Considering that CSF p-tau235 increases late during preclinical AD [15], it is expected that in cohorts richer in CU cases (especially A+T−), other CSF p-tau biomarkers that abnormally emerge earlier in the AD continuum (such as p-tau231 and p-tau217) [15] would provide a superior performance identifying CSF amyloidosis in asymptomatic individuals. The gene discussed is MAPT; the disease is Alzheimer disease.