{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T21:55:43Z","timestamp":1792446943822,"version":"4.5.0"},"reference-count":76,"publisher":"American Medical Association (AMA)","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Netw Open"],"abstract":"\n Importance<\/jats:title>\n In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed.<\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To evaluate the utility of plasma phosphorylated tau 217 (p-tau217), assess its performance as a beta-amyloid (A\u03b2) biomarker in participants with RHI exposure at risk for CTE, and explore concordance with CTE neuropathology in a postmortem subsample.<\/jats:p>\n <\/jats:sec>\n \n Design, Setting, and Participants<\/jats:title>\n This longitudinal, multicenter, case-control study used data from the Diagnostics, Imaging, and Genetics Network for the Objective Study and Evaluation of CTE (DIAGNOSE CTE) Research Project, collected from September 2016 to October 2023. Participants were former American football players (case participants) and asymptomatic men unexposed to RHI (control participants). A subsample had available neuropathologic data.<\/jats:p>\n <\/jats:sec>\n \n Exposures<\/jats:title>\n RHI, traumatic encephalopathy syndrome (TES) diagnoses, and levels of CTE certainty.<\/jats:p>\n <\/jats:sec>\n \n Main Outcomes and Measures<\/jats:title>\n \n Plasma p-tau217 (classified as positive [\u22650.63 pg\/mL], intermediate [0.40-0.62 pg\/mL], and negative [&amp;lt;0.40 pg\/mL]), A\u03b2\u2013positron emission tomography (PET;\n 18<\/jats:sup>\n F-florbetapir; with A\u03b2-positive defined as a standardized uptake value ratio [SUVR] \u22651.10), and tau-PET (\n 18<\/jats:sup>\n F-flortaucipir). TES diagnoses were assigned by multidisciplinary consensus conference. Analyses of postmortem brains controlled for age, race, and\n APOE<\/jats:italic>\n \u03b54 status.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Among 231 participants (mean [SD] age, 57.75 [8.25] years), 177 were former football players (117 professional and 60 college) and 54 were unexposed participants. Former football players had higher baseline mean (SD) p-tau217 concentrations than unexposed participants (0.35 [0.26] pg\/mL vs 0.27 [0.14] pg\/mL;\n P<\/jats:italic>\n \u2009=\u2009.008), although this was driven by a higher proportion of A\u03b2-PET\u2013positive participants among former players. Plasma p-tau217 increased over time across the sample (B\u2009=\u20090.207 [95% CI, 0.117-0.298];\n P<\/jats:italic>\n \u2009&amp;lt;\u2009.001), with no significant time\u2009\u00d7\u2009exposure group interactions. Among football players, p-tau217 showed no time\u2009\u00d7\u2009group interactions with TES diagnosis, TES-CTE certainty, or RHI metrics. Higher p-tau217 concentration correlated with higher global A\u03b2-PET SUVR (B\u2009=\u20090.058 [95% CI, 0.053-3.501;\n P<\/jats:italic>\n \u2009=\u2009.01), with a few discordant cases (5 participants were p-tau217\u2013negative and A\u03b2-PET\u2013positive; 7 participants were p-tau217\u2013positive and A\u03b2-PET\u2013negative). P-tau217 had similar areas under the curve for projecting A\u03b2-PET positivity as cerebrospinal fluid (CSF) p-tau181\/A\u03b242 and CSF A\u03b240\/42 measures (p-tau217: AUC, 0.88 [95% CI, 0.80-0.96]; CSF p-tau181\/A\u03b242: AUC, 0.89 [95% CI, 0.79-1.00]; CSF A\u03b240\/42: AUC, 0.85 [95% CI, 0.72-0.98]). Among 9 brain donors, 6 had CTE (stages II-IV; none with Alzheimer disease). Seven had negative or intermediate p-tau217, concordant with A\u03b2-PET. Two p-tau217 outliers with stage III CTE had normal concentrations upon additional testing.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Relevance<\/jats:title>\n The findings of this study suggest that plasma p-tau217 concentration is unlikely to be useful for the detection of CTE, but it does show utility for ruling out A\u03b2 pathology in participants at risk for CTE.<\/jats:p>\n <\/jats:sec>","DOI":"10.1001\/jamanetworkopen.2026.22966","type":"journal-article","created":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T15:30:18Z","timestamp":1783956618000},"page":"e2622966","source":"Crossref","is-referenced-by-count":1,"title":["Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy"],"prefix":"10.1001","volume":"9","author":[{"given":"Annalise E.","family":"Miner","sequence":"first","affiliation":[{"name":"Boston University CTE Center and Alzheimer\u2019s Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, United Kingdom"},{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, M\u00f6lndal, Sweden"},{"name":"UK Dementia Research Institute at UCL, London, United Kingdom"},{"name":"Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay, Hong Kong, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaj","family":"Blennow","sequence":"additional","affiliation":[{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, M\u00f6lndal, Sweden"},{"name":"Paris Brain Institute, ICM, Piti\u00e9-Salp\u00eatri\u00e8re Hospital, Sorbonne University, Paris, France"},{"name":"Neurodegenerative Disorder Research Center, Division of Life Sciences and Medicine, and Department of Neurology, Institute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, University of Science, Hefei, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenna R.","family":"Groh","sequence":"additional","affiliation":[{"name":"Boston University CTE Center and Alzheimer\u2019s Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alpana","family":"Singh","sequence":"additional","affiliation":[{"name":"Banner Sun Health Research Institute, Sun City, Arizona"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kari","family":"Dieckhoff","sequence":"additional","affiliation":[{"name":"Banner Sun Health Research Institute, Sun City, Arizona"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yorghos","family":"Tripodis","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles H.","family":"Adler","sequence":"additional","affiliation":[{"name":"Department of Neurology, Mayo Clinic College of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura J.","family":"Balcer","sequence":"additional","affiliation":[{"name":"Departments of Neurology, Population Health and Ophthalmology, NYU Grossman School of Medicine, New York, New 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