Evidence map›Paper›PMID 41185063›Full record

ArticleAlzheimer's research & therapy2025

Longitudinal characteristics of plasma biomarkers in Chinese older adults with Alzheimer's disease.

Ruixian Li, Lin Liu, Jie Yang, Wenhui Chai, Mingkai Zhang, Min Wei, Yongzhe Wei, Xuanqian Wang, Shuyu Zhang, Jinghua Wang and 2 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2025. 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

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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. How does type 2 diabetes modify the risk of Alzheimer's disease?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
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

12 authors.

Ruixian Li *Department of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Lin Liu *Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, No.5 Kelian Road, Shenzhen, 518132, China.
Jie YangDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Wenhui ChaiChangji Hui Autonomous Prefecture People's Hospital, Changji, Xinjiang, China.
Mingkai ZhangDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Min WeiDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Yongzhe WeiDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Xuanqian WangDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Shuyu ZhangDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China.
Jinghua WangDepartment of Neurology, The Affiliated Hospital of Hangzhou Normal University, No.126 Wenzhou Road, Gongshu District, Hangzhou, 310015, China. 20201018@hznu.edu.cn.
Tengfei GuoInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, No.5 Kelian Road, Shenzhen, 518132, China. tengfei.guo@szbl.ac.cn.
Ying HanDepartment of Neurology, XuanWu Hospital of Capital Medical University, No.45 Changchun Street, Beijing, 100053, China. hanying@xwh.ccmu.edu.cn.

Funding

China Postdoctoral Science Foundation 2023T160439Guangdong Basic and Applied Basic Science Foundation for Distinguished Young Scholars 2023B1515020113National Natural Science Foundation of China 82327809, 82020108013National Natural Science Foundation of China 82422027, U24A20340Open Research Fund of the State Key Laboratory of Cognitive Neuroscience and Learning CNLZD2101, CNLZD2303STI2030-Major Projects 2022ZD0211800
6 · The paper itself

Abstract

backgroundWhile cross-sectional associations between plasma biomarkers and Alzheimer’s disease (AD) pathology and cognition are well established, their longitudinal relationships remain less elucidated. We aimed to explore the utility of plasma β-amyloid (Aβ) 42/Aβ40 and glial fibrillary acidic protein (GFAP) in detecting and predicting AD progression, particularly considering neuroinflammation as a key contributor.

methodsUtilizing data from the Sino Longitudinal Study on Cognitive Decline (SILCODE), 455 older Chinese participants with available plasma Aβ42/Aβ40 and GFAP data were enrolled. Based on cohort-derived thresholds of plasma Aβ42/Aβ40 (A) and GFAP (As), participants were divided into four groups: A + As+, A + As-, A-As+, and A-As-. We employed generalized linear models to examine the cross-sectional and longitudinal associations between plasma Aβ42/Aβ40, GFAP, and their combination with plasma phosphorylated tau (p-tau), residual hippocampal volume (rHCV), and cognitive function.

resultsAmong 455 participants (mean [SD] age at baseline, 66.11 [6.73] years; 282 [61.98%] female), the A + As + group consistently demonstrated the highest baseline levels and fastest longitudinal increases in plasma p-tau, alongside the lowest baseline levels and fastest longitudinal deterioration of rHCV and cognition. Lower baseline plasma Aβ42/Aβ40 was associated with worse memory and language cognitive function and higher baseline and accelerated increases in plasma p-tau181 and p-tau217. Elevated baseline plasma GFAP was significantly associated with higher baseline plasma p-tau181 and p-tau217, reduced rHCV and cognition, and predicted more rapid increases in plasma p-tau181 and p-tau217, and faster declines in rHCV and cognition. Longitudinally, plasma GFAP slope was positively related to the slopes of plasma p-tau181 and p-tau217 and rapid decreases in global, memory, and executive cognitive function. In contrast, the plasma Aβ42/Aβ40 slope showed a negative correlation only with the p-tau181 slope.

conclusionsThese findings demonstrate the superior predictive utility of plasma GFAP in identifying and predicting plasma p-tau increase, neurodegeneration, and cognitive decline than plasma Aβ42/Aβ40 alone. Critically, the combination of both biomarkers yielded the most optimal results, highlighting their synergistic value for early detection and tracking of AD progression.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesGlial Fibrillary Acidic ProteinPeptide FragmentsAgedBiomarkersChinaCross-Sectional StudiesDisease ProgressionEast Asian PeopleFemaleHippocampusHumansLongitudinal StudiesMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)BiomarkersGFAP protein, humanGlial Fibrillary Acidic ProteinPeptide Fragmentstau ProteinsAlzheimer's diseaseAmyloid-βAstrocyte activationGFAPPlasma biomarkers

Identifiers

PMID41185063
PMCPMC12581300

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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.