Evidence map›Paper›PMID 41231544›Full record

ArticleClinical chemistry2026

Diagnostic Value of Serum p-tau217 in Alzheimer Disease: Equal to Plasma in Levels and Clinical Utility?

Andrea L Benedet, Burak Arslan, Kubra Tan, Hanna Huber, Ilaria Pola, Guglielmo Di Molfetta, Hlin Kvartsberg, Anna Orduña Dolado, Shorena Janelidze, Kaj Blennow and 4 more

Erratum issuedAbstract read
In one paragraph

Article in Clinical chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Andrea L BenedetDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Burak ArslanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID 0000-0001-7229-3226
Kubra TanDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Hanna HuberDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Ilaria PolaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Guglielmo Di MolfettaDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Hlin KvartsbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID 0000-0002-4481-508X
Anna Orduña DoladoClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.
Shorena JanelidzeClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.ORCID 0000-0003-3930-4354
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Malmö, Lund University, Lund, Sweden.ORCID 0000-0001-8467-7286
Pedro Rosa-NetoTranslational Neuroimaging Laboratory, Department of Neurology and Neurosurgery, Psychiatry and Pharmacology and Therapeutics, McGill University Research Centre for Studies in Aging, Montreal Neurological Institute-Hospital, Douglas Research Institute, McGill University, Montreal, Canada.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Funding

AD Strategic Fund 22HLT07AD Strategic Fund ADSF-21-831376-CAD Strategic Fund ADSF-21-831377-CAD Strategic Fund ADSF-21-831381-CAD Strategic Fund ADSF-24-1284328-CAlzheimer Drug Discovery Foundation 201809-2016862Alzheimer's Association NIRG-12-92090Alzheimer's Association NIRP-12-259245Alzheimer's Association Research Fellowship AARFD-22-974564Bluefield ProjectBrain Canada FoundationCanadian Consortium of Neurodegeneration and Aging MOP-11-51-31CIHR 159815CIHR 162303CIHR MOP-11-51-31CIHR RFN 152985Cure Alzheimer's FundErling-Persson Family FoundationEuropean Union Joint Programme-Neurodegenerative Disease Research JPND2021-00694European Union's Horizon Europe 101053962Familjen Rönströms StiftelseFonds de Recherche du Québec-Santé 2020-VICO-279314Fonds de Recherche du Québec-Santé 2024-VICO-356138GHR Foundation 2022-00775Hjärnfonden, Sweden FO2022-0270Knut and Alice Wallenberg Foundation 2022-0231Konung Gustaf V:s och Drottning Victorias FrimurarestiftelseLund University AF-980907Marie Skłodowska-Curie grantNational Institute for Health and Care Research University College London Hospitals Biomedical Research CentreOlav Thon FoundationParkinson Foundation of Sweden 1412/22Regionalt Forskningsstöd 2022-1259Rönström Family FoundationSkåne University Hospital Foundation 2020-O000028Stiftelsen för Gamla TjänarinnorSwedish Alzheimer Foundation AF-940262Swedish Brain Foundation FO2021-0293Swedish Federal Government 2022-Projekt0080Swedish Research Council 2019-02397Swedish Research Council 2022-01018Swedish Research Council 2023-00356Swedish State Support for Clinical Research ALFGBG-71320UK Dementia Research Institute 2017-00915UK Dementia Research Institute 2022-00732UK Dementia Research Institute AF-930351UK Dementia Research Institute AF-939721UK Dementia Research Institute AF-968270UK Dementia Research Institute ALFGBG-715986UK Dementia Research Institute ALFGBG-965240UK Dementia Research Institute ALZ2022-0006UK Dementia Research Institute FO2017-0243UK Dementia Research Institute JPND2019-466-236UK Dementia Research Institute SG-23-1038904UK Dementia Research Institute SG-23-1061717UK Dementia Research Institute UKDRI-1003UK Dementia Research Institute ZEN24-1069572University of GothenburgWeston Brain Institute
6 · The paper itself

Abstract

backgroundPhosphorylated tau 217 (p-tau217) has emerged as a leading blood-based biomarker for Alzheimer disease (AD). While typically measured in plasma, serum is a widely used matrix in clinical laboratories, yet few p-tau217 assays have been validated for serum. Evaluating serum p-tau217 performance is essential for expanding its use in clinical and research settings, particularly for cohorts with only serum samples available.

methodsWe quantified p-tau217 in plasma and serum from individuals within the AD continuum (n = 100; mean age 72.5 ± 5.0 years; 54% female) using 6 assays across 4 platforms. Spearman correlation, Passing-Bablok regression, and receiver operating characteristics analysis were used to assess intermatrix agreement and diagnostic performance. Specific validation parameters (e.g., precision, parallelism, dilution linearity, stability) were evaluated in both matrices.

resultsHigh correlations between plasma and serum were observed for most assays (ρ > 0.8), though plasma often yielded higher concentrations. Notably, the Lumipulse assay showed near-perfect correlation (ρ = 0.98) and minimal bias. Fold changes in p-tau217 levels across the AD continuum were comparable between matrices, though cutoffs for detecting AD pathology differed. Applying plasma-derived cutoffs to serum resulted in misclassification rates ranging from 16% to 47%, except for Lumipulse (10% in serum vs 5% in plasma). Not all assays performed equally in serum, as reflected in validation metrics.

conclusionsSerum p-tau217, across multiple platforms, shows strong correlations with plasma p-tau217 and reflected comparable patterns across the AD continuum. However, absolute concentrations differed for most assays, thus requiring differing disease specific cutoffs. Most of the evaluated platforms demonstrated reliable quantification of p-tau217 in serum, yielding satisfactory validation performance. These findings support serum as a viable alternative to plasma for p-tau217 quantification in both research and clinical settings, provided matrix-specific validation is ensured.

Indexed as

Alzheimer Diseasetau ProteinsAgedAged, 80 and overBiomarkersFemaleHumansMalePhosphorylationBiomarkerstau Proteins

Identifiers

PMID41231544
PMCPMC12865796

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.