ArticleBrain and behavior2025
Association of the Lipidome With Alzheimer's Disease and the Mediated Effect of Metabolites: A Two-Step Mendelian Randomization Study.
Article in Brain and behavior, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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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
1 citing paper in PubMed.
- Betaine: A Promising Natural Product for Neurological and Psychiatric Diseases.Current neuropharmacology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
objectiveThis study aimed to explore the causal effects of lipidome on Alzheimer's disease (AD) and the mediated effects of the metabolites using Mendelian randomization (MR).
methodsData were obtained in genome-wide association studies, and single-nucleotide polymorphisms were screened according to the underlying assumptions of MR. Subsequently, weighted inverse variance was used to analyze the causality of lipidome with AD as well as the mediated effects of metabolites. Finally, MR-Egger, Cochran's Q, and sensitivity analysis were used to assess horizontal pleiotropy, heterogeneity, and robustness of the results, respectively.
resultsThe MR analysis showed that phosphatidylcholine (PC) (15:0_18:2) (mediated proportion: 18.30%, p = 0.024) and phosphatidylethanolamine (PE) (18:0_18:2) (mediated proportion: 14.60%, p = 0.028) mediated the reduction of AD risk by lowering betaine levels, which revealed lipidomic susceptibility. The MR-Egger intercept showed no horizontal pleiotropy for all results (p ≥ 0.05). Cochran's Q showed heterogeneity in some of the results. Sensitivity analysis indicated that all results were robust.
conclusionOur findings reveal the pathways through which PC (15:0_18:2) and PE (18:0_18:2) mediated the reduction of AD risk by lowering betaine levels.
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Registered trials
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