Deprivation and Threat: Dimensions of Early Experience and Neural Development

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 DESCRIPTION (provided by applicant): Extensive research finds robust links between mental health and childhood adversity (CA), encompassing diverse exposures from child abuse to poverty. Despite the strength and consistency of these findings, the mechanisms producing such links remain poorly specified. In particular, past research has failed to identify how specifi environmental experiences influence specific neural processes. Such limitations arise from the difficulty of precisely quantifying relevant CA and neural variables in children. The current proposal addresses these limitations by capitalizing on a unique, well characterized NIH-funded longitudinal cohort of children where multiple aspects of CA have been precisely assessed and use of rigorous neuroimaging methods to quantify functioning in specific neural circuits. We will use these methods to test a novel conceptual framework delineating how specific types of environmental experience influence specific neural processes, addressing Objective 1 of the NIMH Strategic Plan. Our model argues that different types of CA have distinct effects on neural development. The central distinction we make is between trauma and deprivation. Trauma exposure involves harm or threat of harm, resulting in fear learning mediated by limbic pathways that are well characterized in animals and conserved across species. We argue that child trauma alters development of circuits in the Negative Valence System that support emotional learning encompassing amygdala and ventromedial prefrontal cortex (PFC). In contrast, deprivation involves absence of expected cognitive and social inputs and environmental complexity. Animal research shows that deprivation disrupts development in PFC and parietal cortex by hijacking the typical process of synaptic pruning. Thus we predict that social-cognitive deprivation influences Cognitive Control Systems, resulting in age-specific reductions in thickness and volume of dorsolateral PFC and superior parietal cortex and reduced performance on cognitive control tasks supported by these areas. Clearly, trauma and deprivation are correlated. Our unique design will measure these experiences on separate dimensions informed by rich preliminary data indicating distinct effects of trauma and deprivation on neural development even in samples with high exposure co-occurrence. Our proposed conceptual model will be tested by acquiring structural and functional MRI data on an existing sample of 300 children (1/3 in poverty, 1/3 near poverty, and 1/3 middle class) followed since early childhood with significant variability in CA exposure. Psychopathology has been measured in previous waves of the study and will be collected multiple times during the study period. Study findings will provide critical information about how specific dimensions of environmental experience influence specific neural processes. Elucidating these mechanisms will not only build knowledge of how adverse environments alter neural development in ways that increase risk for psychopathology, but will also suggest possible targets for preventive interventions aimed at reducing psychopathology risk in children exposed to trauma and deprivation.