Altered Aβ homeostasis plays a crucial role in AD pathogenesis: mutations in genes involved in Aβ generation, including APP, PSEN1, and PSEN2 are known to cause early-onset, familial AD (EOAD) [5, 6]; and as the most important risk factor for late-onset, sporadic AD (LOAD), APOE ε4-encoded ApoE4 accelerates early seeding of Aβ pathology and compromises Aβ metabolism and clearance through multiple pathways [7–9]. This evidence concerns the gene APOE and Alzheimer disease.