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Plasma P-tau181 and P-tau217 in Patients With Traumatic Encephalopathy Syndrome With and Without Evidence of Alzheimer Disease Pathology
Open accessAbstract
BACKGROUND AND OBJECTIVES: Traumatic encephalopathy syndrome (TES) has overlapping clinical symptoms with Alzheimer disease (AD). AD pathology commonly co-occurs with chronic traumatic encephalopathy (CTE) pathology. There are currently no validated CTE biomarkers. AD-specific biomarkers such as plasma P-tau181 and P-tau217 may help to identify patients with TES who have AD pathology. METHODS: We measured plasma P-tau181 and P-tau217 (Meso Scale Discovery electrochemiluminescence) in patients with TES, mild cognitive impairment/dementia with biomarker-confirmed AD ("AD"), and healthy controls ("HC"). Patients underwent amyloid-beta (Aβ)-PET and a subset underwent tau-PET using [18F]Flortaucipir. We compared plasma P-tau levels controlling for age and sex and also performed AUC analyses to evaluate the accuracy of group differentiation. In patients with TES, we evaluated associations between plasma P-tau, years of repetitive head impact exposure, and tau-PET. Four TES patients with autopsy-confirmed CTE were described qualitatively. RESULTS: = 0.13). Patients with AD had higher tau-PET tracer uptake than Aβ(+) TES and were well differentiated using P-tau181 (AUC = 0.81 [0.68-0.94]) and P-tau217 (AUC = 0.86 [0.73-0.98]). Plasma P-tau correlated with the tau-PET signal in Aβ(+) TES but not in Aβ(-) TES, and there was no association between plasma P-tau and years of repetitive head impact exposure. TES patients with severe CTE and no AD at autopsy had low P-tau181 and P-tau217 levels. DISCUSSION: Measuring P-tau181 and P-tau217 in plasma may be a feasible and scalable fluid biomarker for identifying AD pathology in TES. Low plasma P-tau levels may be used to increase clinical suspicion of CTE over AD as a primary pathology in TES. Currently, there is no support for P-tau181 or P-tau217 as in vivo biomarkers of CTE tau. Larger studies of patients with pathologically confirmed CTE are needed. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that (1) among patients with TES and abnormal Aβ-PET scans, elevated plasma P-tau can differentiate between affected individuals and HCs; (2) low plasma P-tau may help identify patients with TES who do not have Alzheimer; and (3) plasma P-tau181 and P-tau217 are not useful biomarkers of patients with TES who do not have AD.
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“It appears to be more specific for AD pathology, at least compared to frontotemporal dementia and chronic traumatic encephalopathy (85, 91, 92), but it is increased in prion disease (83).”
From All the Tau We Cannot See (2023) · cites this paper as [91]
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1 retracted
Dementia prevention, intervention, and care: 2020 report of the Lancet Commission
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“We then evaluated how well plasma P-tau181 and P-tau217 discriminated between participants with TES (stratified by Aβ status) and AD.”
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“Participants with AD met clinical research criteria for probable AD dementia10 or MCI.18 To maximize specificity of underlying AD pathology, all participants with AD had both Aβ-PET and tau-PET imaging consistent with AD.”
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Qualitative Assessment of Verbal Fluency Performance in Frontotemporal Dementia
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Metadata
- Authors
- Asken, B. M., Tanner, J. A., VandeVrede, L., Mantyh, W. G., Casaletto, K. B., Staffaroni, A. M., La Joie, R., Iaccarino, L., Soleimani-Meigooni, D., Rojas, J. C., Gardner, R. C., Miller, B. L., Grinberg, L. T., Boxer, A. L., Kramer, J. H., & Rabinovici, G. D.
- Affiliations
- University of Minnesota (US)
- From the Memory and Aging Center (B.M.A.T.C., J.A.T., L.V., W.G.M., K.B.C., A.M.S., R.L.J., L.I., D.S.-M., J.C.R., R.C.G., B.L.M., L.T.G., A.L.B., J.H.K., G.D.R.), Department of Neurology, Weill Institute for Neurosciences, University of California San Francisco; Department of Neurology (W.G.M.), University of Minnesota, Minneapolis; San Francisco Veterans Affairs Medical Center (R.C.G.); and Department of Radiology & Biomedical Imaging, University of California (G.D.R.), San Francisco.
- ORCID
- Venue
- Neurology
- Published
- 2022-08-09
- Volume
- 99
- Issue
- 6
- Pages
- e594-e604
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC9442622
- OpenAlex
- W4280514047
- Cited by
- 40
- References
- 51
- Citations by year
- 2026: 11 · 2025: 12 · 2024: 7 · 2023: 8 · 2022: 2
- FWCI
- 4.73
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health
- National Institute on Aging (K23AG059888, R01AG045611, U01AG057195, R01AG064314, R01AG048234, R21AG069252, K23AG061253, L30 AG069301, K23AG031861, RF1AG032289, K99AG065501, K24AG045333, R01AG038791, U19AG063911, P01AG019724, R01AG060477, P30AG062422, K23AG073514, R01AG032289, R01AG072475, T32AG023481)
- National Institute of Neurological Disorders and Stroke (U54NS100717, K23NS095755, U54NS092089)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
- Keywords
- traumatic encephalopathy syndrome, chronic traumatic encephalopathy, Alzheimer's disease, p-tau181, p-tau217, fluid biomarkers, tau PET, amyloid PET, differential diagnosis, mild cognitive impairment, dementia, 18F-flortaucipir, electrochemiluminescence
- MeSH terms
- Chronic Traumatic Encephalopathy, Alzheimer Disease, Dementia, Humans, Syndrome, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography
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