The earlier onset and increased prevalence of AD in DS could be explained in part by the triplication of Hsa21 genes increasing the risk of AD and promoting the production of Aβ and the aberrant phosphorylation of Tau, such as SOD1, BACE2, S100β or DYRK1A. Moreover, the trisomic Ts65Dn and Ts1Cje mouse models of DS exhibited aberrant phosphorylation of Tau (Liu et al., 2008; Shukkur et al., 2003). The gene discussed is BACE2; the disease is Alzheimer disease.