Evidence mapPaperPMID 41083880Full record

SynthesisJournal of neurology2025

The role of APOE ε4 in modulating the relationship between non-genetic risk factors and dementia: a system review and meta-analysis.

Xiao-Tong Huang, Liang-Yu Huang, Chen-Chen Tan, Jie-Mei Wei, Xin-Hao Zhang, Lan Tan, Wei Xu

Abstract readMeta-AnalysisSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Biological psychiatry global open science · 2026
    Article
  2. Review
  3. Review
  4. 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

7 authors.

Xiao-Tong HuangDepartment of Neurology, Qingdao Municipal Hospital Group, Qingdao University, Donghai Middle Road, No. 5, Qingdao, 266000, Shandong, China.
Liang-Yu HuangDepartment of Neurology, Qingdao Municipal Hospital Group, Qingdao University, Donghai Middle Road, No. 5, Qingdao, 266000, Shandong, China.
Chen-Chen TanDepartment of Neurology, Qingdao Municipal Hospital Group, Qingdao University, Donghai Middle Road, No. 5, Qingdao, 266000, Shandong, China.
Jie-Mei WeiDepartment of Neurology, Linyi Central Hospital, Linyi, 276400, Shandong, China.
Xin-Hao ZhangMedical College, Qingdao University, Qingdao, Shandong, China.
Lan TanDepartment of Neurology, Qingdao Municipal Hospital Group, Qingdao University, Donghai Middle Road, No. 5, Qingdao, 266000, Shandong, China.
Wei XuDepartment of Neurology, Qingdao Municipal Hospital Group, Qingdao University, Donghai Middle Road, No. 5, Qingdao, 266000, Shandong, China. dr_xuwei@qdu.edu.cn.ORCID http://orcid.org/0000-0002-3310-5875

Funding

Taishan Scholar Foundation of Shandong Province tsqn202211375
6 · The paper itself

Abstract

backgroundThe ε4 allele of the apolipoprotein E gene (APOE ε4) is the strongest genetic risk factor for dementia. However, it remains unclear whether APOE ε4 status modulates the associations of non-genetic risk factors and dementia risk. This study aims to comprehensively evaluate this potential modulating role.

methodsA systematic search of electronic databases was conducted up to June 2023. Population-based longitudinal studies were included if they reported associations of risk factors with all-cause dementia (ACD) or Alzheimer's disease (AD) stratified by APOE ε4 status. Subgroup and meta-regression analyses were performed to test stratification effects by APOE ε4.

resultA total of 170 studies (173 factors) were included, with 48 factors for meta-analyses. Meta-regression confirmed significant modification effect by APOE ε4 status for nine risk factors. Stronger associations in APOE ε4 carriers were found for nonsteroidal anti-inflammatory drugs, statins, frequent drinking, and high systolic blood pressure; in noncarriers, stronger associations were observed for light-to-moderate alcohol consumption, female sex, physical activity, diabetes, and loneliness. Diabetes specifically increased AD risk only in APOE ε4 noncarriers. Additionally, the subgroup analyses stratified by APOE ε4 status indicated that nine other factors may influence risk differentially between carriers and noncarriers, though the associations were not significant in meta-regression (vitamin E intake, heart failure, serum neurofilament light chain, serum testosterone, agitation, air NO

conclusionEvidence from the current investigation suggests that APOE ε4 defines distinct etiological pathways for dementia, underscoring the promise of genotype-tailored prevention strategies.

Indexed as

Apolipoprotein E4DementiaAlzheimer DiseaseHumansRisk FactorsApolipoprotein E4Alzheimer’s diseaseAPOE ε4CohortDementiaLongitudinalRisk factor

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.