Memory suppression in individuals with alcohol use disorder: Evidence for altered brain functional coupling

Alcohol use disorder (AUD) has been associated with impairments in inhibitory control, episodic memory, and heightened salience of alcohol-related cues, yet the neural mechanisms underlying voluntary suppression of alcohol memories remain poorly understood. The present study aimed to investigate behavioral and neurofunctional correlates of memory inhibition in abstinent AUD individuals using an adapted Think/No-Think Alcohol paradigm combined with task-based functional connectivity analyses. Forty-one participants (26 abstinent individuals with alcohol use disorder; 15 controls) completed encoding, Think/No-Think (during functional magnetic resonance imaging) and retrieval phases.Individuals with AUD showed reduced encoding and overall recall performance, while suppression-induced forgetting was comparable between groups. At the neural level, during attempts to suppress alcohol-related memories, AUD participants exhibited increased connectivity between reward-related subcortical regions and prefrontal, perceptual, and interoceptive cortices, whereas controls preferentially recruited classic top-down memory control circuitry, suggesting more selective top-down modulation of memory and perceptual representations during suppression. In contrast, during suppression of non-alcohol memories, AUD participants showed stronger fronto-posterior coupling than controls, indicating that suppression-related control mechanisms remained recruitable but were engaged in a stimulus-dependent manner, alongside evidence of generalized salience-related modulation of perceptual processing. Additionally, during the recall of alcohol-related stimuli, the AUD group showed stronger coupling within salience and valuation circuitry, while controls engaged goal-directed and perceptual imagery systems. Within the AUD group, craving, particularly compulsivity, was associated with greater recall of suppressed alcohol-related memories and with altered functional connectivity in regulatory and salience networks. Together, the findings indicate that memory control in AUD is characterized not by overt behavioral suppression failure but by salience-biased redistribution of neural recruitment. These results highlight neural-level vulnerability in memory regulation that may contribute to craving persistence and relapse risk, providing potential targets for neurocognitive interventions aimed at strengthening memory control in individuals with AUD.