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Creators/Authors contains: "Clark, D. Angus"

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  1. Abstract

    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);pPERMUTATIONvalues < 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%;pPERMUTATION < 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.

     
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  2. Abstract Background

    Although early life exposure to chronic disadvantage is associated with deleterious outcomes, 40%–60% of exposed youth continue to thrive. To date, little is known about the etiology of these resilient outcomes.

    Methods

    The current study examined child twin families living in disadvantaged contexts (N = 417 pairs) to elucidate the etiology of resilience. We evaluated maternal reports of the Child Behavior Checklist to examine three domains of resilience and general resilience.

    Results

    Genetic, shared, and nonshared environmental influences significantly contributed to social resilience (22%, 61%, 17%, respectively) and psychiatric resilience (40%, 28%, 32%, respectively), but academic resilience was influenced only by genetic and nonshared environmental influences (65% and 35%, respectively). These three domains loaded significantly onto a latent resilience factor, with factor loadings ranging from 0.60 to 0.34. A common pathway model revealed that the variance common to all three forms of resilience was predominantly explained by genetic and non‐shared environmental influences (50% and 35%, respectively).

    Conclusions

    These results support recent conceptualizations of resilience as a multifaceted construct influenced by both genetic and environmental influences, only some of which overlap across the various domains of resilience.

     
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