Interleukin-6 and Depressive Mood Symptoms: Mediators of the Association Between Childhood Abuse and Cognitive Performance in Middle-Aged Adults

People exposed to abuse in childhood showed cognitive deficits in middle-age, due in part to their elevated levels of inflammation and depressed mood. Abstract Background Childhood abuse is a risk factor for the development of cognitive deficits in adulthood, a relation that is likely mediated by stress-sensitive psychological and physiological indicators. Purpose To evaluate whether the link between exposure to childhood abuse and cognitive function in middle adulthood is mediated by interleukin-6 (IL-6), metabolic risk, and depressive mood symptoms. Methods Participants were 770 adults aged 40–65 recruited from the community, who completed the following: (i) a questionnaire assessing exposure to abuse prior to age 18, (ii) a phone interview assessing current depressive mood symptoms, and (iii) a home visit that included blood sampling for evaluation of IL-6 and assessment of metabolic risk indices. A follow-up telephone assessment evaluating cognitive function was completed by 555 of the participants. Structural equation modeling was used to test study hypotheses. Results Childhood abuse predicted higher levels of IL-6, depressive mood symptoms, and metabolic risk scores (p < .05). The relation between childhood abuse and poorer cognitive performance was mediated by IL-6 (p = .046) and depressive mood symptoms (p = .023), but not metabolic risk. IL-6 and depressive mood symptoms significantly mediated the relation between childhood abuse and adult cognitive function. Conclusions Exposure to early abuse conveys enduring physiological and psychological effects, which may contribute to cognitive deficits that are evident by middle adulthood. Increased vulnerability for cognitive decline among adults with a history of early trauma and the mediating roles of IL-6 and depressive mood symptoms point to the potential value of interventions that address inflammation or depression, singly or together, to prevent cognitive decline in this at-risk population.