The deposition of amyloid-β (Aβ) derived from the cleavage of amyloid precursor protein (APP) by β and γ-secretases and the hyperphosphorylation of Tau (a microtubule-associated protein) are the hallmarks of AD (Bertram and Tanzi, 2005; Jin et al., 2011). This evidence concerns the gene APP and Alzheimer disease.