A plethora of potential pathways, such as increased oxidative stress, ER-mediated misfolding of proteins, as well as a decline in proteasome/autophagic stimulated protein clearing, and aging-associated events, accelerate the Aβ and tau deposition in AD (López Salon et al., 2000; Hoozemans et al., 2005). This evidence concerns the gene MAPT and Alzheimer disease.