Despite near 50 risk loci have been implicated in AD, such as amyloid precursor protein (App) and interleukin 34 (Il-34), among others [10], a wide body of literature provides compelling evidence of genetic pleiotropy for AD, having a quasi ‘monogenetic role’ of apolipoprotein E (ApoE) [11] because it confers a strong genetic risk for AD, cardiovascular and neurogenerative diseases [12, 13]. This evidence concerns the gene APP and Alzheimer disease.