Emerging Role of Epigenetic Mechanisms in Alcohol Addiction

Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression s...

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Published inAlcoholism, clinical and experimental research Vol. 41; no. 4; pp. 666 - 680
Main Authors Berkel, Tiffani D.M., Pandey, Subhash C.
Format Journal Article
LanguageEnglish
Published England 01.04.2017
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Abstract Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD. The epigenetic influence on synaptic plasticity appears to be instrumental in the development of alcoholism via histone deacetylase (HDAC)‐induced chromatin remodeling. Aberrant DNA methylation mechanisms are also important in regulating expression of various genes and associated biological pathways during alcoholism. Stratification of subjects by alcohol use disorder (AUD) phases is useful as epigenetic mechanisms uniquely regulate acute exposure/binge‐drinking, post‐dependence, and withdrawal effects. HDAC and DNA methyltransferase (DNMT) inhibitors consistently attenuate AUD phenotypes, and histone methyltransferase (HMT) inhibitors warrant exploration.
AbstractList Alcohol use disorder ( AUD ) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD , and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD . Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD . More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD .
Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD.
Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and post-exposure withdrawal on epigenetically-induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD.
Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD. The epigenetic influence on synaptic plasticity appears to be instrumental in the development of alcoholism via histone deacetylase (HDAC)‐induced chromatin remodeling. Aberrant DNA methylation mechanisms are also important in regulating expression of various genes and associated biological pathways during alcoholism. Stratification of subjects by alcohol use disorder (AUD) phases is useful as epigenetic mechanisms uniquely regulate acute exposure/binge‐drinking, post‐dependence, and withdrawal effects. HDAC and DNA methyltransferase (DNMT) inhibitors consistently attenuate AUD phenotypes, and histone methyltransferase (HMT) inhibitors warrant exploration.
Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD.Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD.
Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental factors are known to contribute to the development of AUD, and recent studies on alcohol exposure and subsequent changes in gene expression suggest the importance of epigenetic mechanisms. In particular, histone modifications and DNA methylation have emerged as important regulators of gene expression and associated phenotypes of AUD. Given the therapeutic potential of epigenetic targets, this review aims to summarize the role of epigenetic regulation in our current understanding of AUD by evaluating known epigenetic signatures of brain regions critical to addictive behaviors in both animal and human studies throughout various stages of AUD. More specifically, the effects of acute and chronic alcohol exposure, tolerance, and postexposure withdrawal on epigenetically induced changes to gene expression and synaptic plasticity within key brain regions and the associated behavioral phenotypes have been discussed. Understanding the contribution of epigenetic regulation to crucial signaling pathways may prove vital for future development of novel biomarkers and treatment agents in ameliorating or preventing AUD. The epigenetic influence on synaptic plasticity appears to be instrumental in the development of alcoholism via histone deacetylase (HDAC)-induced chromatin remodeling. Aberrant DNA methylation mechanisms are also important in regulating expression of various genes and associated biological pathways during alcoholism. Stratification of subjects by alcohol use disorder (AUD) phases is useful as epigenetic mechanisms uniquely regulate acute exposure/binge-drinking, post-dependence, and withdrawal effects. HDAC and DNA methyltransferase (DNMT) inhibitors consistently attenuate AUD phenotypes, and histone methyltransferase (HMT) inhibitors warrant exploration.
Author Pandey, Subhash C.
Berkel, Tiffani D.M.
AuthorAffiliation 3 Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, 60612 USA
1 Center for Alcohol Research in Epigenetics, Department of Psychiatry
2 Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago
AuthorAffiliation_xml – name: 2 Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago
– name: 3 Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, 60612 USA
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– sequence: 2
  givenname: Subhash C.
  surname: Pandey
  fullname: Pandey, Subhash C.
  email: scpandey@uic.edu
  organization: University of Illinois at Chicago
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Fri Jul 11 06:28:51 EDT 2025
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Thu Apr 24 23:06:20 EDT 2025
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Issue 4
Keywords DNA Methylation
Histone Methylation
Amygdala
Alcoholism
Epigenetics
Anxiety
Histone Acetylation
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
Copyright © 2017 by the Research Society on Alcoholism.
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Snippet Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental...
Alcohol use disorder ( AUD ) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and...
Alcohol use disorder (AUD) is a complex brain disorder with an array of persistent behavioral and neurochemical manifestations. Both genetic and environmental...
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SourceType Open Access Repository
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StartPage 666
SubjectTerms Alcoholism
Alcoholism - diagnosis
Alcoholism - genetics
Alcoholism - metabolism
Amygdala
Animals
Anxiety
Cyclic AMP Response Element-Binding Protein - genetics
Cyclic AMP Response Element-Binding Protein - metabolism
DNA Methylation
DNA Methylation - physiology
Epigenesis, Genetic - physiology
Epigenetics
Histone Acetylation
Histone Acetyltransferases - genetics
Histone Acetyltransferases - metabolism
Histone Methylation
Humans
Title Emerging Role of Epigenetic Mechanisms in Alcohol Addiction
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facer.13338
https://www.ncbi.nlm.nih.gov/pubmed/28111764
https://www.proquest.com/docview/1861590808
https://www.proquest.com/docview/1891871402
https://pubmed.ncbi.nlm.nih.gov/PMC5378655
Volume 41
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