Tau, amyloid, and hypometabolism in the logopenic variant of primary progressive aphasia

A 57-year-old right-handed woman had an 8-year history of progressive word retrieval and repetition deficits, consistent with the logopenic variant of Alzheimer disease.1 She was studied using the novel hyperphosphorylated-tau tracer 18F-AV-1451,2 in conjunction with metabolic (18F-fluorodeoxyglucose [FDG]) and β-amyloid (18F-florbetapir) PET (figure). Areas with high tau, such as the left inferior parietal lobule, had decreased metabolism. By contrast, some areas with high amyloid, such as striated cortex, had normal metabolism. This case illustrates tau sparing of primary cortex and provides preliminary in vivo evidence that regional tau is more closely linked to hypometabolism than amyloid density.