Psychopathology as long-term sequelae of maltreatment and socioeconomic disadvantage: Neurocognitive development perspectives.

Neuroscience research underscores the critical impact of adverse experiences on brain development. Yet, there is limited understanding of the specific pathways linking adverse experiences to accelerated or delayed brain development and their ultimate contributions to psychopathology. Here, we present new longitudinal data demonstrating that neurocognitive functioning during adolescence, as affected by adverse experiences, predicts psychopathology during young adulthood. The sample included 167 participants (52% male) assessed in adolescence and young adulthood. Adverse experiences were measured by early maltreatment experiences and low family socioeconomic status. Cognitive control was assessed by neural activation and behavioral performance during the Multi-Source Interference Task. Psychopathology was measured by self-reported internalizing and externalizing symptomatology. Results indicated that higher maltreatment predicted heightened frontoparietal activation during cognitive control, indicating delayed neurodevelopment, which, in turn predicted higher internalizing and externalizing symptomatology. Furthermore, higher maltreatment predicted a steeper decline in frontoparietal activation across adolescence, indicating neural plasticity in cognitive control-related brain development, which was associated with lower internalizing symptomatology. Our results elucidate the crucial role of neurocognitive development in the processes linking adverse experiences and psychopathology. Implications of the findings and directions for future research on the effects of adverse experiences on brain development are discussed.

Parenting, emotion regulation, and externalizing symptomatology as adolescent antecedents to young adult health risk behaviors.

This study used longitudinal data to elucidate how trajectories of negative parenting across adolescence are associated with young adult health risk behaviors (HRBs) by testing difficulties with emotion regulation and externalizing symptomatology as sequential underlying mediators. The sample included 167 adolescents (53% males, Mage  = 14 at Time 1 and Mage  = 18 at Time 5) who were assessed five times. Adolescents self-reported on negative parenting, emotion regulation, externalizing symptomatology, and engagement in HRBs. Results suggest that increasingly negative parenting across adolescence has adverse consequences for emotion regulation development and in turn, externalizing symptomatology, which confers risk for young adult HRBs. Results offer insights towards mechanisms for prevention and intervention and public health policy aimed at reducing the prevalence and consequences of engagement in HRBs.

Transactional relations between developmental trajectories of executive functioning and internalizing and externalizing symptomatology in adolescence.

Adolescence is a period of social, physical, and neurobiological transitions that may leave individuals more vulnerable to the development of internalizing and externalizing symptomatology. Extant research demonstrates that executive functioning (EF) is associated with psychopathology outcomes in adolescence; however, it has yet to be examined how EF and psychopathology develop transactionally over time. Data were collected from 167 adolescents (47% female, 13-14 years old at Time 1) and their primary caregiver over 4 years. At each time point, adolescents completed three behavioral tasks that capture the underlying dimensions of EF, and both adolescents and their primary caregiver completed measures of adolescent psychopathology. Latent growth curve modeling was used to test the associations between initial levels and trajectories of EF and psychopathology. Results indicated that higher initial levels of internalizing and externalizing symptomatology were associated with lower EF at Time 4 (controlling for Time 1 EF). Initial levels of EF did not predict changes in internalizing and externalizing symptomatology. These findings suggest that early psychopathology may be a risk factor for maladaptive EF development in adolescence.

A 4-year longitudinal neuroimaging study of cognitive control using latent growth modeling: developmental changes and brain-behavior associations.

