The pathological hallmarks of AD in the central nervous system (CNS) are: (i) the extracellular accumulation of APP-derived Aβ oligomers and other materials into dense senile plaques; (ii) the intraneuronal hyperphosphorylation of the microtubule-binding protein tau which induces its aggregation into neurofibrillary tangles (NFTs); and (iii) chronic inflammation [4]. This evidence concerns the gene MAPT and Alzheimer disease.