18F-flortaucipir tau positron emission tomography distinguishes established progressive supranuclear palsy from controls and Parkinson disease: A multicenter study

Objective(18)F-flortaucipir (formerly F-18-AV1451 or F-18-T807) binds to neurofibrillary tangles in Alzheimer disease, but tissue studies assessing binding to tau aggregates in progressive supranuclear palsy (PSP) have yielded mixed results. We compared in vivo F-18-flortaucipir uptake in patients meeting clinical research criteria for PSP (n=33) to normal controls (n=46) and patients meeting criteria for Parkinson disease (PD; n=26). MethodsParticipants underwent magnetic resonance imaging and positron emission tomography for amyloid- (C-11-PiB or F-18-florbetapir) and tau (F-18-flortaucipir). F-18-flortaucipir standardized uptake value ratios were calculated (t=80-100 minutes, cerebellum gray matter reference). Voxelwise and region-of-interest group comparisons were performed in template space, with receiver operating characteristic curve analyses to assess single-subject discrimination. Qualitative comparisons with postmortem tau are reported in 1 patient who died 9 months after F-18-flortaucipir. ResultsClinical PSP patients showed bilaterally elevated F-18-flortaucipir uptake in globus pallidus, putamen, subthalamic nucleus, midbrain, and dentate nucleus relative to controls and PD patients (voxelwise p<0.05 family wise error corrected). Globus pallidus binding best distinguished PSP patients from controls and PD (area under the curve [AUC]=0.872 vs controls, AUC=0.893 vs PD). PSP clinical severity did not correlate with F-18-flortaucipir in any region. A patient with clinical PSP and pathological diagnosis of corticobasal degeneration had severe tau pathology in PSP-related brain structures with good correspondence between in vivo F-18-flortaucipir and postmortem tau neuropathology. Interpretation(18)F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. Ann Neurol 2017;82:622-634