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Related Experiment Video

Updated: Aug 4, 2025

Lipidomics and Transcriptomics in Neurological Diseases
09:58

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

3.5K

Lipids and amyotrophic lateral sclerosis: A two-sample Mendelian randomization study.

Kailin Xia1,2,3,4,5, Veronika Klose3, Josef Högel2

  • 1Department of Neurology, Peking University Third Hospital, Beijing, China.

European Journal of Neurology
|March 31, 2023
PubMed
Summary

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Genetically predicted higher lipid levels, particularly low-density lipoprotein cholesterol (LDL-C), increase amyotrophic lateral sclerosis (ALS) risk. LDL-C also mediates the link between polyunsaturated fatty acids and ALS.

Area of Science:

  • Genetics
  • Neuroscience
  • Metabolic Disorders

Background:

  • Observational studies suggest a link between lipid metabolism and amyotrophic lateral sclerosis (ALS) risk, but findings are controversial and potentially biased.
  • Mendelian randomization (MR) offers a robust method to investigate genetically determined risk factors, mitigating bias.

Purpose of the Study:

  • To investigate the genetically determined relationship between lipid metabolism and ALS risk using a bidirectional MR analysis.
  • To explore the mediating role of low-density lipoprotein cholesterol (LDL-C) in the pathway from polyunsaturated fatty acids (PUFAs) to ALS risk.

Main Methods:

  • Utilized genome-wide association study (GWAS) summary-level data for various lipids (total cholesterol, HDL-C, LDL-C, ApoA1, ApoB) and ALS.
  • Performed bidirectional MR analysis to assess genetic associations between lipids and ALS.
Keywords:
Mendelian randomizationamyotrophic lateral sclerosisgeneticsinstrumental variableslipids

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  • Conducted mediation analysis to evaluate LDL-C's role in the PUFA-ALS pathway.

    • Main Results:

    • Genetically predicted elevated lipid levels, especially LDL-C, are associated with increased ALS risk (OR 1.028, p=0.006).
    • Apolipoprotein levels showed similar associations with ALS risk as their corresponding lipoproteins.
    • No evidence was found for ALS influencing lipid levels or a link between LDL-C-modifying lifestyles and ALS.
    • LDL-C was identified as a mediator in the pathway from linoleic acid (a PUFA) to ALS.

    Conclusions:

    • This study provides strong genetic evidence supporting a positive association between elevated lipid levels and ALS risk.
    • Demonstrated a significant mediating role of LDL-C in the relationship between PUFAs and ALS.
    • Findings reinforce the importance of lipid metabolism in ALS pathogenesis.