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18F‐flortaucipir tau positron emission tomography distinguishes established progressive supranuclear palsy from controls and Parkinson disease: A multicenter study
| Content Provider | Semantic Scholar |
|---|---|
| Author | Schonhaut, Daniel R. McMillan, Corey T. Spina, Salvatore Dickerson, Bradford C. Siderowf, Andrew D. Devous, Michael D. Tsai, Richard M. Winer, Joseph R. Russell, David S. Litvan, Irene Roberson, Erik D. Seeley, William W. Grinberg, Lea Tenenholz Kramer, Joel H. Miller, Bruce L. Pressman, Peter S. Nasrallah, Ilya M. Baker, Suzanne L. Gomperts, Stephen N. Johnson, Keith A. Grossman, Murray Jagust, William J. Boxer, Adam L. Rabinovici, Gil D. |
| Copyright Year | 2017 |
| Abstract | 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. |
| Starting Page | 1719 |
| Ending Page | 1727 |
| Page Count | 9 |
| File Format | PDF HTM / HTML |
| DOI | 10.1002/ana.25060 |
| Alternate Webpage(s) | https://cloudfront.escholarship.org/dist/prd/content/qt01j9450z/qt01j9450z.pdf?t=p9uz6p |
| PubMed reference number | 28980714 |
| Alternate Webpage(s) | https://doi.org/10.1002/ana.25060 |
| Journal | Medline |
| Volume Number | 82 |
| Journal | Annals of neurology |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |