According to the current understanding of molecular pathogenesis, the main hallmarks of Alzheimer’s disease are the abnormal deposition of amyloid plaques in the brain, composed of β-amyloid peptide (Aβ), and neurofibrillary tangles, containing hyperphosphorylated tau proteins.2,10,11 The amyloid cascade theory proposes that Aβ formation is directly responsible for triggering tau phosphorylation and formation of neurofibrillary tangles, leading to neuronal loss and cognitive deficits.12-14. The gene discussed is MAPT; the disease is Alzheimer disease.