Plasma phosphorylated tau 217 and phosphorylated tau 181 as biomarkers in Alzheimer's disease and frontotemporal lobar degeneration: a retrospective diagnostic performance study
Open accessAbstract
Background Plasma tau phosphorylated at threonine 217 (p-tau217) and plasma tau phosphorylated at threonine 181 (p-tau181) are associated with Alzheimer's disease tau pathology. We compared the diagnostic value of both biomarkers in cognitively unimpaired participants and patients with a clinical diagnosis of mild cognitive impairment, Alzheimer's disease syndromes, or frontotemporal lobar degeneration (FTLD) syndromes.Methods In this retrospective multicohort diagnostic performance study, we analysed plasma samples, obtained from patients aged 18-99 years old who had been diagnosed with Alzheimer's disease syndromes (Alzheimer's disease dementia, logopenic variant primary progressive aphasia, or posterior cortical atrophy), FTLD syndromes (corticobasal syndrome, progressive supranuclear palsy, behavioural variant frontotemporal dementia, non-fluent variant primary progressive aphasia, or semantic variant primary progressive aphasia), or mild cognitive impairment; the participants were from the University of California San Francisco (UCSF) Memory and Aging Center, San Francisco, CA, USA, and the Advancing Research and Treatment for Frontotemporal Lobar Degeneration Consortium (ARTFL; 17 sites in the USA and two in Canada). Participants from both cohorts were carefully characterised, including assessments of CSF p-tau181, amyloid-PET or tau-PET (or both), and clinical and cognitive evaluations. Plasma p-tau181 and p-tau217 were measured using electrochemiluminescence-based assays, which differed only in the biotinylated antibody epitope specificity. Receiver operating characteristic analyses were used to determine diagnostic accuracy of both plasma markers using clinical diagnosis, neuropathological findings, and amyloid-PET and tau-PET measures as gold standards. Difference between two area under the curve (AUC) analyses were tested with the Delong test.Findings Data were collected from 593 participants (443 from UCSF and 150 from ARTFL, mean age 64 years [SD 13], 294 [50%] women) between July 1 and Nov 30, 2020. Plasma p-tau217 and p-tau181 were correlated (r=0·90, p<0·0001). Both p-tau217 and p-tau181 concentrations were increased in people with Alzheimer's disease syndromes (n=75, mean age 65 years [SD 10]) relative to cognitively unimpaired controls (n=118, mean age 61 years [SD 18]; AUC=0·98 [95% CI 0·95-1·00] for p-tau217, AUC=0·97 [0·94-0·99] for p-tau181; p diff=0·31) and in pathology-confirmed Alzheimer's disease (n=15, mean age 73 years [SD 12]) versus pathologically confirmed FTLD (n=68, mean age 67 years [SD 8]; AUC=0·96 [0·92-1·00] for p-tau217, AUC=0·91 [0·82-1·00] for p-tau181; p diff=0·22). P-tau217 outperformed p-tau181 in differentiating patients with Alzheimer's disease syndromes (n=75) from those with FTLD syndromes (n=274, mean age 67 years [SD 9]; AUC=0·93 [0·91-0·96] for p-tau217, AUC=0·91 [0·88-0·94] for p-tau181; p diff=0·01). P-tau217 was a stronger indicator of amyloid-PET positivity (n=146, AUC=0·91 [0·88-0·94]) than was p-tau181 (n=214, AUC=0·89 [0·86-0·93]; p diff=0·049). Tau-PET binding in the temporal cortex was more strongly associated with p-tau217 than p-tau181 (r=0·80 vs r=0·72; p diff<0·0001, n=230).Interpretation Both p-tau217 and p-tau181 had excellent diagnostic performance for differentiating patients with Alzheimer's disease syndromes from other neurodegenerative disorders. There was some evidence in favour of p-tau217 compared with p-tau181 for differential diagnosis of Alzheimer's disease syndromes versus FTLD syndromes, as an indication of amyloid-PET-positivity, and for stronger correlations with tau-PET signal. Pending replication in independent, diverse, and older cohorts, plasma p-tau217 and p-tau181 could be useful screening tools to identify individuals with underlying amyloid and Alzheimer's disease tau pathology.Funding US National Institutes of Health, State of California Department of Health Services, Rainwater Charitable Foundation, Michael J Fox foundation, Association for Frontotemporal Degeneration, Alzheimer's Association.
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Plasma p-tau217 often shows a superior association with temporal lobe tau load compared to other plasma biomarkers, including other p-tau species.
