Altered brain functional connectivity linked to memory suppression in individuals with alcohol use disorder

Individuals are able to voluntarily suppress unwanted thoughts or memories, a phenomenon commonly referred to as memory suppression or suppression-induced forgetting. Although alcohol use disorder (AUD) has been associated with impairments in inhibitory control, episodic memory, and heightened salience of alcohol-related cues, the neural mechanisms underlying the suppression of alcohol-related memories remain poorly understood. The present study aimed to investigate behavioral and neurofunctional correlates of memory inhibition in abstinent individuals with AUD using an adapted Think/No-Think Alcohol paradigm combined with task-based functional connectivity analyses. Forty-one participants (26 abstinent individuals with AUD; 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, suggesting increased engagement of salience and reward systems during suppression demands, whereas controls preferentially recruited classic top-down memory control circuitry. 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 suggest 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.