Substantial evidence supports the efficacy of cognitive bias modification (CBM) for attention and interpretation. However, CBM targeting memory bias (CBM-M) remains underexplored despite its clinical relevance. This study examines the effectiveness and neurobiological mechanisms of CBM-M.

Fifty-eight individuals with elevated anxious and depressive personality traits (>1 SD) were randomly assigned to either CBM-M or sham training (n = 29 per group) in a parallel, double-blind, randomized controlled trial. The intervention involved eight sessions over 1 month. CBM-M aimed to enhance positive autobiographical memory (AM) recall by focusing on positive and negative words, whereas sham training lacked this enhancement module. Anxiety and depressive traits and symptoms, explicit and implicit memory biases, and AM specificity were assessed. Additionally, intrinsic functional connectivity was measured via functional magnetic resonance imaging, and cortisol levels were assayed via saliva collected at 10 time points across 2 days before and after the intervention.

Both groups showed reduced anxiety and depressive traits from pre- to post-intervention. Compared with sham training, CBM-M specifically reduced stress vulnerability, negative explicit memory bias, and daytime cortisol levels, with a large effect size. Improvement in memory bias correlated with stress vulnerability and cortisol reductions. CBM-M also enhanced amygdala functional connectivity with the anteromedial orbitofrontal cortex in comparison with sham training from pre- to post-intervention.

CBM-M reduced stress vulnerability and elicited neural changes in amygdala–anteromedial orbitofrontal cortex interactions, which were involved in social reward and AM recall. Future research should identify the most responsive populations and elucidate underlying mechanisms.

Reward can influence cognitive control; however, dysfunctional interactions between reward and cognitive control in adolescents with major depressive disorder (MDD) remain unclear.

We recruited 35 adolescents with MDD and 29 healthy controls (HC) who completed the AX version of the Continuous Performance Test (AX-CPT) under reward and non-reward conditions, while undergoing functional Near-Infrared Spectroscopy (fNIRS).

Adolescents with MDD exhibited slower response times and higher error rates compared to healthy controls. Under reward conditions, they responded more quickly but made more errors. Hierarchical Drift Diffusion Modeling (HDDM) revealed that adolescents with MDD showed a reduced starting bias toward more rewarding responses and a broader decision threshold in reward contexts. Neuroimaging results indicated that the MDD group showed diminished activation differences in the left dorsolateral prefrontal cortex (DLPFC), left ventrolateral prefrontal cortex (VLPFC), and right VLPFC in response to cues requiring high versus low cognitive control. Additionally, they exhibited weaker functional connectivity between these regions during reward-related cognitive control. Correlation analyses further showed that greater anhedonia severity was associated with poorer behavioral performance and less flexible activation in the prefrontal cortex.

Cognitive control impairments in depressed adolescents may be related to dysfunction in the motivational system. Our findings provide behavioral, computational, and neural evidence for the Expected Value of Control (EVC) theory. Diminished reward sensitivity and inflexible cognitive control may jointly contribute to these deficits, highlighting the importance of considering motivational factors in the diagnosis and intervention of cognitive control impairments in adolescents with depression.

Bipolar Disorder (BD) is a disorder in which cognitive function is relatively preserved but social functioning is markedly impaired. Interestingly, studies on BD show that the patients have a strong desire for social rewards. Hypersensitivity to social rewards in BD has not yet been sufficiently examined through experimental methods, although recent studies have pointed out that their reward hypersensitivity is the cause of symptoms and dysfunction.

The purpose of this study was to investigate whether patients with BD are hypersensitive to social rewards using the social value capture task.

Groups of 25 BD and healthy control (HC) each completed the social value attention capture task. This task consists of a practice phase in which associative learning of social rewards with specific stimuli occurs, and a test phase in which the stimuli associated with rewards appear as distractors during the participants performing a selective attention task. We also recorded event-related potential (ERP) in the practice phase in order to investigate BDs’ cortical activity for social reward.

showed significantly decreased accuracy rate and increased reaction time in the high social reward-associated distractor trials of the test phase in the BD compared to the HC. As a result of analysis in ERP components, P3 amplitude for social reward was significantly greater in the BD than the HC.

BD patients exhibit behavioral and physiological hypersensitivity to social rewards that might contribute to social dysfunction.

No significant relationships.