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Prog Neuropsychopharmacol Biol Psychiatry. 2020 Mar 8;97:109771. doi: 10.1016/j.pnpbp.2019.109771. Epub 2019 Oct 24.

Causal effects of serum metabolites on amyotrophic lateral sclerosis: A Mendelian randomization study.

Author information

1
Clinical Research Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
2
Department of Rheumatism and Immunology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
3
Department of Hematopathology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
4
Department of Hematopathology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Electronic address: Swallow3956@sina.com.

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that is affected by both genetic and environmental factors. Nowadays, OMIC technologies, such as genomics and metabolomics, are providing a systematic readout of genetic structures and physiological states for understanding human diseases. However, the comprehensive analysis of cross-omics is often lacking. Here, we conducted a Mendelian randomization analysis to provide a comprehensive analysis of metabolomics and genomics to estimate the causal relationships between non-targeted human serum metabolites and the development of ALS. Using genetic variants as predictors, our study detected 18 metabolites that might have causal effects on the development of ALS, including a group of gamma-glutamyl amino acids. Our findings suggested that glutathione metabolism dysfunction might be involved in the pathogenesis of ALS. Furthermore, our study provides a novel method to understand the pathogenesis of human diseases and develop therapeutic strategies for diseases by combining metabolomics with genomics.

KEYWORDS:

Amyotrophic lateral sclerosis; GSH metabolism dysfunction; Mendelian randomization; Serum metabolite

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