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Research highlights risk factors across systems, from person to community, for understanding antisocial behavior. However, limited research used person-centered analyses to investigate how individual, familial, neighborhood, and structural risk factors cluster and relate to antisocial behavior. We applied latent profile analysis to questionnaires and Census-derived data ( N = 478; Northeast sample). A five-profile solution fit best (1: Low Risk; 2: Elevated Personality Risk; 3: Elevated Family and Structural Risk; 4: Elevated Personality, Family, and Neighborhood Risk; 5: Elevated Neighborhood and Structural Risk). We compared profiles across questionnaire-based, interview-based, and criminal record outcomes. The Elevated Personality, Family, and Neighborhood Risk profile had the strongest relationship to risky behavior and an antisocial personality disorder diagnosis. The Elevated Neighborhood and Structural Risk profile showed the strongest relationship to number of crimes. These results elucidate patterns of co-occurring risk within-people, across systems, and reveal important commonalities and dissociations among forms of antisocial behavior.

Youth antisocial behavior (AB) is associated with deficits in socioemotional processing, reward and threat processing and executive functioning. These deficits are thought to emerge from differences in neural structure, functioning and connectivity, particularly within the default, salience and frontoparietal networks. However, the relationship between AB and the organization of these networks remains unclear. To address this gap, the current study applied unweighted, undirected graph analyses to resting-state functional magnetic resonance imaging data in a cohort of 161 adolescents (95 female) enriched for exposure to poverty, a risk factor for AB. As prior work indicates that callous-unemotional (CU) traits may moderate the neurocognitive profile of youth AB, we examined CU traits as a moderator. Using multi-informant latent factors, AB was found to be associated with less efficient frontoparietal network topology, a network associated with executive functioning. However, this effect was limited to youth at low or mean levels of CU traits, indicating that these neural differences were specific to those high on AB but not CU traits. Neither AB, CU traits nor their interaction was significantly related to default or salience network topologies. Results suggest that AB, specifically, may be linked with shifts in the architecture of the frontoparietal network.

Gun violence is a major public health problem and costs the United States $280 billion annually (1). Although adolescents are disproportionately impacted (e.g. premature death), we know little about how close adolescents live to deadly gun violence incidents and whether such proximity impacts their socioemotional development (2, 3). Moreover, gun violence is likely to shape youth developmental outcomes through biological processes—including functional connectivity within regions of the brain that support emotion processing, salience detection, and physiological stress responses—though little work has examined this hypothesis. Lastly, it is unclear if strong neighborhood social ties can buffer youth from the neurobehavioral effects of gun violence. Within a nationwide birth cohort of 3,444 youth (56% Black, 24% Hispanic) born in large US cities, every additional deadly gun violence incident that occurred within 500 meters of home in the prior year was associated with an increase in behavioral problems by 9.6%, even after accounting for area-level crime and socioeconomic resources. Incidents that occurred closer to a child's home exerted larger effects, and stronger neighborhood social ties offset these associations. In a neuroimaging subsample (N = 164) of the larger cohort, living near more incidents of gun violence and reporting weaker neighborhood social ties were associated with weaker amygdala–prefrontal functional connectivity during socioemotional processing, a pattern previously linked to less effective emotion regulation. Results provide spatially sensitive evidence for gun violence effects on adolescent behavior, a potential mechanism through which risk is biologically embedded, and ways in which positive community factors offset ecological risk.

Convergent research identifies a general factor (“P factor”) that confers transdiagnostic risk for psychopathology. Large-scale networks are key organizational units of the human brain. However, studies of altered network connectivity patterns associated with the P factor are limited, especially in early adolescence when most mental disorders are first emerging. We studied 11,875 9- and 10-year olds from the Adolescent Brain and Cognitive Development (ABCD) study, of whom 6593 had high-quality resting-state scans. Network contingency analysis was used to identify altered interconnections associated with the P factor among 16 large-scale networks. These connectivity changes were then further characterized with quadrant analysis that quantified the directionality of P factor effects in relation to neurotypical patterns of positive versus negative connectivity across connections. The results showed that the P factor was associated with altered connectivity across 28 network cells (i.e., sets of connections linking pairs of networks);p_PERMUTATIONvalues < 0.05 FDR-corrected for multiple comparisons. Higher P factor scores were associated with hypoconnectivity within default network and hyperconnectivity between default network and multiple control networks. Among connections within these 28 significant cells, the P factor was predominantly associated with “attenuating” effects (67%;p_PERMUTATION < 0.0002), i.e., reduced connectivity at neurotypically positive connections and increased connectivity at neurotypically negative connections. These results demonstrate that the general factor of psychopathology produces attenuating changes across multiple networks including default network, involved in spontaneous responses, and control networks involved in cognitive control. Moreover, they clarify mechanisms of transdiagnostic risk for psychopathology and invite further research into developmental causes of distributed attenuated connectivity.

The family stress model (FSM) is an influential family process model that posits that socioeconomic disadvantage impacts child outcomes via its effects on the parents. Existing evaluations of the FSM are constrained by limited measures of socioeconomic disadvantage, cross‐sectional research designs, and reliance on non‐population‐based samples. The current study tested the FSM in a subsample of the Fragile Families and Child Wellbeing Study (N = 2,918), a large population‐based study of children followed from birth through the age of nine. We employed a longitudinal framework and used measures of socioeconomic disadvantage beyond economic resources. Although the hypothesized FSM pathways were identified in the longitudinal model (e.g., economic pressure at the age of one was associated with maternal distress at the age of three, maternal distress at the age of three was associated with parenting behaviors at the age of five), the effects of socioeconomic disadvantage at childbirth on youth socioemotional outcomes at the age of nine did not operate through all of the hypothesized mediators. In longitudinal change models that accounted for the stability in constructs, multiple indicators of socioeconomic disadvantage at childbirth were indirectly associated with youth externalizing behaviors at the age of nine via either economic pressure at the age of one or changes in maternal warmth from ages 3 to 5. Greater economic pressure at the age of one, increases in maternal distress from ages 1 to 3, and decreases/increases in maternal warmth/harshness from ages 3 to 5 were also directly associated with increases in externalizing behaviors from ages 5 to 9. Results provide partial support for the FSM across the first decade of life.