“Nonetheless, plasma p‐tau217 often shows a superior association with temporal lobe tau load compared to other plasma biomarkers (including other p‐tau species), 13 , 25 , 36”
From Machine learning prediction of tau‐PET in Alzheimer's disease using plasma, MRI, and clinical data (2025) · cites this paper as [36]
The Results report a stronger association between plasma p-tau217 and temporal tau-PET binding than between p-tau181 and that measure (r=0.80 versus 0.72). They do not establish that p-tau217 has a stronger association than other plasma biomarkers more broadly; neither p-tau marker showed a significant association in the amyloid-PET-negative subgroup. The indexed passages provide section labels but no page numbers. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSeveral recent studies have reported that plasma biomarkers have excellent diagnostic accuracy for AD, with sensitivity or specificity often exceeding 90%.
“Several recent studies have reported that plasma biomarkers have excellent diagnostic accuracy for AD, with sensitivity or specificity often exceeding 90% (refs. 4–10).”
From Diagnosis of Alzheimer's disease using plasma biomarkers adjusted to clinical probability (2024) · cites this paper as [7]
The Discussion (page unavailable) reports that plasma P-tau217 and P-tau181 distinguished AD from non-AD disorders with high accuracy (AUCs >0.90), supporting the claim of excellent diagnostic accuracy. It does not establish the more specific claim that sensitivity or specificity often exceeded 90%: the reported figures are AUCs, which are different measures. (LLM, conf=0.86)
Experimental — accuracy not yet measuredElevated phosphorylated tau concentrations in either CSF or plasma suggest that underlying Alzheimer's disease pathology is likely to be the cause of the frontotemporal dementia clinical syndrome.
“Although total tau and amyloid β concentrations are not sensitive or specific for any of the frontotemporal lobar degeneration proteinopathies, elevated phosphorylated tau concentrations in either CSF or plasma suggest that underlying Alzheimer's disease pathology is likely to be the cause of the frontotemporal dementia clinical syndrome.49,55,56”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [56]
The Results report higher plasma P-tau217 and P-tau181 in autopsy-confirmed Alzheimer’s disease than in FTLD, and the Discussion describes patients with a clinical FTLD-spectrum syndrome whose elevated plasma P-tau accompanied Alzheimer’s pathology at autopsy. The Introduction calls CSF tau measurements established Alzheimer’s biomarkers, but our copy does not establish the more specific claim about elevated phosphorylated tau in CSF in this clinical setting. (LLM, conf=0.84)
Experimental — accuracy not yet measuredp-tau217 exhibits larger-fold changes compared with p-tau181 and p-tau231, often achieving high discrimination, with areas under the curve (AUC) exceeding 90%.
“Notably, p-tau217 exhibits larger-fold changes compared with p-tau181 and p-tau231,10 often achieving high discrimination, with areas under the curve (AUC) exceeding 90%.19,23”
From Diagnostic Accuracy of a Plasma Phosphorylated Tau 217 Immunoassay for Alzheimer Disease Pathology (2024) · cites this paper as [23]
Total tau and amyloid β concentrations are not sensitive or specific for any of the frontotemporal lobar degeneration proteinopathies.
“Although total tau and amyloid β concentrations are not sensitive or specific for any of the frontotemporal lobar degeneration proteinopathies, elevated phosphorylated tau concentrations in either CSF or plasma suggest that underlying Alzheimer's disease pathology is likely to be the cause of the frontotemporal dementia clinical syndrome.49,55,56”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [56]
The Introduction discusses amyloid and tau measurements as established Alzheimer’s disease biomarkers, but does not assess whether total tau or amyloid-β concentrations identify FTLD proteinopathies. The Results compare phosphorylated tau across AD, FTLD-tau and FTLD-TDP; searches for total tau, amyloid-β concentrations and FTLD specificity found no passage establishing the quoted claim. Page numbers were not available in our copy. (LLM, conf=0.72)
Experimental — accuracy not yet measured
Plasma tau has emerged as a marker of neuronal distress and appears in several neurodegenerative diseases, including preclinical AD.
“Like NfL (neurofilament light chain), plasma tau has emerged as a marker of neuronal distress. It appears in several different neurodegenerative diseases, including importantly even preclinical AD patients (76–85).”
From All the Tau We Cannot See (2023) · cites this paper as [85]
Plasma tau appears to be more specific for AD pathology compared to frontotemporal dementia and chronic traumatic encephalopathy, but is increased in prion disease.
