Evidence map›Paper›PMID 41478832›Full record

ArticleThe journal of prevention of Alzheimer's disease2026

Association of plasma p-tau and p-tau/Aβ ratio with Alzheimer's pathology.

Xuhui Chen, Mingxing Jiang, Laihong Zhang, Jiayi Zhu, Anqi Li, Zhengbo He, Xin Zhou, Yalin Zhu, Chen Zhang, Cong Wang and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article 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 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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

  1. Diagnostic accuracy of plasma p-tau217 against amyloid PET: A meta-analysis of technical platform variability and ratio versus single marker comparisons.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Pooled it
  2. Article
  3. 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

21 authors.

Xuhui ChenDepartment of Neurology, Peking University First Hospital, Beijing 100034, China; Department of Neurology, Peking University Shenzhen Hospital, Shenzhen 518132, China.
Mingxing JiangShenzhen Medical Academy of Research and Translation, Shenzhen 518132, China; Westlake University, Hangzhou 310024, China.
Laihong ZhangInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China.
Jiayi ZhuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; School of Biology and Biological Engineering, South China University of Technology, Guangzhou 510641, China.
Anqi LiInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; Division of Life Science, The Hong Kong University of Science and Technology, Hong Kong 999077, China.
Zhengbo HeInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China.
Xin ZhouInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; School of Biomedical Engineering, Hainan University, Haikou 570228, China.
Yalin ZhuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China; Division of Life Science, The Hong Kong University of Science and Technology, Hong Kong 999077, China.
Chen ZhangDepartment of Neurology, Peking University First Hospital, Beijing 100034, China.
Cong WangDepartment of Neurology, Peking University First Hospital, Beijing 100034, China.
Mingxu LiDepartment of Neurology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, China.
Yiying WangInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China.
Xinyue MaInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China.
Binhui LiuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China.
Rong MaInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China.
Yipeng JinInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China.
Xiang FanDepartment of Medical Imaging, Peking University Shenzhen Hospital, Shenzhen 518132, China.
Zhen LiuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China.
Tengfei GuoInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China. Electronic address: tengfei.guo@szbl.ac.cn.
Yong-An SunDepartment of Neurology, Peking University First Hospital, Beijing 100034, China. Electronic address: sya@bjmu.edu.cn.
Guoyu LanInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen 518132, China. Electronic address: langy@szbl.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasma phosphorylated tau (p-tau) and β-amyloid (Aβ) are promising biomarkers for Alzheimer's disease (AD). However, it remains unclear whether combining p-tau with Aβ provides better predictive performance than using p-tau alone.

objectivesTo evaluate the predictive utility of plasma p-tau and Aβ combinations for AD-related pathology, brain atrophy, and cognitive decline. DESIGN, SETTING, AND

participantsThis study included 352 participants from the Greater-Bay Area Healthy Aging Brain Study (GHABS) cohort in China, classified into 227 Aβ-negative and 125 Aβ-positive individuals. MEASUREMENTS: Participants underwent Aβ positron emission tomography (PET) and plasma biomarker assessments. Plasma concentrations of p-tau181, p-tau217, p-tau231, Aβ42, and Aβ40 were quantified on the Quanterix HD-X and Lumipulse G1200 platform.

resultsAmong the individual plasma p-tau variants, p-tau217 consistently outperformed p-tau181 and p-tau231. The combination of p-tau biomarkers (p-tau181, p-tau217, and p-tau231) with Aβ42 or the Aβ42/40 ratio further improved discrimination between Aβ+/CU (cognitively unimpaired) and Aβ-/CU individuals. Both p-tau/Aβ42 and p-tau/(Aβ42/40) exhibited slightly stronger or comparable associations with Aβ PET burden, baseline and longitudinal measures of hippocampal atrophy, AD-typical cortical thinning, and cognitive decline, relative to p-tau alone.

conclusionsThe head-to-head comparisons indicate that p-tau217 is the most robust biomarker among the variants tested, and p-tau/Aβ ratios perform comparably or slightly better than p-tau alone in reflecting AD pathology, potentially providing complementary information for early detection and monitoring of disease progression.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBraintau ProteinsAgedAged, 80 and overAtrophyBiomarkersChinaCognitive DysfunctionCohort StudiesFemaleHumansMaleMiddle AgedPhosphorylationAmyloid beta-PeptidesBiomarkersMAPT protein, humantau ProteinsAlzheimer’s diseaseBrain atrophyCognitive declinePlasma biomarkerP-tauΒ-amyloid

Identifiers

PMID41478832
PMCPMC12988372

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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.