C-reactive protein and affective inhibition in bipolar disorder
Amy T Peters1, Caitlin E Millett2, Jessica Harder2
1Massachusetts General Hospital, Boston, MA, United States of America; Harvard Medical School, Boston, MA, United States of America.
Background:
Individuals with bipolar disorder (BD) experience cognitive and affective processing deficits that often persist beyond the remission of acute mood symptoms. One possible biological mechanism for these deficits involves the potential effects of chronic low-grade peripheral inflammation on brain function. Peripheral inflammation has been associated with reduced executive functioning and memory performance, as well as altered reward processing in BD, but whether it is also implicated in cognitive-affective processing remains unknown.
Method:
Peripheral inflammation was measured by serum C-reactive protein (CRP) in 119 adults with BD I or II, age 18-65. All participants completed the Affective Go/No-Go Task, a measure of cognitive-emotional processing. Correlations of CRP with discrimination of and response times to Negative, Positive, and Neutral words were performed before and after adjustment for severity of residual depressive symptoms and other demographic and clinical characteristics associated with inflammation.
Results:
Increased CRP was significantly associated with reduced negative target discriminability, which was also significantly reduced compared to positive and neutral target conditions. Additionally, greater CRP was associated with faster response times for both negative hits and commissions, as well as positive commissions.
Conclusions:
This study adds to existing research demonstrating associations between inflammation and cognition or reward sensitivity and motivation separately in BD, by raising the possibility that inflammation is also implicated in the integration of cognitive-affective processing. Assessment of these associations over time is warranted to determine involvement of inflammation and cognitive-emotional processing in course of illness and identify critical periods for possible modulation of inflammation.
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