CSF levels of p-tau increased in the earliest disease stages (i.e., in asymptomatic individuals with CSF or PET evidence of abnormal Aβ accumulation) and appeared to reach a plateau or even decrease in later symptomatic stages of AD (Fagan et al., 2014; Mattsson-Carlgren et al., 2020a; Janelidze et al., 2021a). This evidence concerns the gene MAPT and Alzheimer disease.