Tau, amyloid, and hypometabolism in a patient with posterior cortical atrophy

Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. We report a patient with posterior cortical atrophy (visual variant of Alzheimer disease) who was studied using the novel tau tracer (18) FAV-1451 in conjunction with (11) CPittsburgh compound B (PIB; amyloid) and (18) Ffluorodeoxyglucose (FDG) positron emission tomography. Whereas (11) CPIB bound throughout association neocortex, (18) FAV-1451 was selectively retained in posterior brain regions that were affected clinically and showed markedly reduced (18) FFDG uptake. This provides preliminary in vivo evidence that tau is more closely linked to hypometabolism and symptomatology than amyloid.