Prefrontal activation in preschool children is associated with maternal adversity and child temperament: A preliminary fNIRS study of inhibitory control.

Exposure to adversity is a well-documented risk factor for cognitive, behavioral, and mental health problems. In fact, the consequences of adversity may be intergenerational. A growing body of research suggests that maternal exposures to adversity, including those prior to childbirth, are associated with offspring biobehavioral development. In a sample of 36 mothers and their preschool-age children (mean child age = 4.21 ± 0.92 years), we used functional near-infrared spectroscopy to replicate and extend this work to include brain activation during inhibitory control in young children. We found that measures of maternal exposure to adversity, including cumulative, childhood, and preconception exposures, were significantly and positively associated with activation in the right frontopolar prefrontal cortex (PFC) and in the left temporal and parietal clusters during inhibitory control. In addition, and consistent with previous findings, children's increased negative affect and decreased effortful control were associated with increased right PFC activation during inhibitory control. These findings provide preliminary evidence that maternal and dispositional risk factors are linked to alterations in PFC functioning during the preschool years. Children of mothers with a history of exposure to adversity, as well as children who are less temperamentally regulated, may require increased neural resources to meet the cognitive demands of inhibitory control.

A network analysis of psychopathology in young Black children: Implications for predicting outcomes in adolescence.

OBJECTIVE: Network analysis may identify specific symptoms involved in the maintenance and development of psychopathology. This approach, however, has not been applied to the study of young Black children, a population facing unique challenges and developmental risks. It is also unclear whether network analysis identifies early symptoms in Black children that are linked to their longer-term difficulties and strengths in adolescence. METHODS: We conducted a network analysis of emotional and behavioral difficulties in 1238 Black (non-Hispanic) children from the age-3 assessment in the Future of Families and Child Wellbeing Study (47 % female). We also explored whether early childhood symptoms predict subsequent caregiver-reported internalizing and externalizing problems, and youth-reported social competencies and extracurricular and community involvement, at the age-15 assessment. RESULTS: We identified specific symptoms of externalizing and emotional reactivity as central in the network. Symptoms of emotional reactivity were also involved in comorbidity, bridging different communities of symptoms. Using elastic net models, we identified specific central and bridge symptoms, but also peripheral network symptoms, that contributed uniquely to the prediction of internalizing and externalizing problems in adolescence. Early childhood symptoms were less predictive of positive outcomes in adolescence. CONCLUSIONS: This study identified central and bridge symptoms in young Black children, an underrepresented population in network analysis research. Some of these central and bridge symptoms, but also peripheral network symptoms, may be useful targets in early interventions to prevent long-term difficulties. Conversely, network approaches to understanding early psychopathology may have less utility for predicting Black children's subsequent strengths in adolescence.

Fetal Gene Regulatory Gene Deletions are Associated with Poor Cognition and Altered Cortical Morphology in Schizophrenia and Community-Based Samples.

Schizophrenia spectrum disorders (SSDs) are characterized by substantial clinical and genetic heterogeneity. Multiple recurrent copy number variants (CNVs) increase risk for SSDs; however, how known risk CNVs and broader genome-wide CNVs influence clinical variability is unclear. The current study examined associations between borderline intellectual functioning or childhood-onset psychosis, known risk CNVs, and burden of deletions affecting genes in 18 previously validated neurodevelopmental gene-sets in 618 SSD individuals. CNV associations were assessed for replication in 235 SSD relatives and 583 controls, and 9,930 youth from the Adolescent Brain Cognitive Development (ABCD) Study. Known SSD- and neurodevelopmental disorder (NDD)-risk CNVs were associated with borderline intellectual functioning in SSD cases (odds ratios (OR) = 7.09 and 4.57, respectively); NDD-risk deletions were nominally associated with childhood-onset psychosis (OR = 4.34). Furthermore, deletion of genes involved in regulating gene expression during fetal brain development was associated with borderline intellectual functioning across SSD cases and non-cases (OR = 2.58), with partial replication in the ABCD cohort. Exploratory analyses of cortical morphology showed associations between fetal gene regulatory gene deletions and altered gray matter volume and cortical thickness across cohorts. Results highlight contributions of known risk CNVs to phenotypic variability in SSD and the utility of a neurodevelopmental framework for identifying mechanisms that influence phenotypic variability in SSDs, as well as the broader population, with implications for personalized medicine approaches to care.