AD is characterized by abnormal synaptic functions due to a plethora of pathogenic mechanisms including mitochondrial dysfunction, neuroinflammation and oxidative stress that cause alterations of protein homeostasis and lead to development of AD molecular hallmarks such as deposition of both amyloid-β (Aβ) and phosphorylation of microtubule-associated protein Tau (i.e., neurofibrillary tangles, NFTs) in the brain [27, 28]. This evidence concerns the gene MAPT and Alzheimer disease.