Head‐to‐head comparison of clinical performance of CSF phospho‐tau T181 and T217 biomarkers for Alzheimer's disease diagnosis
Open accessAbstract
Introduction: Phosphorylated tau (p‐tau) in cerebrospinal fluid (CSF) is an established Alzheimer's disease (AD) biomarker. Novel immunoassays targeting N‐terminal and mid‐region p‐tau181 and p‐tau217 fragments are available, but head‐to‐head comparison in clinical settings is lacking. Methods: N‐terminal‐directed p‐tau217 (N‐p‐tau217), N‐terminal‐directed p‐tau181 (N‐p‐tau181), and standard mid‐region p‐tau181 (Mid‐p‐tau181) biomarkers in CSF were evaluated in three cohorts (n = 503) to assess diagnostic performance, concordance, and associations with amyloid beta (Aβ). Results: CSF N‐p‐tau217 and N‐p‐tau181 had better concordance (88.2%) than either with Mid‐p‐tau181 (79.7%–82.7%). N‐p‐tau217 and N‐p‐tau181 were significantly increased in early mild cognitive impairment (MCI)‐AD (A+T–N–) without changes in Mid‐p‐tau181 until AD‐dementia. N‐p‐tau217 and N‐p‐tau181 identified Aβ pathophysiology (area under the curve [AUC] = 94.8%–97.1%) and distinguished MCI‐AD from non‐AD MCI (AUC = 82.6%–90.5%) signficantly better than Mid‐p‐tau181 (AUC = 91.2% and 70.6%, respectively). P‐tau biomarkers equally differentiated AD from non‐AD dementia (AUC = 99.1%–99.8%). Discussion: N‐p‐tau217 and N‐p‐tau181 could improve diagnostic accuracy in prodromal‐AD and clinical trial recruitment as both identify Aβ pathophysiology and differentiate early MCI‐AD better than Mid‐p‐tau181.
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CSF p-tau epitopes increase in the preclinical phase of the disease, prior to symptom onset and before substantial tau PET ligand retention.
“Our data, like prior studies,18,28,31 shows an increase of CSF p-tau epitopes in the preclinical phase of the disease, prior to symptom onset and before substantial tau PET ligand retention.”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [28]
The Introduction reports that CSF p-tau217 begins to increase in preclinical familial Alzheimer’s disease, supporting an increase before symptoms. The Discussion also describes early increases in N-terminal p-tau biomarkers. Neither passage establishes that these increases precede substantial tau-PET ligand retention; the Introduction reports a correlation with tau-PET, not that timing. (LLM, conf=0.84)
Experimental — accuracy not yet measuredCSF p-tau217 might better discriminate AD from other neurodegenerative diseases than CSF p-tau181.
“Recent reports have suggested that CSF p-tau217 might better discriminate AD from other neurodegenerative diseases24,27, 28, 29, 30 than CSF p-tau181.”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [28]
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Self-citationPlasma p‐tau immunoassays in clinical research for Alzheimer's disease
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Self-citationProteomic profiling of circulating plasma exosomes reveals novel biomarkers of Alzheimer’s disease
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Self-citationCSF p-tau205: a biomarker of tau pathology in Alzheimer’s disease
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Self-citationPlasma biomarkers for neurodegenerative disorders: ready for prime time?
