Early Childhood Deprivation and Psychopathology: Identifying Neurodevelopmental Pathways of Risk

PROJECT SUMMARY/ABSTRACT Experiences of childhood adversity are common in the United States and account for a substantial proportion of pediatric-onset psychopathology. Understanding mechanistic pathways that contribute to this heightened psychopathology risk is, therefore, of critical consequence to public health. The Dimensional Model of Adversity

and Psychopathology (DMAP) proposes that adverse experiences characterized by deprivation (e.g., neglect) may have distinct neurodevelopmental consequences in the frontoparietal network that confer risk for pediatric psychopathology. While existing theory emphasizes the importance of early childhood experiences of deprivation

in shaping development in the frontoparietal network, existing neurodevelopmental research on childhood adversity is primarily cross-sectional and has focused almost exclusively on neural and mental health outcomes in adolescent samples. In two highly related pediatric neuroimaging samples with rich assessment of early

childhood adversity exposure and psychopathology (Sample 1: R01MH115004; Sample 2: R01MH120314), we seek to address these gaps in the literature and Goal 2 of the NIMH strategic plan by identifying neurodevelopmental pathways linking deprivation with transdiagnostic psychopathology risk first in early

childhood and then longitudinally from early childhood through adolescence. The proposed study will first examine concurrent associations of deprivation with altered frontoparietal network activation during cognitive control (Aim 1). We hypothesize that deprivation will be associated with worse cognitive control performance and

reduced activation in the frontoparietal network (Sample 1). Next, we will characterize early childhood deprivation-related alterations to trajectories of cortical structure in the frontoparietal control network (Aim 2). We hypothesize that deprivation will be associated with blunted intra-individual longitudinal trajectories of cortical

thinning in the frontoparietal network (Sample 2). Finally, we will examine deprivation-related alterations to brain function and structural development as potential mechanisms contributing to childhood and adolescent psychopathology (Aim 3). We hypothesize that decreased activation in the frontoparietal network during cognitive

control will mediate the association of early childhood deprivation with concurrent psychopathology (Sample 1). Furthermore, we predict that altered longitudinal trajectories of cortical structure in the frontoparietal control network will mediate the association of early childhood deprivation with adolescent psychopathology. Training

aims include advanced training in functional magnetic resonance imaging (fMRI) analysis, longitudinal modeling of neuroimaging data, and latent modeling of pediatric psychopathology. The applicant’s training will be supported by her sponsor’s and consultants’ expertise in these areas and extensive institutional resources.

Findings will have implications for population health by identifying pathways of transdiagnostic psychopathology risk that can inform future early intervention efforts for childhood adversity involving deprivation.