Despite theoretical models suggesting developmental changes in neural substrates of cognitive control in adolescence, empirical research has rarely examined intraindividual changes in cognitive control-related brain activation using multi-wave multivariate longitudinal data. We used longitudinal repeated measures of brain activation and behavioral performance during the multi-source interference task (MSIT) from 167 adolescents (53% male) who were assessed annually over four years from ages 13 to 17 years. We applied latent growth modeling to delineate the pattern of brain activation changes over time and to examine longitudinal associations between brain activation and behavioral performance. We identified brain regions that showed differential change patterns: (1) the fronto-parietal regions that involved bilateral insula, bilateral middle frontal gyrus, left pre-supplementary motor area, left inferior parietal lobule, and right precuneus; and (2) the rostral anterior cingulate cortex (rACC) region. Longitudinal confirmatory factor analyses of the fronto-parietal regions revealed strong measurement invariance across time implying that multivariate functional magnetic resonance imaging data during cognitive control can be measured reliably over time. Latent basis growth models indicated that fronto-parietal activation decreased over time, whereas rACC activation increased over time. In addition, behavioral performance data, age-related improvement was indicated by a decreasing trajectory of intraindividual variability in response time across four years. Testing longitudinal brain-behavior associations using multivariate growth models revealed that better behavioral cognitive control was associated with lower fronto-parietal activation, but the change in behavioral performance was not related to the change in brain activation. The current findings suggest that reduced effects of cognitive interference indicated by fronto-parietal recruitment may be a marker of a maturing brain that underlies better cognitive control performance during adolescence.

Bidirectional links between adolescent brain function and substance use moderated by cognitive control.

BACKGROUND: No clear consensus exists as to whether neurodevelopmental abnormalities among substance users reflect predisposing neural risk factors, neurotoxic effects of substances, or both. Using a longitudinal design, we examined developmental patterns of the bidirectional links between neural mechanisms and substance use throughout adolescence. METHOD: 167 adolescents (aged 13-14 years at Time 1, 53% male) were assessed annually four times. Risk-related neural processing was assessed by blood-oxygen-level-dependent responses in the insula during a lottery choice task, cognitive control by behavioral performance during the Multi-Source Interference Task, and substance use by adolescents' self-reported cigarette, alcohol, and marijuana use. RESULTS: Latent change score modeling indicated that greater substance use predicted increased insula activation during risk processing, but the effects of insula activation on changes in substance use were not significant. The coupling effect from substance use to insula activation was particularly strong for adolescents with low cognitive control, which supports the theorized moderating role of cognitive control. CONCLUSIONS: Our results elucidate how substance use may alter brain development to be biased toward maladaptive decision-making, particularly among adolescents with poor cognitive control. Furthermore, the current findings underscore that cognitive control may be an important target in the prevention and treatment of adolescent substance use given its moderating role in the neuroadaptive effects of substance use on brain development.

Socioeconomic Risk for Adolescent Cognitive Control and Emerging Risk-Taking Behaviors.

This study examined whether cognitive control mediated the association between socioeconomic status (SES; composite of income-to-needs ratio and parent education) and changes in risk-taking behaviors. The sample included 167 dyads of adolescents (53% male; Mage  = 14.07 years at Time 1) and their parents, assessed annually across 4 years. Parents reported socioeconomic variables at Time 1. Adolescents reported risk-taking behaviors at Times 1 and 4, and completed a functional magnetic resonance imaging cognitive control task at Times 2 and 3. Lower SES was associated with lower behavioral (but not neural) cognitive control, which was associated with increases in risk-taking behaviors. The findings suggest that elevated socioeconomic risk may compromise cognitive control which can cascade into maladaptive behaviors in adolescence.

Neural Cognitive Control Moderates the Relation between Negative Life Events and Depressive Symptoms in Adolescents.

The present longitudinal study examined the role of neural cognitive control in the relation between negative and positive life events and depressive symptoms in adolescents. The sample comprised 138 adolescents (52% male, Mage = 13.49 at baseline) and their parents. At Time 1, adolescents participated in a functional neuroimaging session in which neural cognitive control was measured as hemodynamic activity during an inhibitory control task, and parents reported on adolescents' positive and negative life events within the past year. Adolescents and parents reported on adolescent depressive symptoms at Time 1, Time 2 (1 year later), and Time 3 (2 years later). Conditional latent growth curve model was used to test the main and interaction effects of neural cognitive control and positive/negative life events on the growth factors of depressive symptoms. Higher neural cognitive control moderated the relation between negative life events and the intercept of depressive symptoms. Adolescents with higher neural cognitive control did not experience higher depressive symptoms when confronted with more negative life events, whereas their counterparts with lower neural cognitive control did. The interaction effect between neural cognitive control and positive life events on depressive symptoms was not significant. Results suggest that neural cognitive control acts as a protective factor such that adolescents with higher neural cognitive control are protected against depressionogenic effects of negative life events, whereas adolescents with lower cognitive control are at greater risk for depressive symptoms in response to negative life events.

