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Educational attainment, brain cortical structure, and sarcopenia

A Mendelian randomization study

Bibliographic Data

ID22072243
AuthorsYunqing Zhang (0009-0000-5525-5834), Ruideng Wang (0000-0001-6562-7152, Peking University), Zhengyang Chen (0000-0003-1293-8146, Peking University), Fang Zhou (0000-0002-5542-2994, Peking University), Shilong Su (0000-0001-9489-820X, Peking University, corresponding author)
Year2024
Volume12
Pages1415343-1415343
Publication date2024-10-23
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueFrontiers in Public Health (JOURNAL)
Journal identifiersISSN: 2296-2565 • E-ISSN: 2296-2565
PublisherFrontiers Media SA (PUBLISHER • CH)
DOI10.3389/fpubh.2024.1415343
PMID39507653
OpenAlexW4403699930
LanguageEN
Citations received1
References cited38

Background Previous observational studies have suggested associations between high-level educational attainment (EA) and a lower risk of sarcopenia. However, the causality inferred from those studies was subjected to residual confounding and reverse causation. The protective effect of EA on sarcopenia may be mediated via changes in brain cortical structure. The aim of this study was to use a two-step Mendelian randomization (MR) analysis to illustrate the causal relationship between EA, brain cortical structure, and sarcopenia. Methods Instrumental variables at the genome-wide significance level were obtained from publicly available datasets, and inverse variance weighted as the primary method was used for MR analysis. We perform several sensitivity analyses, including Cochran Q test, MR-Egger intercept test, leave-one-out analyses, and MR Pleiotropy Residual Sum and Outlier to evaluate the reliability of the results. Results EA was causally associated with increased appendicular lean mass ( β = 0.25, 95% confidence interval (CI): 0.19 to 0.31, p = 2.25 × 10 −15 ), hand grip strength (left: β = 0.042, 95% CI: 0.013 to 0.071, p = 4.77 × 10 −3 and right: β = 0.050, 95% CI: 0.022 to 0.079, p = 5.17 × 10 −4 ), and usual walking pace (β = 0.20, 95% CI: 0.18 to 0.22, p = 6.16 × 10 −83 ). In addition, EA was associated with increased brain cortical surface area ( β = 4082.36, 95% CI: 2513.35 to 5681.38, p = 3.40 × 10 −7 ) and cortical thickness (TH) ( β = 0.014, 95% CI: 0.0045 to 0.023, p = 3.45 × 10 −3 ). Regarding the causal effect of EA on usual walking pace, the mediatory effect of TH was 0.0069 and the proportion of mediation by TH was 3.43%. Conclusion The study will have revealed the protective causal effect of EA on sarcopenia, which provides a reference for the prevention of sarcopenia at the public health level. We also will have found EA could affect the brain cortical structure, and the brain cortical structure could mediate the protective effect of EA against sarcopenia risk

Biology · Confidence interval · Confounding · Mendelian randomization · Sarcopenia · Cognitive Abilities and Testing · Cognitive and developmental aspects of mathematical skills · Genetic Associations and Epidemiology · Medicine · Genetics · Internal Medicine

  • Ultrasonographic assessment of thenar muscles for diagnosing sarcopenic obesity in patients with schizophrenia

    Open Access•Gabriel Yan, Guoyu Yan et al.•Frontiers in Psychiatry•2025

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    Open Access•Martin Lövdén, Laura Fratiglioni et al.•Psychological Science in the…•2020

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Unique citing works1
Citations per year1
Citation span2025 - 2025 (1)
Citation velocityrecent
Highly citedNo
Citation typesNeutral: 1

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