Symposia
Health Psychology / Behavioral Medicine - Adult
Amy Peters, Ph.D.
Massachusetts General Hospital and Harvard Medical School
Boston, Massachusetts
Background: Individuals with mood disorders (bipolar disorder, major depression, dysthymia) experience cognitive and affective processing deficits that have been identified as risk markers for onset and recurrence of mood symptoms. Biological mechanisms subserving these behavioral deficits may relate to the effects of chronic low-grade inflammation, hypothalamic-pituitary-adrenal (HPA)-axis dysfunction, and their interactions, on brain function. However, few studies have directly linked measures of immune and endocrine function with performance-based measures of cognitive-affective processing or their neural substrates in individuals with mood disorders.
Methods: Data from three studies will be presented. First, in a sample of 119 adults with bipolar disorder, associations between peripheral inflammation (as measured by C-reactive protein [CRP]) and affective inhibition are determined. Second, in a sample of 39 adolescents (age 12-17) with depressive spectrum disorders and 29 healthy controls (HC), associations between peripheral inflammation (as measured by interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1beta), depressive symptom dimensions, and emotion perception are determined. Third, in a sample of 41 adults with major depression or bipolar disorder and 23 HC, associations of cortisol with neural engagement during emotion perception are determined.
Results: In bipolar disorder, increased CRP was associated with reduced negative, but not positive or neutral, target discriminability. In depressed adolescents, higher inflammatory proteins were associated with depressed mood and somatic symptoms of depression, but not anhedonia, and associated with reduced accuracy for identifying angry, fearful, and neutral facial expressions. In adults with depression or bipolar disorder, increased cortisol was associated with hypoactivation of fronto-parietal and striatal regions during the processing of fearful and angry faces.
Conclusions: Immunoendocrine biomarkers may represent possible targets for modulating cognitive-affective processing deficits in transdiagnostic mood disorders. Hypotheses that might explain shared sequelae of immune and HPA-axis dysregulation (e.g., glucocorticoid resistance), will be discussed.