Genetics and Epigenetics of Substance Use Disorders

Topic Information

Dear Colleagues,

Investigations of the genetic and epigenetic factors in substance use disorders have significantly advanced our understanding of these complex conditions. Genetic research has identified numerous markers associated with addiction, emphasizing the role of the dopamine system in reward pathways. Epigenetic studies have further elucidated how environmental factors, such as stress and drug exposure, can modify gene expression. These modifications can influence the risk of developing SUDs, explaining the variations in susceptibility among individuals with similar genetic backgrounds. The relevance of this research lies in its potential to inform personalized treatment and prevention strategies, tailored to an individual’s unique genetic and epigenetic profile. Future research directions include exploring the intricate interactions between genetic predispositions and environmental influences, as well as developing targeted interventions that consider both genetic and epigenetic factors. This comprehensive approach promises to enhance the effectiveness of treatments and improve outcomes for individuals affected by SUDs.

The Topic Issue encourages researchers to submit original manuscripts and reviews that examine the genetic and epigenetic mechanisms in substance use disorders.

Dr. Aleksandra Suchanecka
Prof. Dr. Anna Maria Grzywacz
Dr. Kszysztof Chmielowiec
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Brain Sciences brainsci	2.8	5.6	2011	17.6 Days	CHF 2200	Submit
Current Issues in Molecular Biology cimb	3.0	3.7	1999	16.3 Days	CHF 2200	Submit
Epigenomes epigenomes	3.5	4.4	2017	25.5 Days	CHF 1600	Submit
Genes genes	2.8	5.5	2010	14.6 Days	CHF 2600	Submit
International Journal of Molecular Sciences ijms	4.9	9.0	2000	17.8 Days	CHF 2900	Submit
DNA dna	-	-	2021	36 Days	CHF 1000	Submit

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Published Papers (2 papers)

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Open AccessArticle

Validation of GDAP1 and HECW2 as Epigenetic Markers of Alcohol Use Disorder in Blood and Brain

by Ariane Wiegand, Marion Friske, Susanne Edelmann, Annika Bender, Lea Fischer, Peter Zill, Gabriele Koller, Georgy Bakalkin, Wolfgang H. Sommer, Anita C. Hansson and Vanessa Nieratschker

Int. J. Mol. Sci. 2025, 26(22), 10840; https://doi.org/10.3390/ijms262210840 - 8 Nov 2025

Cited by 1 | Viewed by 572

Abstract

Alcohol use disorder (AUD) is associated with widespread epigenetic alterations, including changes in DNA methylation (DNAm). This multi-cohort study validated and extended previous findings on DNAm of HECW2 and GDAP1 in AUD, assessed sex differences, and explored DNAm in blood and brain tissue [...] Read more.

Alcohol use disorder (AUD) is associated with widespread epigenetic alterations, including changes in DNA methylation (DNAm). This multi-cohort study validated and extended previous findings on DNAm of HECW2 and GDAP1 in AUD, assessed sex differences, and explored DNAm in blood and brain tissue in humans and rats. DNAm was measured via pyrosequencing in human blood (N_Ctrl = 341, N_AUD = 258), postmortem frontal cortex (Brodmann area 9; discovery cohort: N_Ctrl = 10, N_AUD = 13, replication cohort: N_Ctrl = 64, N_AUD = 55) and rat blood and medial prefrontal cortex (N_Ctrl = 16, N_AUD = 15). Gene expression was assessed in human postmortem brain by quantitative real-time PCR. AUD-associated DNAm differences in HECW2 and GDAP1 were replicated in human blood. While decreased GDAP1 DNAm was only observed in men, HECW2 hypomethylation was present in both sexes. In brain tissue, initial DNAm increases in AUD and HECW2 gene expression decreases were not validated in the replication cohort. In rats, HECW2 hypomethylation appeared in the prelimbic cortex but not in blood. Our findings support the involvement of HECW2 and GDAP1 DNAm in AUD, revealing sex-specific and tissue-dependent epigenetic patterns. The opposing DNAm directionality in blood and brain underscores the complexity of alcohol-related epigenetic modifications and suggests the need for multi-tissue, cross-species, and longitudinal studies to clarify causal mechanisms. Full article

(This article belongs to the Topic Genetics and Epigenetics of Substance Use Disorders)

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Open AccessArticle

Alcohol Preference Impacts Multi-Organ Transcriptome in MetALD

by Saumya Sikhwal, Tyler C. Gripshover, Rui S. Treves and Josiah E. Hardesty

Genes 2025, 16(10), 1121; https://doi.org/10.3390/genes16101121 - 23 Sep 2025

Cited by 1 | Viewed by 824

Abstract

Background/Objectives: Alcohol use disorder (AUD) is a major public health issue with rising global occurrence and metabolic consequences. Modeling the addictive behaviors associated with AUD remains inadequate and elusive. Even more so, models that are representative of AUD in concert with excessive caloric [...] Read more.

Background/Objectives: Alcohol use disorder (AUD) is a major public health issue with rising global occurrence and metabolic consequences. Modeling the addictive behaviors associated with AUD remains inadequate and elusive. Even more so, models that are representative of AUD in concert with excessive caloric intake are limited. Some consequences of chronic alcohol use overlap with the metabolic phenotype of hypercaloric diets. Recently characterized metabolic dysfunction-associated steatotic liver disease with increased alcohol intake (MetALD) helps to differentiate these conditions. This study aims to investigate metabolic phenotypes and gene expression alterations in MetALD mice that are grouped by alcohol preference based on blood phosphatidylethanol levels and alcohol consumption. Methods: Mice were fed high-fat and chow diets, with water and 10% EtOH, for 13 weeks. mRNA sequencing was performed across multiple tissues including brain, liver, skeletal muscle, ileum, and white adipose tissue, and gut microbiome diversity was evaluated via 16S sequencing. Results: Key findings included reduced glucagon in alcohol-preferring mice with no significant differences in dyslipidemia and hepatic steatosis. Additionally, we observed reduced gut microbiome diversity and Wnt signaling with elevated acute-phase response genes in ileum tissue. Reduced Wnt and Hippo signaling in the brain and liver, respectively, was also revealed. Other gene ontologies discovered included increased neural inflammation and adipose mitochondrial translation. Nek3, Ntf3, Cux1, and Irf6 expression changes were shared across at least three tissues and may be potential biomarkers of alcohol addiction. Conclusions: This novel model assists future intervention research in the characterization of MetALD and identifies potential biomarkers of alcohol preference. Full article

(This article belongs to the Topic Genetics and Epigenetics of Substance Use Disorders)

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