Although the molecular mechanisms involved in the etiology and pathogenesis of AD have not been completely elucidated, the accumulation of β-amyloid (Aβ) and hyperphosphorylation of tau in the brain is the hallmarks of AD, and microglia-mediated neuroinflammation is well known to be related to the onset and progression of AD due to the release of proinflammatory mediators [2, 3]. The gene discussed is MAPT; the disease is Alzheimer disease.