A review of Mendelian randomization in amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis is a relatively common and rapidly progressive neurodegenerative disease that, in the majority of cases, is thought to be determined by a complex gene-environment interaction. Exponential growth in the number of performed genome-wide association studies combined with th...
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Published in | Brain (London, England : 1878) Vol. 145; no. 3; pp. 832 - 842 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Oxford University Press
29.04.2022
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Abstract | Amyotrophic lateral sclerosis is a relatively common and rapidly progressive neurodegenerative disease that, in the majority of cases, is thought to be determined by a complex gene-environment interaction. Exponential growth in the number of performed genome-wide association studies combined with the advent of Mendelian randomization is opening significant new opportunities to identify environmental exposures that increase or decrease the risk of amyotrophic lateral sclerosis. Each of these discoveries has the potential to shape new therapeutic interventions. However, to do so, rigorous methodological standards must be applied in the performance of Mendelian randomization. We have reviewed Mendelian randomization studies performed in amyotrophic lateral sclerosis to date. We identified 20 Mendelian randomization studies, including evaluation of physical exercise, adiposity, cognitive performance, immune function, blood lipids, sleep behaviours, educational attainment, alcohol consumption, smoking and type 2 diabetes mellitus. We have evaluated each study using gold standard methodology supported by the Mendelian randomization literature and the STROBE-Mendelian randomization checklist. Where discrepancies exist between Mendelian randomization studies, we suggest the underlying reasons. A number of studies conclude that there is a causal link between blood lipids and risk of amyotrophic lateral sclerosis; replication across different datasets and even different populations adds confidence. For other putative risk factors, such as smoking and immune function, Mendelian randomization studies have provided cause for doubt. We highlight the use of positive control analyses in choosing exposure single nucleotide polymorphisms (SNPs) to make up the Mendelian randomization instrument, use of SNP clumping to avoid false positive results due to SNPs in linkage and the importance of multiple testing correction. We discuss the implications of survival bias for study of late age of onset diseases such as amyotrophic lateral sclerosis and make recommendations to mitigate this potentially important confounder. For Mendelian randomization to be useful to the amyotrophic lateral sclerosis field, high methodological standards must be applied to ensure reproducibility. Mendelian randomization is already an impactful tool, but poor-quality studies will lead to incorrect interpretations by a field that includes non-statisticians, wasted resources and missed opportunities. |
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AbstractList | Amyotrophic lateral sclerosis is a relatively common and rapidly progressive neurodegenerative disease that, in the majority of cases, is thought to be determined by a complex gene–environment interaction. Exponential growth in the number of performed genome-wide association studies combined with the advent of Mendelian randomization is opening significant new opportunities to identify environmental exposures that increase or decrease the risk of amyotrophic lateral sclerosis. Each of these discoveries has the potential to shape new therapeutic interventions. However, to do so, rigorous methodological standards must be applied in the performance of Mendelian randomization. We have reviewed Mendelian randomization studies performed in amyotrophic lateral sclerosis to date. We identified 20 Mendelian randomization studies, including evaluation of physical exercise, adiposity, cognitive performance, immune function, blood lipids, sleep behaviours, educational attainment, alcohol consumption, smoking and type 2 diabetes mellitus. We have evaluated each study using gold standard methodology supported by the Mendelian randomization literature and the STROBE–Mendelian randomization checklist. Where discrepancies exist between Mendelian randomization studies, we suggest the underlying reasons. A number of studies conclude that there is a causal link between blood lipids and risk of amyotrophic lateral sclerosis; replication across different datasets and even different populations adds confidence. For other putative risk factors, such as smoking and immune function, Mendelian randomization studies have provided cause for doubt. We highlight the use of positive control analyses in choosing exposure single nucleotide polymorphisms (SNPs) to make up the Mendelian randomization instrument, use of SNP clumping to avoid false positive results due to SNPs in linkage and the importance of multiple testing correction. We discuss the implications of survival bias for study of late age of onset diseases such as amyotrophic lateral sclerosis and make recommendations to mitigate this potentially important confounder. For Mendelian randomization to be useful to the amyotrophic lateral sclerosis field, high methodological standards must be applied to ensure reproducibility. Mendelian randomization is already an impactful tool, but poor-quality studies will lead to incorrect interpretations by a field that includes non-statisticians, wasted resources and missed opportunities. Amyotrophic lateral sclerosis is a relatively common and rapidly progressive neurodegenerative disease that, in the majority of cases, is thought to be determined by a complex gene–environment interaction. Exponential growth in the number of performed genome-wide association studies combined with the advent of Mendelian randomization is opening significant new opportunities to identify environmental exposures that increase or decrease the risk of amyotrophic lateral sclerosis. Each of these discoveries has the potential to shape new therapeutic interventions. However, to do so, rigorous methodological standards must be applied in