The main hypothesis for the neurotoxicity and synaptic dysfunction in AD are extracellular amyloid-β (Aβ) senile plaques and intracellular neurofibrillary tangles (NFTs) of phosphorylated tau (p-tau), although many other mechanisms involved in AD pathogenesis have been described, such as neuroinflammation, oxidative stress, or metabolic dysfunction [16]. Here, MAPT is linked to Alzheimer disease.