“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 [85]
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Self-citationAshton, N. J., Brum, W. S., Molfetta, G. D., Benedet, A. L., Arslan, B., Jonaitis, E. M., Langhough, R. E., Cody, K. A., Wilson, R. H., Carlsson, C. M., et al. (2023) · medRxiv · doi:10.1101/2023.07.11.23292493 · Cited by 50 · see citing works
Self-citationPromising Blood Biomarkers for Clinical Use in Alzheimer’s Disease: A Focused Update
Park, S. A., Jang, Y. J., Kim, M. K., Lee, S. M., & Moon, S. Y. (2022) · Journal of Clinical Neurology · doi:10.3988/jcn.2022.18.4.401 · Cited by 47 · see citing works
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Clinical and diagnostic implications of Alzheimer's disease copathology in Lewy body disease
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- Authors
- Thijssen, E. H., La Joie, R., Strom, A., Fonseca, C., Iaccarino, L., Wolf, A., Spina, S., Allen, I. E., Cobigo, Y., Heuer, H., VandeVrede, L., Proctor, N. K., Lago, A. L., Baker, S., Sivasankaran, R., Kieloch, A., Kinhikar, A., Yu, L., Valentin, M.-A., Jeromin, A., Zetterberg, H., Hansson, O., Mattsson-Carlgren, N., Graham, D., Blennow, K., Kramer, J. H., Grinberg, L. T., Seeley, W. W., Rosen, H., Boeve, B. F., Miller, B. L., Teunissen, C. E., Rabinovici, G. D., Rojas, J. C., Dage, J. L., & Boxer, A. L.
- Affiliations
- University of California, San Francisco (US)
- Eli Lilly (United States) (US)
- Lawrence Berkeley National Laboratory (US)
- Quanterix (United States) (US)
- Sahlgrenska University Hospital (SE)
- Lund University (SE)
- Biogen (United States) (US)
- Mayo Clinic (US)
- Amsterdam Neuroscience (NL)
- Corresponding author
- Boxer, Adam L
- ORCID
- Thijssen, Elisabeth H
- Strom, Amelia
- Fonseca, Corrina
- Iaccarino, Leonardo
- Wolf, Amy
- Spina, Salvatore
- Allen, Isabel E
- Cobigo, Yann
- Heuer, Hilary
- VandeVrede, Lawren
- Proctor, Nicholas K
- Lago, Argentina Lario
- Baker, Suzanne
- Sivasankaran, Rajeev
- Kinhikar, Arvind
- Yu, Lili
- Zetterberg, Henrik
- Hansson, Oskar
- Graham, Danielle
- Blennow, Kaj
- Kramer, Joel H
- Grinberg, Lea T
- Seeley, William W
- Rosen, Howard
- Boeve, Bradley F
- Miller, Bruce L
- Teunissen, Charlotte E
- Rabinovici, Gil D
- Rojas, Julio C
- Dage, Jeffrey L
- Boxer, Adam L
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2021-09
- Volume
- 20
- Issue
- 9
- Pages
- 739-752
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC8711249
- OpenAlex
- W3194829575
- Cited by
- 607
- References
- 40
- Citations by year
- 2026: 127 · 2025: 161 · 2024: 119 · 2023: 101 · 2022: 87 · 2021: 11
- FWCI
- 57.94
- Type
- journal article
- Language
- en
- Update notices
- erratum (2021-10-01)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (submittedVersion, other-oa)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- Alzheimer's Association (AARF-16\u2013443577, 443577)
- National Center for Advancing Translational Sciences (LEFFTDS U01 AG045390)
- National Institute of Neurological Disorders and Stroke (U54NS092089)
- National Institute on Aging
- American College of Radiology
- Association for Frontotemporal Degeneration
- Rainwater Charitable Foundation
- NIH (R01 AG045611, U24AG21886, K24AG053435, R01AG038791, P50AG016574, K99AG065501, U19AG063911, P50AG023501, P01AG019724)
- Vetenskapsrådet (2018\u201302532, 02532)
- Little Family Foundation
- European Research Council (681712)
- Michael J Fox Foundation for Parkinson's Research
- Alzheimer's Drug Discovery Foundation (201809\u20132016862, 2016862, 201809)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- Alzheimer's disease, frontotemporal lobar degeneration, plasma biomarkers, diagnostic accuracy, mild cognitive impairment, tau PET, amyloid PET, primary progressive aphasia, corticobasal syndrome, progressive supranuclear palsy, behavioral variant frontotemporal dementia, posterior cortical atrophy, logopenic variant primary progressive aphasia, semantic dementia, electrochemiluminescence assay
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Diagnosis, Differential, Female, Humans, Male, Middle Aged, Phosphorylation, Predictive Value of Tests, Retrospective Studies, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography, Frontotemporal Lobar Degeneration, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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