In contrast, the downstream hyperphosphorylation of neurofibrillary tau tangles and their spread from the medial temporal lobe to the neocortex is thought to be contingent on a crucial threshold of Aβ load and is frequently recognised to have stronger associations with clinical decline in AD.37 Our group and others have demonstrated strong links between regional tau deposition and cortical thinning in MCI and AD patients,37–39 supporting the idea that tau, not Aβ, is the primary driver of downstream neurodegenerative processes. The gene discussed is MAPT; the disease is Alzheimer disease.