The majority of AD is sporadic, but mutations in APOE, particularly in the APOE ε4 allele, encoding a lipid carrier protein, APP, PSEN1, and PSEN2 (which encode γ-secretase regulators), increase the individual likelihood of developing AD, probably through the impaired clearance of Aβ plaques [2,7,8]. This evidence concerns the gene APP and Alzheimer disease.