It is generally believed that neurodegeneration in AD is caused by elevated levels of an abnormal form of the amyloid-β (Aβ) peptide, Aβ42, that forms extracellular oligomers and aggregates, and the hyper-phosphorylation of the microtubule-associated protein Tau, promoting its disassociation from axonal microtubules and deposition in insoluble neurofibrillary fibrillary tangles [1,2,3,4]. This evidence concerns the gene MAPT and Alzheimer disease.