaving enzyme 1 (BACE1), which, with γ-secretase, raises levels of β-amyloid peptides leading to amyloid aggregation and plaque formation [19]. This evidence concerns the gene BACE1 and Alzheimer disease.