Alzheimer’s disease is neuropathologically characterized by the formation and extracellular deposition of insoluble plaques, consisting of the 38–43 amino acid long peptide amyloid-β (Aβ) and intracellular neurofibrillary tangles of the tau protein, as well as a substantial neuronal loss [1]. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.