β -amyloid (Aβ), an amyloid precursor protein (APP) that is abnormally cleaved by the β-site APP cleavage enzyme 1 (BACE1) and γ-secretase, significantly contributes to AD pathology; the accumulation of this peptide in the hippocampus and cortex causes neuronal cell dysfunction and cognitive deficits in AD patients [2]. This evidence concerns the gene APP and Alzheimer disease.