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@ARTICLE{Xia:258246,
      author       = {Xia, Kailin and Klose, Veronika and Högel, Josef and
                      Huang, Tao and Zhang, Linjing and Dorst, Johannes and Fan,
                      Dongsheng and Ludolph, Albert C},
      title        = {{L}ipids and amyotrophic lateral sclerosis: {A} two-sample
                      {M}endelian randomization study.},
      journal      = {European journal of neurology},
      volume       = {30},
      number       = {7},
      issn         = {1351-5101},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2023-00592},
      pages        = {1899 - 1906},
      year         = {2023},
      abstract     = {Previous 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.},
      keywords     = {Humans / Amyotrophic Lateral Sclerosis: epidemiology /
                      Amyotrophic Lateral Sclerosis: genetics / Cholesterol, LDL:
                      genetics / Mendelian Randomization Analysis / Genome-Wide
                      Association Study / Risk Factors / Polymorphism, Single
                      Nucleotide / Triglycerides: genetics / Mendelian
                      randomization (Other) / amyotrophic lateral sclerosis
                      (Other) / genetics (Other) / instrumental variables (Other)
                      / lipids (Other) / Cholesterol, LDL (NLM Chemicals) /
                      Triglycerides (NLM Chemicals)},
      cin          = {Clinical Study Center Ulm / AG Zhan},
      ddc          = {610},
      cid          = {I:(DE-2719)5000077 / I:(DE-2719)1910005},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 354 -
                      Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36999624},
      doi          = {10.1111/ene.15810},
      url          = {https://pub.dzne.de/record/258246},
}