One possible explanation for this is that in early stages of the AD continuum, namely preclinical and prodromal AD (cohort 1), Aβ and neurodegeneration are required to increase levels of BD-tau in blood, while in later stages, MCI and dementia (cohort 3), the presence of Aβ pathology can increase blood BD-tau in absence of N positivity in CSF. The gene discussed is MAPT; the disease is Alzheimer disease.