Evidence map›Paper›PMID 41761301›Full record

ArticleJournal of translational medicine2026

Baseline plasma p-tau217/Aβ42 as a sensitive marker for the severity of Alzheimer's disease continuum.

Wen-Zheng Liu, Mei Xue, Ze-Hu Sheng, Yu-Qian Wei, Ya-Hui Ma, Jie-Qiong Li, Jing-Hui Song, Song Chi, Ya-Nan Ou, Alzheimer’s Disease Neuroimaging Initiative

Abstract read
In one paragraph

Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Wen-Zheng LiuDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Mei XueDepartment of Neurology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 26400, China.
Ze-Hu ShengDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing Medical University, Chongqing, 400016, China.
Yu-Qian WeiQingdao University, Qingdao, 266000, China.
Ya-Hui MaDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Jie-Qiong LiDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Jing-Hui SongDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Song ChiDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China.
Ya-Nan OuDepartment of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, 266000, China. ouyanan0522@163.com.
Alzheimer’s Disease Neuroimaging Initiative

Funding

National Natural Science Foundation of China 82501704Taishan Scholar Foundation of Shandong Province tsqn202312391Taishan Scholar Foundation of Shandong Province tsqn202408400
6 · The paper itself

Abstract

backgroundPlasma p-tau217/Aβ42 has shown promising diagnostic accuracy for Alzheimer’s disease (AD), but its prognostic utility for AD risk and clinical phenotype remains unclear.

methodsWe analyzed 580 participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Diagnostic performance of p-tau217/Aβ42 for cognitively normal (CN) vs. AD was evaluated. Cox regression and linear mixed-effects models were used to investigate the relationships of plasma p-tau217/Aβ42 with AD risk, cognitive decline and brain atrophy. We also quantified the incremental predictive value of p-tau217/Aβ42 for AD risk, cognitive decline and brain atrophy beyond demographic data and the Mini-Mental State Examination (MMSE). Mediation analyses were conducted to test whether brain structure accounted for associations between p-tau217/Aβ42 and cognition.

resultsPlasma p-tau217/Aβ42 levels were elevated in individuals with amyloid and tau pathology. Combining plasma p-tau217/Aβ42 with MMSE discriminated AD from CN individuals (AUC = 0.988). Higher p-tau217/Aβ42 predicted faster cognitive decline and greater hippocampal atrophy (P < 0.001), increased explained variance for cognitive decline and brain atrophy (ΔmR² = 0.016–0.121). Hippocampal volumes partially mediated the relationships of p-tau217/Aβ42 with cognition (5.3–14.8%). In non-demented participants, the high-risk group of p-tau217/Aβ42 showed higher AD risk (HR = 7.45, 95% CI 4.36–12.74) and faster cognitive decline, remaining significant among those with preserved baseline cognition (MMSE > 28). The addition of p-tau217/Aβ42 improved AD risk prediction beyond MMSE and covariates (ΔC = 0.040), increased time-dependent AUC at 2 years (ΔAUC = 0.030), reduced prediction error (ΔBrier = − 0.017), improved reclassification (NRI/IDI; all P < 0.05).

conclusionPlasma p-tau217/Aβ42 is a strong prognostic biomarker for AD progression, adding value beyond demographics and brief cognitive screening. It supports a practical blood-first approach for risk stratification and prioritizing confirmatory testing, with additional utility for diagnostic support and trial enrichment.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesPeptide FragmentsSeverity of Illness Indextau ProteinsAgedAtrophyBiomarkersBrainCognitionFemaleHumansMalePhosphorylationAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersPeptide Fragmentstau ProteinsAlzheimer’s diseaseBiomarkerBrain structureCognitive assessmentPlasma p-tau217/Aβ42Predictive performance

Identifiers

PMID41761301
PMCPMC12955328

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LicenceCC BY-NC-ND
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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.