In the brains of postmortem AD patients, CDK5 level was found to be elevated (Lee et al., 1999), leading to an upregulation of the activities of presenilin 1 (PS1) and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), resulting in increased Aβ production and tau hyperphosphorylation (D’Mello, 2021). This evidence concerns the gene BACE1 and Alzheimer disease.