ArticleScientific reports2020
Mendelian randomization implies no direct causal association between leukocyte telomere length and amyotrophic lateral sclerosis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Causal association between telomere length and female reproductive endocrine diseases: a univariable and multivariable Mendelian randomization analysis.Journal of ovarian research · 2024Article
- Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024Review
- Protective Effects of Lovastatin in a Population-Based ALS Study and Mouse Model.Annals of neurology · 2023Article
- Genetically predicted telomere length and its relationship with neurodegenerative diseases and life expectancy.Computational and structural biotechnology journal · 2022Article
- Leukocyte telomere length and amyotrophic lateral sclerosis: a Mendelian randomization study.Orphanet journal of rare diseases · 2021Article
Corrections and comments
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Authors and funding
6 authors at 20 institutions in 15 countries.
Funding
Abstract
We employed Mendelian randomization (MR) to evaluate the causal relationship between leukocyte telomere length (LTL) and amyotrophic lateral sclerosis (ALS) with summary statistics from genome-wide association studies (n = ~ 38,000 for LTL and ~ 81,000 for ALS in the European population; n = ~ 23,000 for LTL and ~ 4,100 for ALS in the Asian population). We further evaluated mediation roles of lipids in the pathway from LTL to ALS. The odds ratio per standard deviation decrease of LTL on ALS was 1.10 (95% CI 0.93-1.31, p = 0.274) in the European population and 0.75 (95% CI 0.53-1.07, p = 0.116) in the Asian population. This null association was also detected between LTL and frontotemporal dementia in the European population. However, we found that an indirect effect of LTL on ALS might be mediated by low density lipoprotein (LDL) or total cholesterol (TC) in the European population. These results were robust against extensive sensitivity analyses. Overall, our MR study did not support the direct causal association between LTL and the ALS risk in neither population, but provided suggestive evidence for the mediation role of LDL or TC on the influence of LTL and ALS in the European population.
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Registered trials
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