The pathological brain changes typically begin much earlier than the onset of AD clinical symptoms; changes that include the deposition of β-amyloid (Aβ) peptides outside the neurons (i.e., senile or Aβ plaques) and the intraneuronal accumulation of an abnormal form of tau protein (i.e., neurofibrillary tangles, NFTs) (Sperling et al., 2011; Kumar et al., 2015; Hanseeuw et al., 2019). The gene discussed is MAPT; the disease is Alzheimer disease.