Rapid neurodevelopment occurs during adolescence, which may increase the developing brain’s susceptibility to environmental risk and resilience factors. Adverse childhood experiences (ACEs) may confer additional risk to the developing brain, where ACEs have been linked with alterations in BOLD signaling in brain regions underlying inhibitory control. Potential resiliency factors, like a positive family environment, may attenuate the risk associated with ACEs, but limited research has examined potential buffers to adversity’s impact on the developing brain. The current study aimed to examine how ACEs relate to BOLD response during successful inhibition on the Stop Signal Task (SST) in regions underlying inhibitory control from late childhood to early adolescence and will assess whether aspects of the family environment moderate this relationship.

Participants (N= 9,080; Mage= 10.7, range= 9-13.8 years old; 48.5% female, 70.1% non-Hispanic White) were drawn from the larger Adolescent Brain Cognitive Development (ABCD) Study cohort. ACE risk scores were created (by EAS) using parent and child reports of youth’s exposure to adverse experiences collected at baseline to 2-year follow-up. For family environment, levels of family conflict were assessed based on youth reports on the Family Environment Scale at baseline and 2-year follow-up. The SST, a task-based fMRI paradigm, was used to measure inhibitory control (contrast: correct stop > correct go); the task was administered at baseline and 2-year follow-up. Participants were excluded if flagged for poor task performance. ROIs included left and right dorsolateral prefrontal cortex, anterior cingulate cortex, anterior insula, inferior frontal gyrus (IFG), and pre-supplementary motor area (pre-SMA). Separate linear mixed-effects models were conducted to assess the relationship between ACEs and BOLD signaling in ROIs while controlling for demographics (age, sex assigned at birth, race, ethnicity, household income, parental education), internalizing scores, and random effects of subject and MRI model.

Greater ACEs was associated with reduced BOLD response in the opercular region of the right IFG (b= -0.002, p= .02) and left (b= -0.002, p= .01) and right pre-SMA (b= -0.002, p= .01). Family conflict was related to altered activation patterns in the left pre-SMA, where youth with lower family conflict demonstrated a more robust negative relationship (b=.001, p= .04). ACEs were not a significant predictor in other ROIs, and the relationship between ACEs and BOLD response did not significantly differ across time. Follow-up brain-behavior correlations showed that in youth with lower ACEs, there was a negative correlation between increased activation in the pre-SMA and less impulsive behaviors.

Preadolescents with ACE history show blunted activation in regions underlying inhibitory control, which may increase the risk for future poorer inhibitory control with downstream implications for behavioral/health outcomes. Further, results demonstrate preliminary evidence for the family environment’s contributions to brain health. Future work is needed to examine other resiliency factors that may modulate the impact of ACE exposure during childhood and adolescence. Further, clinical scientists should continue to examine the relationship between ACEs and neural and behavioral correlates of inhibitory control across adolescent development, as risk-taking behaviors progress.