In the pathogenesis of AD, neuroinflammation is triggered by Aβ deposition, phosphorylation of tau, and subsequent formation of neurofibrillary tangles, which stimulate microglia to differentiate toward the M1 phenotype; this phenomenon increases the M1/M2 ratio, which promotes cellular stress, neuronal dysfunction, and neurodegeneration [7]. Here, MAPT is linked to Alzheimer disease.