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Poster C129

Multimodal Imaging of Reward Processing in Major Depressive Disorder

Poster Session C - Sunday, April 14, 2024, 5:00 – 7:00 pm EDT, Sheraton Hall ABC

Christopher J. H. Pirrung1 (, Garima Singh1, Jeremy Hogeveen1, Davin Quinn1, James F. Cavanagh1; 1University of New Mexico

Anhedonia represents a deficit in reward processing in Major Depressive Disorder (MDD) that can manifest as diminished pleasure from reward and diminished motivation to seek reward, though these phenotypes are often conflated. In this study we use multimodal imaging to examine the neural correlates of the emotional, pleasure-related deficits of depressive anhedonia. Magnetoencephalography (MEG) and functional magnetic resonance imaging (fMRI) data were collected for 52 participants with MDD and 38 healthy controls. A principal components analysis (PCA) of depression and anxiety questionnaires was used to create composite symptom scores for each participant. Participants completed a probabilistic selection task during the MEG scan and a pseudorandomized doors task during the fMRI. PCA derived three symptom components, correlating with emotional and consummatory anhedonia, anxiety and diminished mood, and apathy/motivational deficits. Spatiotemporal permutation clustering tests of MEG source estimates found significant clusters in ventromedial prefrontal cortex (vmPFC), anterior midcingulate cortex, and bilateral insulae for reward activation greater than punishment. Of these three regions, only vmPFC showed significantly greater activation for healthy controls, compared to MDD individuals. Correlation of this region with composite anhedonia scores showed a significant positive correlation between anhedonia and vmPFC activation within MDD. fMRI showed a significantly larger response to reward, relative to punishment, in vmPFC and nucleus accumbens (NAcc), though this response was diminished in the MDD group. Again, vmPFC activation was positively correlated with anhedonia scores. These findings show convergent validity of complex neural deficits associated with the emotional component of anhedonia.



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