171. The neurocircuitry of increased inflammation in depression: Preliminary results

Abstract

Evidence suggests a cause and effect relationship between inflammatory cytokines and behavioral symptoms relevant to a number of psychiatric illnesses. Previous neuroimaging studies have demonstrated that administration of inflammatory stimuli or cytokines changes activity of basal ganglia nuclei to mediate depressive symptoms, effects that may be mediated by decreased striatal dopamine. Whether the effects of inflammation extend beyond the basal ganglia to other brain regions to contribute to specific behavioral symptoms is unknown. This study examined whether increased inflammation in depression affects functional connectivity between the basal ganglia (striatum) and other brain regions to mediate depressive and neurocognitive symptoms. Wakeful resting-state fMRI pilot data were obtained from 17 currently depressed patients with low versus high inflammation (C-reactive protein ⩽ 3 versus >3 mg/L). Seed-to-whole brain correlations were computed and compared between groups using four predefined striatal seeds. Depressed patients with high inflammation exhibited attenuated functional connectivity between three striatal seeds and thirteen cortical or subcortical brain regions. Of these thirteen significant relationships, inflammation-related compromised connectivity between ventral striatum and both anterior cingulate cortex and amygdala correlated with symptoms of anhedonia and anxiety, whereas decreased connectivity between dorsal striatum and prefrontal cortex was associated with decreased psychomotor performance. Understanding inflammation-associated alterations in neurocircuitry that mediate specific depressive behaviors is important for identifying strategies to diagnose and treat behavioral symptoms in patients with increased inflammation.