Classical hallmarks for AD include extracellular senile plaques formed by the deposition of β-amyloid peptide (Aβ), excessive phosphorylation of the tau protein, and formation of intracellular neurofibrillary tangles—all these processes leading to loss of synapses, neuronal death, and proliferation of astrocytes (Masters et al., 2015). This evidence concerns the gene MAPT and Alzheimer disease.