Evidence map›Paper›PMID 41478816›Full record

ArticleThe journal of prevention of Alzheimer's disease2026

Associations of plasma biomarkers with longitudinal co-pathologies in Alzheimer's disease and cerebral small vessel disease comorbidity.

Jing Yang, Xinyuan Zhao, Yidan Liu, Yangwei Cai, Yuhua Fan, Alzheimer’s Disease Neuroimaging Initiative

Abstract read
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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

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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

6 authors.

Jing YangDepartment of Neurology, The First Affiliated Hospital, Sun Yat-sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China; Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, No.58 Zhongshan Road 2, Guangzhou, 510080, China; National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Xinyuan ZhaoLaboratory of Metabolism and Aging, School of Pharmaceutical Sciences (Shenzhen), Shenzhen Campus of Sun Yat-sen University, No.66 Gongchang Road, Shenzhen, 518107, China.
Yidan LiuDepartment of Neurology, Chengdu Seventh People's Hospital, No.1188, Shuangxing Avenue, Chengdu, 610000, China.
Yangwei CaiDepartment of Cardiology, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, No.32, West Section 2, 1st Ring Road, Chengdu, 610000, China.
Yuhua FanDepartment of Neurology, The First Affiliated Hospital, Sun Yat-sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China; Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, No.58 Zhongshan Road 2, Guangzhou, 510080, China; National Key Clinical Department and Key Discipline of Neurology, No.58 Zhongshan Road 2, Guangzhou, 510080, China. Electronic address: fanyuhua@mail.sysu.edu.cn.
Alzheimer’s Disease Neuroimaging Initiative

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPlasma glial fibrillary acidic protein (GFAP), neurofilament light (NfL), phosphorylated tau217 (p-tau217), and the β-amyloid (Aβ) 42/40 ratio are emerging indicators of neuroinflammation, neurodegeneration, and AD-specific pathology, while their specific roles within Alzheimer's disease (AD) and cerebral small vessel disease (CSVD) comorbidity are not fully understood.

methodsParticipants with normal cognition or mild cognitive impairment were drawn from the Alzheimer's Disease Neuroimaging Initiative database. Multivariable linear regression and linear mixed-effects models were employed to examine associations of baseline plasma biomarkers with neuropathological features and cognition. Furthermore, Cox proportional hazards models assessed the associations of plasma biomarkers with the risk of comorbid AD and CSVD.

resultsIn total populations, elevated GFAP and p-tau217 were significantly associated with greater white matter hyperintensity (WMH) burden, hippocampal atrophy, cerebral Aβ burden, and cognitive decline at baseline and with progression over time (|β| = 0.007 to 1.670, p = 0.047 to <0.0001). Within disease-specific subgroups, GFAP, p-tau217, and Aβ42/40 ratio demonstrated associations with hippocampal atrophy or WMH progression in CSVD (|β| = 0.011 to 0.220, p = 0.046 to 0.010), whereas GFAP, NfL, p-tau217, and Aβ42/40 ratio were linked to hippocampal atrophy and/or WMH progression in typical AD (|β| = 0.013 to 0.191, p = 0.044 to 0.0002). For Cox proportional hazards models, p-tau217 demonstrated greater precision in predicting progression to the CSVD phenotype within the AD subgroup (Hazard ratios = 1.267 to 3.811, p = 0.046 to 0.034).

conclusionThese findings underscore the potential role of plasma biomarkers in elucidating the synergistic mechanisms underlying AD and CSVD comorbidity.

Indexed as

Alzheimer DiseaseCerebral Small Vessel DiseasesAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersCognitive DysfunctionComorbidityDisease ProgressionFemaleGlial Fibrillary Acidic ProteinHippocampusHumansLongitudinal StudiesMagnetic Resonance ImagingMaleAmyloid beta-PeptidesBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament Proteinstau ProteinsAlzheimer’s diseaseCerebral small vessel diseaseComorbidityPlasma biomarker

Identifiers

PMID41478816
PMCPMC12869035

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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.