Religious Social Support Protects against Social Risks for Adolescent Substance Use.

We used a social developmental perspective to identify how prominent social contexts influence substance use during adolescence. Longitudinal data were collected annually from 167 parent-adolescent dyads over four years. We investigated whether parent substance use was related to adolescent substance use directly and indirectly via peer substance use and whether these associations were moderated by religious social support. Structural equation modeling (SEM) analysis indicated significant moderated mediation: Greater parent substance use predicted increases in adolescent substance use indirectly via increased peer substance use when adolescent religious social support was low or average, but not high. These results suggest religious social support may protect adolescents against prominent social risks for intergenerational substance use.

Longitudinal pathways linking family risk, neural risk processing, delay discounting, and adolescent substance use.

BACKGROUND: Current theories in neuroscience emphasize the crucial role of individual differences in the brain contributing to the development of risk taking during adolescence. Yet, little is known about developmental pathways through which family risk factors are related to neural processing of risk during decision making, ultimately contributing to health risk behaviors. Using a longitudinal design, we tested whether neural risk processing, as affected by family multi-risk index, predicted delay discounting and substance use. METHOD: One hundred and fifty-seven adolescents (aged 13-14 years at Time 1, 52% male) were assessed annually three times. Family multi-risk index was measured by socioeconomic adversity, household chaos, and family risk-taking behaviors. Delay discounting was assessed by a computerized task, substance use by questionnaire data, and risk-related neural processing by blood-oxygen-level-dependent (BOLD) responses in the amygdala during a lottery choice task. RESULTS: Family multi-risk index at Time 1 was related to adolescent substance use at Time 3 (after controlling for baseline substance use) indirectly through heightened amygdala sensitivity to risks and greater delay discounting. CONCLUSIONS: Our results elucidate the crucial role of neural risk processing in the processes linking family multi-risk index and the development of substance use. Furthermore, risk-related amygdala activation and delay discounting are important targets in the prevention and treatment of substance use among adolescents growing up in high-risk family environments.

Brains of a feather flocking together? Peer and individual neurobehavioral risks for substance use across adolescence.

Adolescence is a period of heightened susceptibility to peer influences, and deviant peer affiliation has well-established implications for the development of psychopathology. However, little is known about the role of brain functions in pathways connecting peer contexts and health risk behaviors. We tested developmental cascade models to evaluate contributions of adolescent risk taking, peer influences, and neurobehavioral variables of risk processing and cognitive control to substance use among 167 adolescents who were assessed annually for four years. Risk taking at Time 1 was related to substance use at Time 4 indirectly through peer substance use at Time 2 and insular activation during risk processing at Time 3. Furthermore, neural cognitive control moderated these effects. Greater insular activation during risk processing was related to higher substance use for those with greater medial prefrontal cortex activation during cognitive control, but it was related to lower substance use among those with lower medial prefrontal cortex activation during cognitive control. Neural processes related to risk processing and cognitive control play a crucial role in the processes linking risk taking, peer substance use, and adolescents' own substance use.

How Is Religiousness Associated With Adolescent Risk-Taking? The Roles of Emotion Regulation and Executive Function.

Existing literature has demonstrated an association between higher adolescent religiousness and lower risk-taking via higher self-regulation. This study sought to elucidate the roles of emotion regulation and executive function as parallel mediators in the link between religiousness and risk-taking in a sample of 167 adolescents (mean age = 14.13 years, 52% male, 82% White at Time 1). Longitudinal results across three waves utilizing structural equation modeling indicated higher religiousness was associated with higher emotion regulation, whereas religiousness was not associated with executive function. Subsequently, higher emotion regulation and executive function were associated with lower risk-taking. Emotion regulation mediated the association between religiousness and risk-taking. The findings highlight religiousness as a contextual protective factor for adolescents.