the performance of Mendelian randomization. We have reviewed Mendelian randomization studies performed in amyotrophic lateral sclerosis to date. We identified 20 Mendelian randomization studies, including evaluation of physical exercise, adiposity, cognitive performance, immune function, blood lipids, sleep behaviours, educational attainment, alcohol consumption, smoking and type 2 diabetes mellitus. We have evaluated each study using gold standard methodology supported by the Mendelian randomization literature and the STROBE–Mendelian randomization checklist. Where discrepancies exist between Mendelian randomization studies, we suggest the underlying reasons. A number of studies conclude that there is a causal link between blood lipids and risk of amyotrophic lateral sclerosis; replication across different datasets and even different populations adds confidence. For other putative risk factors, such as smoking and immune function, Mendelian randomization studies have provided cause for doubt. We highlight the use of positive control analyses in choosing exposure single nucleotide polymorphisms (SNPs) to make up the Mendelian randomization instrument, use of SNP clumping to avoid false positive results due to SNPs in linkage and the importance of multiple testing correction. We discuss the implications of survival bias for study of late age of onset diseases such as amyotrophic lateral sclerosis and make recommendations to mitigate this potentially important confounder. For Mendelian randomization to be useful to the amyotrophic lateral sclerosis field, high methodological standards must be applied to ensure reproducibility. Mendelian randomization is already an impactful tool, but poor-quality studies will lead to incorrect interpretations by a field that includes non-statisticians, wasted resources and missed opportunities. Amyotrophic lateral sclerosis is the result of a complex interaction between genes and environment, but environmental risk factors remain poorly understood. Julian et al . review the use of Mendelian randomization to try to identify these factors, summarising key findings and proposing methodological improvements for future studies. |
Author | Julian, Thomas H Whittaker, Katherine J Moll, Tobias Harvey, Calum Islam, Mahjabin Zhang, Sai Boddy, Sarah Snyder, Michael P Kurz, Julian Cooper-Knock, Johnathan Shaw, Pamela J McDermott, Christopher |
AuthorAffiliation | 2 Department of Genetics, Stanford University School of Medicine , Stanford, CA, USA 3 Center for Genomics and Personalized Medicine, Stanford University School of Medicine , Stanford, CA, USA 1 Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield , Sheffield, UK |
AuthorAffiliation_xml | – name: 3 Center for Genomics and Personalized Medicine, Stanford University School of Medicine , Stanford, CA, USA – name: 2 Department of Genetics, Stanford University School of Medicine , Stanford, CA, USA – name: 1 Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield , Sheffield, UK |
Author_xml | – sequence: 1 givenname: Thomas H surname: Julian fullname: Julian, Thomas H organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 2 givenname: Sarah surname: Boddy fullname: Boddy, Sarah organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 3 givenname: Mahjabin surname: Islam fullname: Islam, Mahjabin organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 4 givenname: Julian surname: Kurz fullname: Kurz, Julian organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 5 givenname: Katherine J surname: Whittaker fullname: Whittaker, Katherine J organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 6 givenname: Tobias surname: Moll fullname: Moll, Tobias organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 7 givenname: Calum surname: Harvey fullname: Harvey, Calum organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 8 givenname: Sai surname: Zhang fullname: Zhang, Sai organization: Center for Genomics and Personalized Medicine, Stanford University School of Medicine, Stanford, CA, USA – sequence: 9 givenname: Michael P surname: Snyder fullname: Snyder, Michael P organization: Center for Genomics and Personalized Medicine, Stanford University School of Medicine, Stanford, CA, USA – sequence: 10 givenname: Christopher surname: McDermott fullname: McDermott, Christopher organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 11 givenname: Johnathan orcidid: 0000-0002-0873-8689 surname: Cooper-Knock fullname: Cooper-Knock, Johnathan organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK – sequence: 12 givenname: Pamela J surname: Shaw fullname: Shaw, Pamela J organization: Department of Neuroscience, Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34791088$$D View this record in MEDLINE/PubMed |
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Copyright | The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For permissions, please email: journals.permissions@oup.com. The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For permissions, please email: journals.permissions@oup.com 2021 |
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Keywords | epidemiology amyotrophic lateral sclerosis Mendelian randomization |
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License | The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For permissions, please email: journals.permissions@oup.com. https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) |
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Notes | Johnathan Cooper-Knock, Pamela J. Shaw contributed equally to this work. |
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Snippet | Amyotrophic lateral sclerosis is a relatively common and rapidly progressive neurodegenerative disease that, in the majority of cases, is thought to be... |
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SubjectTerms | Amyotrophic Lateral Sclerosis - genetics Diabetes Mellitus, Type 2 Genome-Wide Association Study - methods Humans Lipids Mendelian Randomization Analysis - methods Neurodegenerative Diseases Reproducibility of Results Review |
Title | A review of Mendelian randomization in amyotrophic lateral sclerosis |
URI | https://www.ncbi.nlm.nih.gov/pubmed/34791088 https://pubmed.ncbi.nlm.nih.gov/PMC9050546 |
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