Brain Age Gap Associations with Externalising Behaviours in Youth: A Longitudinal Investigation in the Adolescent Brain Cognitive Development (ABCD) Cohort

Background. Early adolescence is a period of heightened risk for the emergence of externalising psychopathology, making it an important window for identifying neurodevelopmental risk markers. Differences between predicted brain age and chronological age - termed the brain age gap - reflect variation from age-typical patterns of brain structure. While brain age gap has been closely linked with internalising behaviours in adolescence, less is known about its relationship with externalising symptoms. This study examined whether brain age gap in late childhood/early adolescence (9-11 years) is associated with current externalising symptoms and whether it predicts externalising trajectories over seven-year follow-up. Methods. Participants were 10,516 adolescents (aged 9-11 at baseline; up to 18 years at follow-up) from the Adolescent Brain Cognitive Development (ABCD) Study who met inclusion/exclusion criteria. Brain age gap for each participant was derived from an external validated prediction model (Drobinin et al., 2022) applied to baseline measurements of cortical volume, area, and subcortical volume. Linear mixed-effects models were used to test cross-sectional and longitudinal associations between baseline brain age gap and externalising symptoms, as assessed using the Child Behaviour Checklist. Primary models were adjusted for age, sex, pubertal status, and prior to inclusion of sociodemographic covariates (ethnoracial identity and caregiver highest education). Results. A higher/more positive brain age gap was associated with greater externalising symptoms at baseline (B[SE]=0.067[0.033], p=.042), but this association was removed following sociodemographic adjustment (B[SE]=0.056[0.033], p=.088). Longitudinally, a significant brain age gap x age interaction was identified that remained evident after sociodemographic adjustment, with this relationship weakening across adolescence (B[SE]=-0.007[0.003], p=.033). Conclusions. These findings suggest that a more positive brain age gap, indicating more mature-appearing brain structure for age, in late childhood/early adolescence may be associated with externalising psychopathology, but this relationship is likely to be age- and context-dependent rather than a stable marker of persistent behavioural risk.