ArticleIn vivo (Athens, Greece)
Association of Alcohol Use Disorder Risk With
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- FAAH and MAGL inhibition: Evolving approaches to treating substance use disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Review
- Review
- Sweet Taste Receptors' Genetic Variability in Advanced Potential Targets of Obesity.Nutrients · 2025Article
- Is There a Natural, Non-addictive, and Non-anti-reward, Safe, Gene-based Solution to Treat Reward Deficiency Syndrome? KB220 Variants vs GLP-1 Analogs.Journal of addiction psychiatry · 2024Article
- Review
- The association between theArhiv za higijenu rada i toksikologiju · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimAlcohol use disorder (AUD) is a chronic, multifactorial psychiatric condition with an enormous impact on public health and social cost. Genetic studies suggest a heritability, and genome-wide association studies (GWAS) have revealed genetic polymorphisms influencing AUD development. Our study aimed to investigate known variants located in ADH1B, DRD2, FAAH, SLC39A8, GCKR, and PDYN genes (rs1229984, rs7121986, rs324420, rs13107325, rs1260326, rs2281285 respectively) in an AUD Greek cohort in order to shed more light on the genetic predisposition to AUD. MATERIALS AND
methodsAlcohol-dependent individuals (n=251) meeting both the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) and the ICD-10 guidelines for alcohol abuse and dependence, and control individuals (n=280) were recruited. DNA was extracted from whole blood and PCR-restriction fragment length polymorphism (RFLP-PCR) or allele-specific PCR method was used for genotyping.
resultsIndividuals carrying the FAAH rs324420 A allele were significantly associated with increased risk of AUD (p<0.0001). SLC39A8 rs13107325 T allele and ADH1B rs1229984 T allele are overrepresented in control subjects (p<0.0001 and p<0.0001, respectively). The associations are maintained following an adjustment for age and sex and Bonferroni correction. GCKR rs13107325, DRD2 rs7121986, and PDYN rs2281285 polymorphisms did not show a significant association with AUD in the studied population after Bonferroni correction.
conclusionSusceptibility to AUD is related to variations in FAAH, ADH1B, and SLC39A8 genes. These polymorphisms could serve as potential biomarkers for AUD risk.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.