Evidence map›Paper›PMID 38253907›Full record

ArticleJournal of neurology2024

Identifying the mediating role of inflammation on the relationship between socioeconomic status and Alzheimer's disease: a Mendelian randomization analysis and mediation analysis.

Chaofan Geng, Ke Meng, Yi Tang

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Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
5.5field-weighted citation impact, top 4% of its field
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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Individual and neighborhood socioeconomic inequality and the risk of dementia: A 14-year follow-up study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Article
  4. Article
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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

3 authors at 2 institutions in 1 country.

Chaofan Geng *Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, National Center for Neurological Disorders, Capital Medical University, 45 Changchun Street, Beijing, 100053, China.
Ke Meng *Department of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, National Center for Neurological Disorders, Capital Medical University, 45 Changchun Street, Beijing, 100053, China.
Yi TangDepartment of Neurology and Innovation Center for Neurological Disorders, Xuanwu Hospital, National Center for Neurological Disorders, Capital Medical University, 45 Changchun Street, Beijing, 100053, China. tangyi@xwhosp.org.
Capital Medical University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesObservational studies have demonstrated a significant association between socio-economic status (SES) and Alzheimer's disease (AD). Nonetheless, the precise biological mechanisms underlying this association remain unclear. Therefore, we adopted a Mendelian Randomization (MR) approach to investigate the causal relationship between SES and genetic susceptibility to AD, as well as to explore the potential mediation effects of inflammation.

methodsLarge-scale cohorts based on publicly available genome-wide association study (GWAS) datasets from European populations were employed for conducting the MR study. The primary criterion utilized was the inverse-variance weighting (IVW) model. Heterogeneity and horizontal pleiotropy were assessed. In addition, multivariate MR (MVMR) was utilized to correct the confounders. Moreover, a two-step MR approach was used to evaluate the potential mediating effects of factors on the causal effects between SES and AD.

resultsAs indicated by the results of the IVW model, educational years (OR = 0.708, 95% CI 0.610-0.821, P < 0.001) and household income (OR = 0.746, 95% CI 0.566-0.982, P = 0.037) was associated with a decreased genetic susceptibility risk for AD. The univariable results showed that the causal effect of educational years on the lower risk of AD remained significant (OR = 0.643, 95% CI 0.467-0.886, P = 0.006). In addition, our findings indicated that C-reactive protein (CRP) played a role in the causal effect of educational years on AD. The proportions of mediation were - 50.08% (95% CI - 92.78; - 7.38%). DISCUSSION: These findings provided evidence supporting the causal effect of educational attainment lower AD risk, with inflammation playing a mediating role. These findings may inform prevention strategies and interventions directed toward AD. Future studies should explore other plausible biological mechanisms.

Indexed as

Alzheimer DiseaseGenetic Predisposition to DiseaseGenome-Wide Association StudyInflammationMediation AnalysisMendelian Randomization AnalysisSocial ClassHumansPolymorphism, Single NucleotideAlzheimer’s diseaseCausal relationshipC-reaction protein (CRP)Mendelian randomization studySocioeconomic status

Identifiers

PMID38253907
OpenAlexW4391098392

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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.