ArticleJournal of medical genetics2020
Diverse types of genomic evidence converge on alcohol use disorder risk genes.
Article in Journal of medical genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Integrating TWAS, chemical-genomic networks, and experimental models: melatonin as a ferroptosis inhibitor in osteoarthritis therapy.Clinical rheumatology · 2026Article
- Modeling Brain Gene Expression in Alcohol Use Disorder with Genetic Animal Models.Current topics in behavioral neurosciences · 2025Review
- Review
- Genetic and environmental influence on alcohol intent and alcohol sips among U.S. children-Effects across sex, race, and ethnicity.PloS one · 2024Article
- Article
- Prioritization of risk genes in multiple sclerosis by a refined Bayesian framework followed by tissue-specificity and cell type feature assessment.BMC genomics · 2022Article
- Genome-Wide Correlation of DNA Methylation and Gene Expression in Postmortem Brain Tissues of Opioid Use Disorder Patients.The international journal of neuropsychopharmacology · 2021Article
- Association of CXCR6 with COVID-19 severity: delineating the host genetic factors in transcriptomic regulation.Human genetics · 2021Article
- Association ofbioRxiv : the preprint server for biology · 2021Article
- Predicting regulatory variants using a dense epigenomic mapped CNN model elucidated the molecular basis of trait-tissue associations.Nucleic acids research · 2021Article
- CSEA-DB: an omnibus for human complex trait and cell type associations.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAlcohol use disorder (AUD) is one of the most common forms of substance use disorders with a strong contribution of genetic (50%-60%) and environmental factors. Genome-wide association studies (GWAS) have identified a number of AUD-associated variants, including those in alcohol metabolism genes. These genetic variants may modulate gene expression, making individuals more susceptible to AUD. A long-term alcohol consumption can also change the transcriptome patterns of subjects via epigenetic modulations.
methodsTo explore the interactive effect of genetic and epigenetic factors on AUD, we conducted a secondary analysis by integrating GWAS, CNV, brain transcriptome and DNA methylation data to unravel novel AUD-associated genes/variants. We applied the mega-analysis of OR (MegaOR) method to prioritise AUD candidate genes (AUDgenes).
resultsWe identified a consensus set of 206 AUDgenes based on the multi-omics data. We demonstrated that these AUDgenes tend to interact with each other more frequent than chance expectation. Functional annotation analysis indicated that these AUDgenes were involved in substance dependence, synaptic transmission, glial cell proliferation and enriched in neuronal and liver cells. We obtained a multidimensional evidence that AUD is a polygenic disorder influenced by both genetic and epigenetic factors as well as the interaction of them.
conclusionWe characterised multidimensional evidence of genetic, epigenetic and transcriptomic data in AUD. We found that 206 AUD associated genes were highly expressed in liver, brain cerebellum, frontal cortex, hippocampus and pituitary. Our studies provides important insights into the molecular mechanism of AUD and potential target genes for AUD treatment.
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