In AD, extracellular amyloid-β (Aβ) deposits and intracellular phosphorylated Tau aggregates form senile plaques and neurofibrillary tangles, respectively, two neuropathological hallmarks that induce neuroinflammation and subsequent neuronal damage associated with cognitive decline and neuropsychiatric symptoms [3,4,5,6,7]. Here, MAPT is linked to Alzheimer disease.