From a histopathological point of view, non-mendelian early- and late-onset sporadic AD share the same molecular pathologies including amyloid-beta (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated 3/4R tau pathology, suggesting that an earlier symptom onset is unlikely to be specifically driven by distinct molecular characteristics of AD pathology11. The gene discussed is MAPT; the disease is Alzheimer disease.