The role of functional emotion circuits in distinct dimensions of psychopathology in youth.

Several mental disorders emerge during childhood or adolescence and are often characterized by socioemotional difficulties, including alterations in emotion perception. Emotional facial expressions are processed in discrete functional brain modules whose connectivity patterns encode emotion categories, but the involvement of these neural circuits in psychopathology in youth is poorly understood. This study examined the associations between activation and functional connectivity patterns in emotion circuits and psychopathology during development. We used task-based fMRI data from the Philadelphia Neurodevelopmental Cohort (PNC, N = 1221, 8-23 years) and conducted generalized psycho-physiological interaction (gPPI) analyses. Measures of psychopathology were derived from an independent component analysis of questionnaire data. The results showed positive associations between identifying fearful, sad, and angry faces and depressive symptoms, and a negative relationship between sadness recognition and positive psychosis symptoms. We found a positive main effect of depressive symptoms on BOLD activation in regions overlapping with the default mode network, while individuals reporting higher levels of norm-violating behavior exhibited emotion-specific lower functional connectivity within regions of the salience network and between modules that overlapped with the salience and default mode network. Our findings illustrate the relevance of functional connectivity patterns underlying emotion processing for behavioral problems in children and adolescents.

Dimensions of early life adversity are differentially associated with patterns of delayed and accelerated brain maturation.

BACKGROUND: Different types of early-life adversity have been associated with children's brain structure and function. However, understanding the disparate influence of distinct adversity exposures on the developing brain remains a major challenge. METHODS: This study investigates the neural correlates of 10 robust dimensions of early-life adversity identified through exploratory factor analysis in a large community sample of youth from the Adolescent Brain Cognitive Development (ABCD) Study. Brain age models were trained, validated, and tested separately on T1-weighted (T1; N = 9524), diffusion tensor (DTI; N = 8834), and resting-state functional (rs-fMRI; N = 8233) magnetic resonance imaging (MRI) data from two time points (mean age = 10.7 years, SD = 1.2, range = 8.9-13.8 years). RESULTS: Bayesian multilevel modelling supported distinct associations between different types of early-life adversity exposures and younger- and older-looking brains. Dimensions generally related to emotional neglect, such as lack of primary and secondary caregiver support, and lack of caregiver supervision, were associated with lower brain age gaps (BAGs), i.e., younger-looking brains. In contrast, dimensions generally related to caregiver psychopathology, trauma exposure, family aggression, substance use and separation from biological parent, and socio-economic disadvantage and neighbourhood safety were associated with higher BAGs, i.e., older-looking brains. CONCLUSIONS: The findings suggest that dimensions of early-life adversity are differentially associated with distinct neurodevelopmental patterns, indicative of dimension-specific delayed and accelerated brain maturation.

Structural brain changes in emotion recognition across the adult lifespan.

Emotion recognition (ER) declines with increasing age, yet little is known whether this observation is based on structural brain changes conveyed by differential atrophy. To investigate whether age-related ER decline correlates with reduced grey matter (GM) volume in emotion-related brain regions, we conducted a voxel-based morphometry analysis using data of the Human Connectome Project-Aging (N = 238, aged 36-87) in which facial ER was tested. We expected to find brain regions that show an additive or super-additive age-related change in GM volume indicating atrophic processes that reduce ER in older adults. The data did not support our hypotheses after correction for multiple comparisons. Exploratory analyses with a threshold of P < 0.001 (uncorrected), however, suggested that relationships between GM volume and age-related general ER may be widely distributed across the cortex. Yet, small effect sizes imply that only a small fraction of the decline of ER in older adults can be attributed to local GM volume changes in single voxels or their multivariate patterns.

Puberty differentially predicts brain maturation in male and female youth: A longitudinal ABCD Study.

Research has demonstrated associations between pubertal development and brain maturation. However, existing studies have been limited by small samples, cross-sectional designs, and inconclusive findings regarding directionality of effects and sex differences. We examined the longitudinal temporal coupling of puberty status assessed using the Pubertal Development Scale (PDS) and magnetic resonance imaging (MRI)-based grey and white matter brain structure. Our sample consisted of 8896 children and adolescents at baseline (mean age = 9.9) and 6099 at follow-up (mean age = 11.9) from the Adolescent Brain and Cognitive Development (ABCD) Study cohort. Applying multigroup Bivariate Latent Change Score (BLCS) models, we found that baseline PDS predicted the rate of change in cortical thickness among females and rate of change in cortical surface area for both males and females. We also found a correlation between baseline PDS and surface area and co-occurring changes over time in males. Diffusion tensor imaging (DTI) analyses revealed correlated change between PDS and fractional anisotropy (FA) for both males and females, but no significant associations for mean diffusivity (MD). Our results suggest that pubertal status predicts cortical maturation, and that the strength of the associations differ between sex. Further research spanning the entire duration of puberty is needed to understand the extent and contribution of pubertal development on the youth brain.