ArticleAlcohol, clinical & experimental research2026
The OPRM1 A118G G Allele Is Associated With Poorer Auditory-Verbal Learning and Memory, Executive Functions, and Working Memory in Veterans Undergoing Residential Treatment for Alcohol Use Disorder.
Article in Alcohol, clinical & experimental research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundThe neurocognitive dysfunction observed in Alcohol Use Disorder (AUD) is related to a complex interplay between genetic, neurobiological, and environmental factors. The μ-opioid receptor (MOR), encoded by the OPRM1 gene, modulates reward processing, stress responsivity, and excitatory-inhibitory activity within prefrontal-limbic and hippocampal circuits implicated in neurocognition. The common A118G (Asn40Asp, rs1799971) polymorphism alters MOR expression and signaling, but its contribution to domain-specific cognitive functioning in AUD, particularly among Veterans, has received limited investigation.
methodsVeterans (n = 127) in residential treatment for AUD completed a neurocognitive battery assessing the following domains of functioning: auditory-verbal and visuospatial learning and memory, executive function, and working memory. Participants were genotyped for OPRM1 A118G, and A homozygotes and G-allele carriers (AG/GG) were compared on the above measures, using bootstrapped generalized linear models, adjusted for age, education, biological sex, race, pre-study alcohol consumption, and brain-derived neurotrophic factor (BDNF) (rs6265) and catechol-O-methyltransferase (COMT) (rs4680) genotypes, which have been previously shown to be associated with neurocognition.
resultsG-allele carriers demonstrated significantly worse performance than A homozygotes on measures of auditory-verbal learning and memory, cognitive flexibility/set shifting, auditory working memory, and on a composite average of all measures. BDNF or COMT genotypes were not associated with any measure, and there were no significant interactions among OPRM1, BDNF, and COMT genotypes.
conclusionsFindings suggest that altered MOR signaling in G-allele carriers may be associated with differences in prefrontal network efficiency, potentially justifying future studies investigating the relationship between OPRM1 and glutamatergic plasticity. The results highlight a potential genetically influenced contributor to the neurocognitive heterogeneity in AUD and underscore the possible value of integrating MOR-related biological markers into neurocognitive assessment of individuals with AUD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.