Structural Home Environment Effects on Developmental Trajectories of Self-Control and Adolescent Risk Taking.

Extant literature has demonstrated that self-control is critical for health and adjustment in adolescence. Questions remain regarding whether there are individuals that may be most vulnerable to impaired self-control development and whether aspects of the structural home environment may predict membership in these subgroups, as well as the behavioral consequences of impaired self-control trajectories. The present study utilized growth mixture modeling and data from 1083 individuals (50% female, 82% White) from age 8.5 to 15 years to identify four latent classes of self-control development. Additionally, higher household chaos and lower socioeconomic status at age 8.5 were associated with maladaptive trajectories of self-control at ages 8.5-11.5. In turn, maladaptive self-control trajectories at ages 8.5-11.5 were associated with higher risk taking at age 15. The results highlight the importance of increased structure and support for at-risk youth.

Positive and Negative Affect and Adolescent Adjustment: Moderation Effects of Prefrontal Functioning.

We examined whether cognitive control moderates the effects of emotion on adolescent internalizing and externalizing symptomatology in a longitudinal study of 138 adolescents. Self-reported positive affect (PA) and negative affect and behavioral and neural indicators of cognitive control, indexed by performance and prefrontal hemodynamic response during a cognitive interference task, were collected at Time 1. Self-reported internalizing and externalizing symptomatology were collected at Time 1 and Time 2 (1 year later). Results indicated that higher PA predicted decreases in externalizing symptomatology, but only for adolescents with poor neural cognitive control. No moderation effects were found for behavioral cognitive control. Findings imply the beneficial effects of PA on the development of externalizing problems among adolescents with poor prefrontal functioning.

Household chaos as a context for intergenerational transmission of executive functioning.

Executive functioning (EF) may be transmitted across generations such that strengths or deficiencies in parent EF are similarly manifested in the child. The present study examined the contributions of parent EF and impulsivity on adolescent EF, and investigated whether household chaos is an environmental moderator that alters these transmission processes. American adolescents (N = 167, 47% female, 13-14 years old at Time 1) completed behavioral measures of EF and reported household chaos at Time 1 and one year later at Time 2. Parents completed behavioral measures of EF and self-reported impulsivity at Time 1. Results indicated that lower parent EF at Time 1 predicted lower adolescent EF at Time 2 (controlling for adolescent EF and IQ at Time 1), but only in the context of high household chaos. Findings suggest that household chaos may be a risk factor that compounds influences of poor parent EF and compromises adolescent EF development.

Leveraging multivariate approaches to advance the science of early-life adversity.

Since the landmark Adverse Childhood Experiences (ACEs) study, adversity research has expanded to more precisely account for the multifaceted nature of adverse experiences. The complex data structures and interrelated nature of adversity data require robust multivariate statistical methods, and recent methodological and statistical innovations have facilitated advancements in research on childhood adversity. Here, we provide an overview of a subset of multivariate methods that we believe hold particular promise for advancing the field's understanding of early-life adversity, and discuss how these approaches can be practically applied to explore different research questions. This review covers data-driven or unsupervised approaches (including dimensionality reduction and person-centered clustering/subtype identification) as well as supervised/prediction-based approaches (including linear and tree-based models and neural networks). For each, we highlight studies that have effectively applied the method to provide novel insight into early-life adversity. Taken together, we hope this review serves as a resource to adversity researchers looking to expand upon the cumulative approach described in the original ACEs study, thereby advancing the field's understanding of the complexity of adversity and related developmental consequences.

Brain Similarity as a Protective Factor in the Longitudinal Pathway Linking Household Chaos, Parenting, and Substance Use.

