Classical neuropathological hallmarks of AD, such as intraneuronal accumulation of hyperphosphorylated Tau protein in neurofibrillary tangles or extracellular deposition of amyloid-β peptide (Aβ) in senile plaques, have been considered as the culprit of neuronal damage; however, they show a weak correlation with memory loss (Selkoe, 2001; Nelson et al., 2012). This evidence concerns the gene MAPT and Alzheimer disease.