Max P. Herzberg

Behavioral inhibition (BI), a temperamental trait; the error-related negativity (ERN), a marker of performance monitoring measured via electroencephalogram; and overcontrol, a phenotype characterized by perfectionism and inflexibility, all show associations with childhood anxiety, obsessive-compulsive symptoms, and social functioning. However, the independent and combined risk for psychiatric and social functioning of these factors is unknown. The present study examined how childhood BI, ERN, and overcontrol independently predict longitudinal psychiatric symptoms and peer functioning. We then examined how overcontrol may mediate the relationship between BI and longitudinal outcomes, as well as how the ERN may moderate this mediation. Caregivers completed baseline (aged 5-6 years; 48% female; 77% White) measures of BI, overcontrol, and psychiatric and peer functioning (N = 123), and children completed a go/no-go task while an electroencephalogram was collected (n = 86). Two years later, parents completed measures of psychiatric symptoms and peer functioning. Findings demonstrated only overcontrol, not BI or ERN, predicted worsening anxiety and peer relations. Overcontrol mediated the relationship between BI and longitudinal anxiety and between BI and longitudinal peer functioning. The ERN did not moderate these mediations. Findings suggest overcontrol confers risk for worsening childhood psychiatric and peer outcomes and may be an understudied mechanism linking BI to these outcomes. Therefore, early identification of the overcontrolled phenotype may be important given its direct association with an exacerbation of psychiatric and peer functioning difficulties across a 2-year period. Moreover, overcontrol may be a clinically useful and potent target for childhood psychiatric and social problems. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

Social Determinants of Health (SDoH) are defined as the non-biological individual and structural factors that shape the socio-environmental conditions of everyday life. SDoH are major drivers of risk for psychiatric disorders across development. However, what remains less clear are the neurobiological mechanisms by which SDoH confers risk for psychopathology, especially in early childhood. Growing evidence suggests that adverse forms of SDoH begin to impact the developing brain from the earliest points in development, including in-utero. Brain-wide associations have been found for brain structure and function, especially in regions that subserve socioemotional and cognitive functions. While most studies have shown SDoH-related delays in brain development and psychopathology risk, a small collection of studies have also shown that SDoH has been related to accelerated brain maturation. These latter findings potentially suggest adaptive or compensatory mechanisms that enhance resilient mental health outcomes in the context of adversity. Future directions include the need for randomized interventions designed to enhance development that target the modifiable SDoH and related socio-environmental factors during distinct periods of brain plasticity. The recruitment and retention of socially diverse research participants, to more precisely elucidate the impacts of SDoH on the developing brain in children experiencing different environments, are also needed.

Childhood exposure to social disadvantage is a major risk factor for psychiatric disorders and poor developmental, educational, and occupational outcomes, presumably because adverse exposures alter the neurodevelopmental processes that contribute to risk trajectories. Yet, given the limited social mobility in the United States and other countries, childhood social disadvantage is frequently preceded by maternal social disadvantage during pregnancy, potentially altering fetal brain development during a period of high neuroplasticity through hormonal, microbiome, epigenetic, and immune factors that cross the placenta and fetal blood–brain barrier. The current study examines prenatal social disadvantage to determine whether these exposures in utero are associated with alterations in functional brain networks as early as birth. As part of the Early Life Adversity and Biological Embedding study, mothers were recruited during pregnancy, prenatal social disadvantage was assessed across trimesters, and their healthy, full-term offspring were imaged using resting-state functional magnetic resonance imaging during the first weeks of life. Multivariate machine learning methods revealed that neonatal functional connectivity (FC) varied as a function of prenatal exposure to social disadvantage (n = 261, R = 0.43, R ² = 0.18), with validation in an independent sample. Alterations in FC associated with prenatal social disadvantage occurred brain-wide and were most pronounced in association networks (fronto-parietal, ventral attention, dorsal attention) and the somatomotor network. Amygdala FC was altered at birth, with a pattern shared across subcortical structures. These findings provide critical insights into how early in development functional networks begin to diverge in the context of social disadvantage and elucidate the functional networks that are most impacted.

