Inflammation following childhood maltreatment is associated with executive functioning decline in older adults
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Abstract
Background: Childhood maltreatment has been linked to cognitive decline in adulthood, specifically within the domains of episodic memory and executive functioning; however, the intermediate pathways underlying this relationship are not well understood. Prior work suggests that systemic inflammation may be one route through which childhood maltreatment leads to later cognitive decline. The current study tested this hypothesis by investigating inflammation as an intermediate pathway by which childhood maltreatment affects episodic memory and executive functioning in adulthood.
Methods: We selected 589 participants (Mean age = 60.8 years) from the Midlife in the United States (MIDUS) Study based on available data for measures of childhood maltreatment (Childhood Trauma Questionnaire (CTQ)), pro-inflammatory biomarkers [C-reactive protein (CRP), interleukin-6 (IL-6), E-selectin, fibrinogen, intracellular adhesion molecule-1 (ICAM-1)], and episodic memory and executive functioning composite scores (Brief Test of Adult Cognition via Telephone (BTACT)). All analyses were conducted using R statistical software; specifically, Spearman’s rank correlations tested associations between CTQ scores, cognition, and biomarker data across the entire cohort. These results informed follow-up mediation models that tested indirect effects of inflammation on relationships between childhood maltreatment and cognitive impairments using model 4 of the PROCESS macro.
Results: Correlations demonstrated significant associations between inflammation and overall childhood maltreatment (total CTQ composite score) as well as specific domains of childhood maltreatment (physical abuse, sexual abuse, emotional abuse, physical neglect CTQ scores; all p < 0.05). Inflammation was also negatively associated with executive functioning (p = 0.004) but not episodic memory performance (p > 0.05). Follow-up mediation analyses revealed significant indirect pathways linking both overall (total CTQ composite; ß = -0.0005, 95% CI [-0.0012, -0.0000]) and specific domains of childhood maltreatment (physical abuse: ß = -0.0023, 95% CI [-0.0056, -0.001]), sexual abuse: ß = -0.0018, 95% CI [-0.004, -0.001]), physical neglect: ß = -0.0023, 95% CI [-0.0056, -0.0000])) to executive functioning through inflammation.
Conclusions: Results suggests that pro-inflammatory biomarkers may help explain the link between exposure to childhood maltreatment and later executive functioning deficits in adulthood. Specific domains of childhood maltreatment may present increased risk for later executive functioning decline through inflammation.