Evidence map›Paper›PMID 41947717›Full record

ArticleEuropean journal of neurology2026

Gene-Environment Interactions for Alzheimer's Disease Pathology in Cognitively Normal Adults: The CABLE Study.

Ze-Xin Guo, Xiao-Yu He, Yi-Jun Ge, Bing Zhao, Liang-Yu Huang, Shi-Dong Chen, Yan Fu, Pei-Yang Gao, Ze-Hu Sheng, Yi-Ming Huang and 2 more

Abstract read
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Article in European journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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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

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Ze-Xin GuoDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.ORCID https://orcid.org/0009-0004-1570-0859
Xiao-Yu HeDepartment of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Yi-Jun GeDepartment of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Bing ZhaoDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
Liang-Yu HuangDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
Shi-Dong ChenDepartment of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Yan FuDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
Pei-Yang GaoDepartment of Neurology & Innovation Center for Neurological Disorders, Xuanwu Hospital, National Center for Neurological Disorders, Capital Medical University, Beijing, China.
Ze-Hu ShengDepartment of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yi-Ming HuangDepartment of Neurology and Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.
Qiong-Yao LiDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.
Lan TanDepartment of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China.

Funding

National Natural Science Foundation of China 82271475
6 · The paper itself

Abstract

backgroundCharacterizing the gene-environment interactions with early pathological changes in Alzheimer's disease (AD) is critical to precision medicine.

methodsWe recruited 1007 cognitively normal participants from the Chinese Alzheimer's Biomarker and LifestylE (CABLE) study. Multiple linear regression models were applied to explore the associations between polygenic risk scores (PRSs) and cerebrospinal fluid (CSF) biomarkers of AD, the interactions between PRSs and potentially modifiable risk factors, and the relationships between lifestyle categories and CSF AD biomarkers.

resultsA higher AD-PRS was associated with more severe amyloidosis, as indicated by pTau/Aβ42 (β = 0.091, p = 0.005) and tTau/Aβ42 (β = 0.092, p = 0.004). There were significant interactions between AD-PRS and three modifiable risk factors (anemia, gingivitis, and anxiety) in AD biomarker ratios. Stratified analyses by AD-PRS indicated that anemia was associated with higher pTau/Aβ42 and tTau/Aβ42 in the first and second quartiles, while gingivitis and anxiety correlated with amyloidosis in the fourth quartile (all p < 0.05). Additionally, a favorable lifestyle was associated with milder amyloidosis in the high genetic risk group.

conclusionsAD-PRS was associated with amyloidosis severity. The associations between modified risk factors (anemia, gingivitis, and anxiety) and biomarker ratios differed by genetic risk strata. Moreover, a healthy lifestyle was associated with less amyloid burden in individuals with high genetic risk. These findings can be used to generate hypotheses for future longitudinal studies to investigate whether targeted management of these factors influences AD pathological progression.

Indexed as

Alzheimer DiseaseGene-Environment InteractionAgedAged, 80 and overAmyloid beta-PeptidesAmyloidosisBiomarkersFemaleGenetic Risk ScoreHumansLife StyleMaleMiddle AgedPeptide FragmentsRisk Factorstau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersPeptide Fragmentstau ProteinsAlzheimer's diseasecerebrospinal fluid biomarkersgene–environmentlifestyleneurodegenerationpolygenic risk score

Identifiers

PMID41947717
PMCPMC13058572

What Socratic holds

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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 Socratic graph.