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Published on: November 30, 2015
Inflammation following childhood maltreatment is associated with episodic memory decline in older adults
Dalia Einstein1, Savana Jurgens1, Erica Howard1
1Psychology Department, The Ohio State University, Columbus, Ohio, USA.
Abstract:
Childhood maltreatment is recognized as a risk factor for cognitive decline in adulthood. However, the mechanisms underlying this association, particularly the role of systemic inflammation, remain understudied. To address this gap, this study investigated the indirect effects of inflammation on the associations between childhood maltreatment and both episodic memory (EM) and executive functioning (EF) performance 10 years after inflammatory measurement in older adults. We selected 590 participants (Mage = 65.5 years) from the Midlife in the United States Study based on available childhood maltreatment, inflammation, and composite cognitive data. Spearman's rank correlations were calculated to test associations among childhood maltreatment, cognition, and inflammation. The results informed follow-up analyses testing the indirect effects of inflammation on the associations between childhood maltreatment and cognition. Correlations demonstrated that inflammation was associated with overall childhood maltreatment as well as with specific domains of childhood maltreatment (i.e., physical abuse, sexual abuse, emotional abuse, and physical neglect), ps = .002-.010. Inflammation was negatively associated with EF, p = .001, and EM, p = .028. Follow-up analyses revealed significant indirect pathways linking overall childhood maltreatment, β = -.0088, SE = 0.0058, 95% CI [-0.0223, -0.00000], to EM performance through inflammation, but no specific domain of maltreatment drove this association. The results suggest that inflammation may help explain links between childhood maltreatment exposure and EM deficits in adulthood. These results elucidate the importance of evaluating childhood maltreatment as a risk factor for later-life cognitive decline, particularly within the context of heightened inflammatory biomarkers.
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