| Background Adverse childhood experiences (ACEs) are strong predictors of psychopathological risks throughout the entire life cycle, and they may have extensive adverse effects on physical and mental health in the early stages of an individual''s development. ACEs not only increase the risk of childhood psychopathology but also may affect sleep quality and lead to impaired cognitive function. However, the early neurobiological mechanisms mediating the cognitive impairment caused by ACEs remain unclear. Objective To explore the association between ACEs exposure and the risk of psychopathology, sleep disorders, and cognitive function, and to examine the mediating role of the putamen volume in the relationship between ACEs and cognitive function from the perspective of neurodevelopment. Methods Data were obtained from the Adolescent Brain Cognitive Development (ABCD) study, involving 10 572 children aged 9~10. The children were divided into five groups based on the cumulative score of ACEs reported by their parents and the children themselves: no-exposure group (0 types of ACEs), the one-exposure group, the two-exposure group, the three-exposure group, and the high-risk exposure group (≥ 4 types of ACEs). Logistic regression analysis was employed to explore the association between ACEs and psychopathological symptoms [T score of the Child Behavior Checklist (CBCL) ≥ 65]. Multiple linear regression analysis was used to investigate the correlations between ACEs and the scores of the Sleep Disturbance Scale for Children (SDSC), the NIH Toolbox Cognition Battery (NIHTB-CB), as well as multiple structures in the cerebral cortex and subcortex. The Bootstrap method was utilized to test the mediating effect of the putamen volume between ACEs and neurocognitive function. Results After controlling for confounders, ACEs cumulative score was correlated with children''s psychopathological symptoms, and there was a dose-response relationship between the two. Compared with the no-exposed group, the high-risk exposure group had a 2.08-fold (OR=2.080, 95% CI: 1.401–3.088) increased risk of internalizing problems and a 3.13-fold (OR=3.132, 95% CI: 1.703–5.760) increased risk of externalizing problems, and the risk of conduct problems was 4.68 times that of the no-exposed group (OR=4.681, 95% CI: 2.528–8.669). ACEs cumulative score positively predicted the total score of SDSC (β=0.080, 95% CI: 0.059–0.102), with relatively stronger predictive effects on sleep-wake transition disorder (β=0.086, 95% CI: 0.063–0.109) and sleep onset and maintenance disorder (β=0.066, 95% CI: 0.043–0.089). In terms of neurocognition and brain structure, ACEs cumulative score negatively predicted the overall cognitive composite score (β=-0.025, 95% CI: -0.050– -0.001), the crystallized cognitive composite score (β=-0.035, 95% CI: -0.060– -0.010), and the volume of the left putamen nucleus (β=-0.025, 95% CI: -0.046– -0.003). The total putamen volume played a partial mediating role in the negative association between ACEs and the overall cognitive composite score (indirect effect value B=-0.002, 95% CI: -0.004– -0.001), accounting for 7.49% of the total effect. Conclusion ACEs exposure may increase the risk of psychopathological and sleep disturbances in children, and may also lead to impaired neurocognitive function. The reduction of the putamen volume may be a potential neurobiological pathway through which ACEs affect children''s neurocognitive function.
【Keywords】 Adverse childhood experiences; Children; Psychopathology; Sleep disturbances; Neurocognitive function; Putamen |