Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer’s disease

See Sarazin et al . (doi:[10.1093/brain/aww041][1]) for a scientific commentary on this article. The advent of the positron emission tomography tracer 18F-AV1451 provides the unique opportunity to visualize the regional distribution of tau pathology in the living human brain. In this study, we tested the hypothesis that tau pathology is closely linked to symptomatology and patterns of glucose hypometabolism in Alzheimer’s disease, in contrast to the more diffuse distribution of amyloid-β pathology. We included 20 patients meeting criteria for probable Alzheimer’s disease dementia or mild cognitive impairment due to Alzheimer’s disease, presenting with a variety of clinical phenotypes, and 15 amyloid-β-negative cognitively normal individuals, who underwent 18F-AV1451 (tau), 11C-PiB (amyloid-β) and 18F-FDG (glucose metabolism) positron emission tomography, apolipoprotein E ( APOE ) genotyping and neuropsychological testing. Voxel-wise contrasts against controls (at P right temporoparietal cortex). In conclusion, tau imaging—contrary to amyloid-β imaging—shows a strong regional association with clinical and anatomical heterogeneity in Alzheimer’s disease. Although preliminary, these results are consistent with and expand upon findings from post-mortem, animal and cerebrospinal fluid studies, and suggest that the pathological aggregation of tau is closely linked to patterns of neurodegeneration and clinical manifestations of Alzheimer’s disease. * Abbreviations : AI =  : asymmetry index DVR = : distribution volume ratio MMSE = : Mini-Mental State Examination PCA = : posterior cortical atrophy PiB = : Pittsburgh compound B PPA = : primary progressive aphasia SUVR = : standardized uptake value ratio [1]: /lookup/doi/10.1093/brain/aww041