AD has, indeed, a diverse pathogenic etiology and the different major processes associated with this disease cover amyloid cascade, glutamatergic, oxidative stress, cholinergic, vascular and epigenetics hypotheses (Table 1) as well as other recent approaches, e.g., the inhibition of Fyn kinase activation by amyloid β-prion interaction and consequent inhibition of Tau hyperphosphorylation [50], identified as promising strategies for treatment against AD [47]. This evidence concerns the gene MAPT and Alzheimer disease.