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Open Access Publications from the University of California

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

  • Author(s): Schonhaut, Daniel R
  • McMillan, Corey T
  • Spina, Salvatore
  • Dickerson, Bradford C
  • Siderowf, Andrew
  • Devous, Michael D
  • Tsai, Richard
  • Winer, Joseph
  • Russell, David S
  • Litvan, Irene
  • Roberson, Erik D
  • Seeley, William W
  • Grinberg, Lea T
  • Kramer, Joel H
  • Miller, Bruce L
  • Pressman, Peter
  • Nasrallah, Ilya
  • Baker, Suzanne L
  • Gomperts, Stephen N
  • Johnson, Keith A
  • Grossman, Murray
  • Jagust, William J
  • Boxer, Adam L
  • Rabinovici, Gil D
  • et al.

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OBJECTIVE:18 F-flortaucipir (formerly 18 F-AV1451 or 18 F-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 18 F-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). METHODS:Participants underwent magnetic resonance imaging and positron emission tomography for amyloid-β (11 C-PiB or 18 F-florbetapir) and tau (18 F-flortaucipir). 18 F-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 18 F-flortaucipir. RESULTS:Clinical PSP patients showed bilaterally elevated 18 F-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 18 F-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 18 F-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.

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