Indeed, SAMP8 mice develop early learning and memory deficiencies since their young age (3–5 months), progressing then toward the development of full AD pathology (8–12 months), where they display the main pathophysiological and clinical features of AD, including the deposition of Aβ 1–40 or 1–42 proteins in hippocampal granules; hyperphosphorylation of tau protein; increase in α-syn, presenilin, oxidative damage, glutamate and nNOS levels; and decrease in ChAT activity [14]. The gene discussed is MAPT; the disease is Alzheimer disease.