Some studies have shown that Aβ pathology in AD might trigger increased production, release, and phosphorylation of tau28,29 and that this likely happens early in the disease course because CSF levels of P-tau increase several years before tau aggregation is detectable by PET.14 In the present study, we used event-based modeling and cross-sectional data to predict the sequence of biomarker abnormality in cognitively unimpaired participants and in those with MCI. The gene discussed is MAPT; the disease is Alzheimer disease.