ArticleBMJ medicine2023
Genetically proxied lean mass and risk of Alzheimer's disease: mendelian randomisation study.
Article in BMJ medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Dementia risk across distinct metabolic profiles in the UK Biobank.GeroScience · 2026Article
- Associations of Sarcopenia and Sarcopenic Obesity Using Different Obesity Definitions With Memory Decline.Journal of diabetes · 2026Article
- Genetically proxied blood pressure, vascular brain injury, and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Article
- Body size and intracranial volume interact with the structure of the central nervous system: A multi-center in vivo neuroimaging study.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Development of a prediction model for cognitive impairment of sarcopenia using multimodal neuroimaging in non-demented older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Bayesian genome-wide TWAS with reference transcriptomic data of brain and blood tissues identified 141 risk genes for Alzheimer's disease dementia.Alzheimer's research & therapy · 2024Article
- Associations of body habitus and its changes with incident dementia in older adults.Journal of the American Geriatrics Society · 2024Article
- Polygenic scores and Mendelian randomization identify plasma proteins causally implicated in Alzheimer's disease.Frontiers in neuroscience · 2024Article
- Interactions between muscle volume and body mass index on brain structure in the UK Biobank.Frontiers in dementia · 2024Article
- Risk factors and mediating mechanisms of restless legs syndrome in patients undergoing maintenance hemodialysis: a longitudinal cohort study combined with Mendelian randomization analysis.Frontiers in neurologyArticle
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To examine whether genetically proxied lean mass is associated with risk of Alzheimer's disease. Design: Mendelian randomisation study. Setting: The UK Biobank study and genome wide association study meta-analyses of Alzheimer's disease and cognitive performance. Participants: Summary level genetic data from: 450 243 UK Biobank participants with impedance measures of lean mass and fat mass; an independent sample of 21 982 patients with Alzheimer's disease and 41 944 controls without Alzheimer's disease; a replication sample of 7329 patients with Alzheimer's disease and 252 879 controls; and 269 867 individuals taking part in a genome wide association study of cognitive performance. Main outcome measure: Effect of genetically proxied lean mass on the risk of Alzheimer's disease, and the related phenotype of cognitive performance. Results: An increase in genetically proxied appendicular lean mass of one standard deviation was associated with a 12% reduced risk of Alzheimer's disease (odds ratio 0.88, 95% confidence interval 0.82 to 0.95, P=0.001). This finding was replicated in an independent cohort of patients with Alzheimer's disease (0.91, 0.83 to 0.99, P=0.02) and was consistent in sensitivity analyses that are more robust to the inclusion of pleiotropic variants. Higher genetically proxied appendicular lean mass was also associated with increased cognitive performance (standard deviation increase in cognitive performance for each standard deviation increase in appendicular lean mass 0.09, 95% confidence interval 0.06 to 0.11, P=0.001), and adjusting for potential mediation through genetically proxied cognitive performance did not reduce the association between appendicular lean mass and risk of Alzheimer's disease. Similar results were found for the outcomes of Alzheimer's disease and cognitive performance when the risk factors of genetically proxied trunk lean mass and whole body lean mass were used, respectively, adjusted for genetically proxied fat mass. Conclusions: These findings suggest that lean mass might be a possible modifiable protective factor for Alzheimer's disease. The mechanisms underlying this finding, as well as the clinical and public health implications, warrant further investigation.
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