Recent research has reported effects of socioeconomic status on neurobehavioral development as early as infancy, including positive associations between income and brain structure, functional connectivity, and behavior later in childhood (Ramphal, Whalen, et al., 2020; Triplett et al., 2022). This study extends this literature by investigating the relation of maternal prenatal social disadvantage (PSD) to neonatal amygdala and hippocampus functional connectivity and whether socioeconomic-related alterations in functional connectivity subsequently predict behavior at age 12 months in a large, socioeconomically diverse sample (N = 261 mother-infant dyads). PSD was assessed across gestation; neonatal magnetic resonance imaging was completed within the first weeks of life; and infant internalizing and externalizing symptoms were evaluated using the Infant-Toddler Social and Emotional Assessment at age 12 months. The results showed that PSD was significantly related to neonatal right amygdala and left hippocampus functional connectivity with prefrontal and motor-related regions. Social disadvantage-related right amygdala and left hippocampus functional connectivity with these regions was subsequently related to infant externalizing and internalizing symptoms at age 12 months. Building off an emerging literature exploring prenatal impacts on neonatal functional connectivity, this study further emphasizes the important role of the maternal environment during gestation on infant brain function and its relationship with externalizing and internalizing behavior in the first years of life. The results suggest that the prenatal socioeconomic environment may be a promising target for interventions aimed at improving infant neurobehavioral outcomes. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Neuroplasticity during sensitive periods, the molecular and cellular process of enduring neural change in response to external stimuli during windows of high environmental sensitivity, is crucial for adaptation to expected environments and has implications for psychiatry. Animal research has characterized the developmental sequence and neurobiological mechanisms that govern neuroplasticity, yet gaps in our ability to measure neuroplasticity in humans limit the clinical translation of these principles. Here, we present a roadmap for the development and validation of neuroimaging and electrophysiology measures that index neuroplasticity to begin to address these gaps. We argue that validation of measures to track neuroplasticity in humans will elucidate the etiology of mental illness and inform the type and timing of mental health interventions to optimize effectiveness. We outline criteria for evaluating putative neuroimaging measures of plasticity in humans including links to neurobiological mechanisms shown to govern plasticity in animal models, developmental change that reflects heightened early life plasticity, and prediction of neural and/or behavior change. These criteria are applied to three putative measures of neuroplasticity using electroencephalography (gamma oscillations, aperiodic exponent of power/frequency) or functional magnetic resonance imaging (amplitude of low frequency fluctuations). We discuss the use of these markers in psychiatry, envision future uses for clinical and developmental translation, and suggest steps to address the limitations of the current putative neuroimaging measures of plasticity. With additional work, we expect these markers will significantly impact mental health and be used to characterize mechanisms, devise new interventions, and optimize developmental trajectories to reduce psychopathology risk.

Adverse experiences and family income in childhood have been associated with altered brain development. While there is a large body of research examining these associations, it has primarily used cross‐sectional data sources and studied adverse experiences and family income in isolation. However, it is possible that low family income and adverse experiences represent dissociable and potentially interacting profiles of risk. To address this gap in the literature, we examined brain structure as a function of adverse experiences in childhood and family income in 158 youths with up to five waves of MRI data. Specifically, we assessed the interactive effect of these two risk factors on six regions of interest: hippocampus, putamen, amygdala, nucleus accumbens, caudate, and thalamus. Adverse experiences and family income interacted to predict putamen volume (B = 0.086, p = 0.011) but only in participants with family income one standard deviation below the mean (slope estimate = −0.11, p = 0.03). These results suggest that adverse experiences in childhood result in distinct patterns of brain development across the socioeconomic gradient. Given previous findings implicating the role of the putamen in psychopathology‐related behaviors, these results emphasize the importance of considering life events and socioeconomic context when evaluating markers of risk. Future research should include interactive effects of environmental exposures and family income to better characterize risk for psychopathology in diverse samples.