The main hypothesis for the neurotoxicity and synaptic dysfunction in AD focuses on the typical pathological hallmarks of the disease, mainly intracellular neurofibrillary tangles (NFTs) of phosphorylated tau (p-tau) and extracellular amyloid-β (Aβ) senile plaques, although many other mechanisms involved in AD pathogenesis have been described [19]. Here, MAPT is linked to Alzheimer disease.