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Self-citationComparison of CSF phosphorylated tau 181 and 217 for cognitive decline
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Phospho‐specific plasma p‐tau181 assay detects clinical as well as asymptomatic Alzheimer's disease
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Impact of the Cannabinoid System in Alzheimer's Disease
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Alzheimer's Disease Biomarker Analysis Using Targeted Mass Spectrometry
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Self-citationT217-Phosphorylation Exacerbates Tau Pathologies and Tau-Induced Cognitive Impairment
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Self-citationPlasma N‐terminal tau fragment is an amyloid‐dependent biomarker in Alzheimer's disease
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The association between rs6859 in NECTIN2 gene and Alzheimer’s disease is partly mediated by pTau
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Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer’s disease
Chongtham, A., Ramakrishnan, A., Farinas, M., Broekaart, D. W. M., Seo, J. H., Zhu, C. W., Sano, M., Shen, L., & Pereira, A. C. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-02998-y · Cited by 9 · see citing works
Targeting tau in Alzheimer’s Disease: rationale, approach and challenges
Aslanyan, A., Foiani, M. S., Giovannucci, T. A., McDade, E., Duff, K., Mummery, C. J., Schöll, M., Wildsmith, K. R., & Paterson, R. W. (2026) · Molecular Neurodegeneration · doi:10.1186/s13024-026-00925-5 · Cited by 10 · see citing works
Islam, T., Kvartsberg, H., Sehrawat, A., Kac, P. R., Becker, B., Olsson, M., Abrahamson, E. E., Zetterberg, H., Ikonomović, M. D., Blennow, K., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.13711 · Cited by 9 · see citing works
Self-citation
- Authors
- Karikari, T. K., Emeršič, A., Vrillon, A., Lantero‐Rodriguez, J., Ashton, N. J., Kramberger, M. G., Dumurgier, J., Hourregue, C., Čučnik, S., Brinkmalm, G., Rot, U., Zetterberg, H., Paquet, C., & Blennow, K.
- Affiliations
- University of Gothenburg (SE)
- Ljubljana University Medical Centre (SI)
- Inserm (FR)
- King's College London (GB)
- University of Ljubljana (SI)
- Université Paris Cité (FR)
- Université de Paris, Cognitive Neurology Center, GHU Nord APHP Hospital Lariboisière Fernand Widal Paris France
- Sahlgrenska University Hospital (SE)
- Corresponding author
- Karikari, Thomas K.
- ORCID
- Venue
- Alzheimer's & Dementia
- Publisher
- Wiley
- Published
- 2020-11-30
- Volume
- 17
- Issue
- 5
- Pages
- 755-767
- ISSN
- 1552-5260 (ISSN-L)
- 1552-5279
- PMC
- PMC8246793
- OpenAlex
- W3106880531
- Cited by
- 143
- References
- 55
- Citations by year
- 2026: 15 · 2025: 17 · 2024: 30 · 2023: 18 · 2022: 42 · 2021: 20 · 2020: 1
- FWCI
- 14.96
- Type
- journal article
- Language
- en
- Update notices
- erratum (2023-06-13)
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Alzheimer s & Dementia (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Alzheimer's Drug Discovery Foundation (2016862, FO2017-0243, 201809, 2017-00915, #ALFGBG-715986, 201809–2016862, JPND2019-466-236, 201809-2016615, #RDAPB‐201809‐2016615, AF-742881)
- BrightFocus Foundation (AF-930627, A2020812F)
- Gun och Bertil Stohnes Stiftelse
- Demensförbundet
- European Commission (201809-2016862, JPND2019‐466‐236)
- Hjärnfonden (FO2017‑0243, FO2017, ALFGBG-715986, #FO2020-0240, JPND2019-466-236)
- Vetenskapsrådet (2017-00915, (#ALFGBG-715986, -201809-2016615, 201809-2016862, 681712, 02532, 2018-, JPND2019-466-236, ALFGBG-720931, FO2017-0243, 2018-02532)
- Alzheimerfonden (#AF-930627, -742881, AF-742881, -715986, -0243, FO2017-0243)
- UK Dementia Research Institute (JPND2019-466–236, #2017-00915, ALFGBG-715986, RDAPB-201809-2016615, FO2017-0243, -0243, -201809-2016615, -715986)
- H2020 European Research Council (681712)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
- Keywords
- Alzheimer's disease, phosphorylated tau
- MeSH terms
- Aged, Alzheimer Disease, Female, France, Humans, Immunoassay, Male, Middle Aged, Phosphorylation, Sweden, Biomarkers, tau Proteins, Cognitive Dysfunction
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