To recapitulate AD pathology, transgenic mouse models carry familial AD gene mutations in the amyloid precursor protein (APP) and/or presenilins (PS) based on the amyloid hypothesis, which postulates an increased production or decreased removal of the APP proteolytic fragment, amyloid β-protein (Aβ), as the primary cause of AD [16]. This evidence concerns the gene PRB2 and Alzheimer disease.