The APOE ε4 gene variant promotes Aβ plaque formation [85], which facilitates the loss of key presynaptic proteins [86], disrupts long-term potentiation and plasticity [87], leads to a reduction in the dendritic density [88], and has a role in the hereditary pathogenesis of AD—up to 4-fold in people in the heterozygous form (APOE3/APOE4 or APOE2/APOE4) and up to 15-fold in the homozygous form (APOE4/APOE4) [69,77,89]. Here, APOE is linked to Alzheimer disease.