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Updated: Sep 16, 2025

Disruption of Frontal Lobe Neural Synchrony During Cognitive Control by Alcohol Intoxication
Published on: February 6, 2019
Brain structural correlates of prior alcohol use disorder and their relation to cognitive impairment in individuals
Kamilla W Miskowiak1, Sofie M Bjerregaard2, Anders Fink-Jensen3
1Neurocognition and Emotion Across Disorders of the Brain Centre (NEAD), Mental Health Services, Capital Region of Denmark, Department of Psychology, University of Copenhagen, Copenhagen, Denmark; Copenhagen Affective Disorder Research Centre (CADIC), Mental Health Center Copenhagen, Rigshospitalet, Denmark.
Background:
Alcohol use disorders (AUD) often co-occur with mood disorders (MD), negatively impacting the clinical course of both disorders and exacerbating cognitive impairments. Neuroimaging studies have demonstrated lower gray matter volume (GMV) and hippocampal volume in MD and AUD, and additionally in the orbitofrontal cortex (OFC), nucleus accumbens (NAc), and white matter (WM) volume in AUD. However, whether the pronounced structural alterations in MD persist after remission from AUD, and their relation to cognitive impairments, remains unclear.
Method:
Individuals with MD with (MD + AUD; n = 42) or without (MD: n = 244) prior comorbid AUD, underwent structural magnetic resonance imaging and neuropsychological testing. We investigated differences in GMV and hippocampal volume between MD + AUD and MD groups, and their associations with cognitive function. Exploratory analyses also examined differences in volume of WM, NAc, and OFC between MD + AUD and MD groups.
Results:
The MD + AUD group had significantly lower GMV (p = 0.02) and hippocampal volume (p = 0.01) than MD group. Lower GMV was associated with poorer global cognition (p = 0.001), while smaller hippocampal volume scaled with lower verbal learning and memory function (p = 0.03). Lower volume was additionally observed in MD + AUD group in the OFC (p = 0.04) and NAc (p = 0.003), but not in WM.
Conclusion:
Individuals with MD and prior AUD exhibit lower brain volume in regions that subserve higher cognitive function and vulnerable to alcohol-induced neurotoxicity. Our data suggests persistent neurobiological alterations despite remission from AUD, and support the use of integrated treatment approaches that enhance neuroplasticity and cognition.
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