Genome-wide meta-analysis of insomnia prioritizes genes associated with metabolic and psychiatric pathways

Insomnia is a heritable, highly prevalent sleep disorder for which no sufficient treatment currently exists. Previous genome-wide association studies with up to 1.3 million subjects identified over 200 associated loci. This extreme polygenicity suggested that many more loci remain to be discovered....

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Published inNature genetics Vol. 54; no. 8; pp. 1125 - 1132
Main Authors Watanabe, Kyoko, Jansen, Philip R., Savage, Jeanne E., Nandakumar, Priyanka, Wang, Xin, Hinds, David A., Gelernter, Joel, Levey, Daniel F., Polimanti, Renato, Stein, Murray B., Van Someren, Eus J. W., Smit, August B., Posthuma, Danielle
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.08.2022
Nature Publishing Group
Subjects
631/208/205/2138
692/699/375/1816
Agriculture
Animal Genetics and Genomics
Biobanks
Biomedical and Life Sciences
Biomedicine
Brain - metabolism
Cancer Research
Gene expression
Gene Function
Gene loci
Genes
Genetic Predisposition to Disease
Genome-wide association studies
Genome-Wide Association Study
Genomes
Human Genetics
Humans
Hypotheses
Insomnia
Meta-analysis
Multifactorial Inheritance
Polymorphism, Single Nucleotide - genetics
Risk
Sample size
Sleep disorders
Sleep Initiation and Maintenance Disorders - genetics
Sleep Initiation and Maintenance Disorders - metabolism
Strategy
United Kingdom > UK
Online AccessGet full text
ISSN1061-4036
1546-1718
1546-1718
DOI10.1038/s41588-022-01124-w

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Abstract Insomnia is a heritable, highly prevalent sleep disorder for which no sufficient treatment currently exists. Previous genome-wide association studies with up to 1.3 million subjects identified over 200 associated loci. This extreme polygenicity suggested that many more loci remain to be discovered. The current study almost doubled the sample size to 593,724 cases and 1,771,286 controls, thereby increasing statistical power, and identified 554 risk loci (including 364 novel loci). To capitalize on this large number of loci, we propose a novel strategy to prioritize genes using external biological resources and functional interactions between genes across risk loci. Of all 3,898 genes naively implicated from the risk loci, we prioritize 289 and find brain-tissue expression specificity and enrichment in specific gene sets of synaptic signaling functions and neuronal differentiation. We show that this novel gene prioritization strategy yields specific hypotheses on underlying mechanisms of insomnia that would have been missed by traditional approaches. Genome-wide association meta-analysis of insomnia in 593,724 cases and 1,771,286 controls identifies 554 risk loci and implicates specific biological pathways through gene prioritization.
AbstractList Insomnia is a heritable, highly prevalent sleep disorder for which no sufficient treatment currently exists. Previous genome-wide association studies with up to 1.3 million subjects identified over 200 associated loci. This extreme polygenicity suggested that many more loci remain to be discovered. The current study almost doubled the sample size to 593,724 cases and 1,771,286 controls, thereby increasing statistical power, and identified 554 risk loci (including 364 novel loci). To capitalize on this large number of loci, we propose a novel strategy to prioritize genes using external biological resources and functional interactions between genes across risk loci. Of all 3,898 genes naively implicated from the risk loci, we prioritize 289 and find brain-tissue expression specificity and enrichment in specific gene sets of synaptic signaling functions and neuronal differentiation. We show that this novel gene prioritization strategy yields specific hypotheses on underlying mechanisms of insomnia that would have been missed by traditional approaches. Genome-wide association meta-analysis of insomnia in 593,724 cases and 1,771,286 controls identifies 554 risk loci and implicates specific biological pathways through gene prioritization.
Insomnia is a heritable, highly prevalent sleep disorder for which no sufficient treatment currently exists. Previous genome-wide association studies with up to 1.3 million subjects identified over 200 associated loci. This extreme polygenicity suggested that many more loci remain to be discovered. The current study almost doubled the sample size to 593,724 cases and 1,771,286 controls, thereby increasing statistical power, and identified 554 risk loci (including 364 novel loci). To capitalize on this large number of loci, we propose a novel strategy to prioritize genes using external biological resources and functional interactions between genes across risk loci. Of all 3,898 genes naively implicated from the risk loci, we prioritize 289 and find brain-tissue expression specificity and enrichment in specific gene sets of synaptic signaling functions and neuronal differentiation. We show that this novel gene prioritization strategy yields specific hypotheses on underlying mechanisms of insomnia that would have been missed by traditional approaches.Insomnia is a heritable, highly prevalent sleep disorder for which no sufficient treatment currently exists. Previous genome-wide association studies with up to 1.3 million subjects identified over 200 associated loci. This extreme polygenicity suggested that many more loci remain to be discovered. The current study almost doubled the sample size to 593,724 cases and 1,771,286 controls, thereby increasing statistical power, and identified 554 risk loci (including 364 novel loci). To capitalize on this large number of loci, we propose a novel strategy to prioritize genes using external biological resources and functional interactions between genes across risk loci. Of all 3,898 genes naively implicated from the risk loci, we prioritize 289 and find brain-tissue expression specificity and enrichment in specific gene sets of synaptic signaling functions and neuronal differentiation. We show that this novel gene prioritization strategy yields specific hypotheses on underlying mechanisms of insomnia that would have been missed by traditional approaches.
Insomnia is a heritable, highly prevalent sleep disorder for which no sufficient treatment currently exists. Previous genome-wide association studies with up to 1.3 million subjects identified over 200 associated loci. This extreme polygenicity suggested that many more loci remain to be discovered. The current study almost doubled the sample size to 593,724 cases and 1,771,286 controls, thereby increasing statistical power, and identified 554 risk loci (including 364 novel loci). To capitalize on this large number of loci, we propose a novel strategy to prioritize genes using external biological resources and functional interactions between genes across risk loci. Of all 3,898 genes naively implicated from the risk loci, we prioritize 289 and find brain-tissue expression specificity and enrichment in specific gene sets of synaptic signaling functions and neuronal differentiation. We show that this novel gene prioritization strategy yields specific hypotheses on underlying mechanisms of insomnia that would have been missed by traditional approaches.
Author Nandakumar, Priyanka
Savage, Jeanne E.
Wang, Xin
Stein, Murray B.
Hinds, David A.
Posthuma, Danielle
Van Someren, Eus J. W.
Watanabe, Kyoko
Gelernter, Joel
Polimanti, Renato
Smit, August B.
Jansen, Philip R.
Levey, Daniel F.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/35835914$$D View this record in MEDLINE/PubMed
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Copyright The Author(s), under exclusive licence to Springer Nature America, Inc. 2022
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Cancer Research
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