Evidence map›Paper›PMID 42247843›Full record

Observational studyThe journal of prevention of Alzheimer's disease2026

Plasma brain-derived p-Tau217 outperforms other p-Tau species in detecting abnormal brain amyloid in an Asian cohort of older people with cerebrovascular disease burden.

Joyce R Chong, Saima Hilal, Narayanaswamy Venketasubramanian, Michael Schöll, Nicholas J Ashton, Henrik Zetterberg, Christopher P Chen, Mitchell K P Lai

Abstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in The journal of prevention of Alzheimer's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–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

4 citing papers in PubMed.

  1. Excitation-inhibition imbalance links amyloid pathophysiology to cognition in non-demented individuals.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Article
  3. Prognostic value of plasma brain-derived pTau.medRxiv : the preprint server for health sciences · 2026
    Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Joyce R ChongDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore; Memory, Aging and Cognition Centre, National University Health Systems, Singapore 117599, Singapore; Wisconsin Alzheimer's Disease Research Center, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA. Electronic address: jrchong@wisc.edu.
Saima HilalDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore; Memory, Aging and Cognition Centre, National University Health Systems, Singapore 117599, Singapore; Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore 117549, Singapore.
Narayanaswamy VenketasubramanianRaffles Hospital, Raffles Neuroscience Centre, Singapore 188770, Singapore.
Michael SchöllDepartment of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden; Dementia Research Centre, Institute of Neurology, University College London, London, UK.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden; Banner Sun Health Research Institute, Sun City, AZ, USA.
Henrik ZetterbergWisconsin Alzheimer's Disease Research Center, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA; Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Sweden; Dementia Research Centre, Institute of Neurology, University College London, London, UK; Paris Brain Institute, ICM, Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France.
Christopher P ChenDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore; Memory, Aging and Cognition Centre, National University Health Systems, Singapore 117599, Singapore.
Mitchell K P LaiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore; Memory, Aging and Cognition Centre, National University Health Systems, Singapore 117599, Singapore. Electronic address: mitchell.lai@dementia-research.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasma brain derived-p-Tau217 (BD-p-Tau217) may outperform total-p-Tau217 in detecting brain amyloid burden and warrants evaluation.

objectivesTo perform head-to-head comparison of plasma BD- as well as total-p-Tau181, p-Tau217 and p-Tau231 for detecting beta-amyloid positivity (Aβ+), evaluate reference ranges for Aβ+, and assess the prognostic utility of BD-p-Tau217 reference ranges.

designObservational study.

settingParticipants recruited from memory clinics and the community in Singapore.

participants213 participants, including 44 cognitively normal, 107 cognitively impaired no dementia, and 62 dementia (mean [SD] age, 73 [1] years; 121 females). MEASUREMENTS: Amyloid status (Aβ- [n = 139] vs Aβ+ [n = 74]) was determined by positron emission tomography (PET). Plasma BD-p-Tau and total-p-Tau were measured using the NULISAseq™ CNS Disease Panel 120. The diagnostic performance for detecting Aβ+, reference ranges (three-range: 95% specificity/95% sensitivity); binary: maximizing Youden index), and the prognostic performance of p-Tau biomarkers were evaluated.

resultsPlasma BD-p-Tau217 (AUC = 0.965) outperformed other BD- and total-p-Tau species in detecting PET Aβ+ (AUC = 0.823-0.937; all p ≤ 0.008). Using a three-range reference, BD-p-Tau217 achieved positive predictive value (PPV) and negative predictive value (NPV) of 90% and 97%, respectively. Proportion of participants in the intermediate-risk group was 7% (n = 14). Applying a binary reference, BD-p-Tau217 achieved both a specificity and sensitivity of 92%, with PPV and NPV of 86% and 96%, respectively. BD-p-Tau217-derived high-risk group exhibited faster cognitive decline than the low-risk group.

conclusionsRisk stratification for PET Aβ+ based on plasma BD-p-Tau217 suggests superior diagnostic and prognostic utility, warranting further validation.

Indexed as

Amyloid beta-PeptidesBrainCerebrovascular Disorderstau ProteinsAgedAsian PeopleBiomarkersDementiaFemaleHumansMalePositron-Emission TomographyReference ValuesSingaporeAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer’s diseaseBrain amyloidBrain-derived p-TauDiagnosisPrognosis

Identifiers

PMID42247843
PMCPMC13264343

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.