ArticleNutrients2024
Causal Association between Circulating Metabolites and Dementia: A Mendelian Randomization Study.
Article in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review of risk factors for vascular dementia using Mendelian randomization: a call for methodologically robust studies to advance knowledge.BMC neurology · 2026Pooled it
- Integrative transcriptomic and genetic analysis implicates fatty acid metabolic reprogramming in perivascular macrophages in Alzheimer's disease.Metabolic brain disease · 2026Article
- Modifiable and clinically actionable exposures for vascular dementia: a structured evidence synthesis of Mendelian randomization studies.Journal of neurology · 2026Review
- Plasma pentadecanoic acid is modestly related to cardiovascular health in CARDIA and ARIC cohorts: observational associations without evidence of causality.Frontiers in nutrition · 2026Article
- Causal associations between circulating metabolites and chronic kidney disease: a Mendelian randomization study.Renal failure · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The causal association of circulating metabolites with dementia remains uncertain. We assessed the causal association of circulating metabolites with dementia utilizing Mendelian randomization (MR) methods. We performed univariable MR analysis to evaluate the associations of 486 metabolites with dementia, Alzheimer's disease (AD), and vascular dementia (VaD) risk. For secondary validation, we replicated the analyses using an additional dataset with 123 metabolites. We observed 118 metabolites relevant to the risk of dementia, 59 of which were lipids, supporting the crucial role of lipids in dementia pathogenesis. After Bonferroni adjustment, we identified nine traits of HDL particles as potential causal mediators of dementia. Regarding dementia subtypes, protective effects were observed for epiandrosterone sulfate on AD (OR = 0.60, 95% CI: 0.48-0.75) and glycoproteins on VaD (OR = 0.89, 95% CI: 0.83-0.95). Bayesian model averaging MR (MR-BMA) analysis was further conducted to prioritize the predominant metabolites for dementia risk, which highlighted the mean diameter of HDL particles and the concentration of very large HDL particles as the predominant protective factors against dementia. Moreover, pathway analysis identified 17 significant and 2 shared metabolic pathways. These findings provide support for the identification of promising predictive biomarkers and therapeutic targets for dementia.
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Registered trials
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