One of the characteristics of Alzheimer’s disease is the extracellular accumulation of β-amyloid peptide (βA)—mainly the βA1-42 isoform—which forms plaques in various regions of the cerebral cortex and intracellular neurofibrillary tangles of hyperphosphorylated tau protein in the hippocampus, medial temporal lobe, isocortical temporal, parietal areas, and frontal lobes, producing loss of regulation of neuronal metabolism such as glutamatergic, cholinergic, and GABAergic neurotransmission [63]. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.