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000258246 1001_ $$0P:(DE-2719)9001677$$aXia, Kailin$$b0$$eFirst author
000258246 245__ $$aLipids and amyotrophic lateral sclerosis: A two-sample Mendelian randomization study.
000258246 260__ $$aOxford [u.a.]$$bWiley-Blackwell$$c2023
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000258246 520__ $$aPrevious observational studies revealed a potential but partially controversial relation between lipid metabolism and the risk of amyotrophic lateral sclerosis (ALS), potentially prone to bias. Therefore, we aimed to study whether lipid metabolism involves genetically determined risk factors for ALS through Mendelian randomization (MR) analysis.Using genome-wide association study summary-level data for total cholesterol (TC) (n = 188,578), high-density lipoprotein cholesterol (HDL-C) (n = 403,943), low-density lipoprotein cholesterol (LDL-C) (n = 440,546), apolipoprotein A1 (ApoA1) (n = 391,193), apolipoprotein B (ApoB) (n = 439,214), and ALS (12,577 cases and 23,475 controls), we implemented a bidirectional MR study to evaluate a genetic relation between lipids and ALS risk. We performed a mediation analysis to assess whether LDL-C is a potential mediator on the pathway from traits of LDL-C-related polyunsaturated fatty acids (PUFAs) to ALS risk.We identified genetically predicted increased lipid levels to be associated with the risk of ALS, whereby elevated LDL-C had the most potent effect (OR 1.028, 95% CI 1.008-1.049, p = 0.006). The effect of increased levels of apolipoproteins on ALS was similar to their corresponding lipoproteins. ALS did not cause any changes in lipid levels. We found no relation between LDL-C-modifying lifestyles and ALS. The mediation analysis revealed that LDL-C could act as an active mediator for linoleic acid, with the mediation effect estimated to be 0.009.We provided high-level genetic evidence verifying the positive link between preclinically elevated lipid and ALS risk that had been described in previous genetic and observational studies. We also demonstrated the mediating role of LDL-C in the pathway from PUFAs to ALS.
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000258246 650_7 $$2Other$$aMendelian randomization
000258246 650_7 $$2Other$$aamyotrophic lateral sclerosis
000258246 650_7 $$2Other$$agenetics
000258246 650_7 $$2Other$$ainstrumental variables
000258246 650_7 $$2Other$$alipids
000258246 650_7 $$2NLM Chemicals$$aCholesterol, LDL
000258246 650_7 $$2NLM Chemicals$$aTriglycerides
000258246 650_2 $$2MeSH$$aHumans
000258246 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: epidemiology
000258246 650_2 $$2MeSH$$aAmyotrophic Lateral Sclerosis: genetics
000258246 650_2 $$2MeSH$$aCholesterol, LDL: genetics
000258246 650_2 $$2MeSH$$aMendelian Randomization Analysis
000258246 650_2 $$2MeSH$$aGenome-Wide Association Study
000258246 650_2 $$2MeSH$$aRisk Factors
000258246 650_2 $$2MeSH$$aPolymorphism, Single Nucleotide
000258246 650_2 $$2MeSH$$aTriglycerides: genetics
000258246 7001_ $$0P:(DE-2719)9001084$$aKlose, Veronika$$b1$$udzne
000258246 7001_ $$aHögel, Josef$$b2
000258246 7001_ $$aHuang, Tao$$b3
000258246 7001_ $$aZhang, Linjing$$b4
000258246 7001_ $$0P:(DE-2719)9001951$$aDorst, Johannes$$b5$$udzne
000258246 7001_ $$00000-0002-6679-0864$$aFan, Dongsheng$$b6
000258246 7001_ $$0P:(DE-2719)2812633$$aLudolph, Albert C$$b7$$eLast author$$udzne
000258246 773__ $$0PERI:(DE-600)2020241-6$$a10.1111/ene.15810$$gVol. 30, no. 7, p. 1899 - 1906$$n7$$p1899 - 1906$$tEuropean journal of neurology$$v30$$x1351-5101$$y2023
000258246 8564_ $$uhttps://onlinelibrary.wiley.com/doi/10.1111/ene.15810
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