BACKGROUND: Socioecological factors such as family environment and parenting behaviors contribute to the development of substance use. While biobehavioral synchrony has been suggested as the foundation for resilience that can modulate environmental effects on development, the role of brain similarity that attenuates deleterious effects of environmental contexts has not been clearly understood. We tested whether parent-adolescent neural similarity-the level of pattern similarity between parent-adolescent functional brain connectivity representing the level of attunement within each dyad-moderates the longitudinal pathways in which household chaos (a stressor) predicts adolescent substance use directly and indirectly via parental monitoring. METHODS: In a sample of 70 parent-adolescent dyads, similarity in resting-state brain activity was identified using multipattern connectivity similarity estimation. Adolescents and parents reported on household chaos and parental monitoring, and adolescent substance use was assessed at a 1-year follow-up. RESULTS: The moderated mediation model indicated that for adolescents with low neural similarity, but not high neural similarity, greater household chaos predicted higher substance use over time directly and indirectly via lower parental monitoring. Our data also indicated differential susceptibility in the overall association between household chaos and substance use: Adolescents with low neural similarity exhibited high substance use under high household chaos but low substance use under low household chaos. CONCLUSIONS: Neural similarity acts as a protective factor such that the detrimental effects of suboptimal family environment and parenting behaviors on the development of adolescent health risk behaviors may be attenuated by neural similarity within parent-adolescent bonds.

Family socioeconomic status and adolescent substance use: The role of parent-adolescent brain similarity and parental monitoring.

Greater neural similarity between parents and adolescents may reduce adolescent substance use. Among 70 parent-adolescent dyads, we tested a longitudinal path model in which family economic environment is related to adolescent substance use, directly and indirectly through parent-adolescent neural similarity and parental monitoring. Neural similarity was measured as parent-adolescent pattern similarity in functional brain connectivity at Time 1. Parents reported socioeconomic status and parental monitoring at Time 1. Adolescents reported parental monitoring at Time 1 and substance use at Time 2. Higher family socioeconomic status was associated with greater neural similarity. Greater neural similarity was associated with lower adolescent substance use, mediated through greater adolescent-perceived parental monitoring. Parent-adolescent neural similarity may attenuate adolescent substance use by bolstering parental monitoring. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Neural Circuit Markers of Familial Risk for Depression Among Healthy Youths in the Adolescent Brain Cognitive Development Study.

BACKGROUND: Family history of depression is a robust predictor of early-onset depression, which may confer risk through alterations in neural circuits that have been implicated in reward and emotional processing. These alterations may be evident in youths who are at familial risk for depression but who do not currently have depression. However, the identification of robust and replicable findings has been hindered by few studies and small sample sizes. In the current study, we sought to identify functional connectivity (FC) patterns associated with familial risk for depression. METHODS: Participants included healthy (i.e., no lifetime psychiatric diagnoses) youths at high familial risk for depression (HR) (n = 754; at least one parent with a history of depression) and healthy youths at low familial risk for psychiatric problems (LR) (n = 1745; no parental history of psychopathology) who were 9 to 10 years of age and from the Adolescent Brain Cognitive Development (ABCD) Study sample. We conducted whole-brain seed-to-voxel analyses to examine group differences in resting-state FC with the amygdala, caudate, nucleus accumbens, and putamen. We hypothesized that HR youths would exhibit global amygdala hyperconnectivity and striatal hypoconnectivity patterns primarily driven by maternal risk. RESULTS: HR youths exhibited weaker caudate-angular gyrus FC than LR youths (α = 0.04, Cohen's d = 0.17). HR youths with a history of maternal depression specifically exhibited weaker caudate-angular gyrus FC (α = 0.03, Cohen's d = 0.19) as well as weaker caudate-dorsolateral prefrontal cortex FC (α = 0.04, Cohen's d = 0.21) than LR youths. CONCLUSIONS: Weaker striatal connectivity may be related to heightened familial risk for depression, primarily driven by maternal history. Identifying brain-based markers of depression risk in youths can inform approaches to improving early detection, diagnosis, and treatment.

Differential Associations of Adversity Profiles with Adolescent Cognitive Control and Psychopathology.

Adverse childhood experiences are common and have long-term consequences for biological and psychosocial adjustment. We used a person-centered approach to characterize distinct profiles of adversity in early adolescence and examined associations with later cognitive control and psychopathology. The sample included 167 adolescents (47% female) and their primary caregivers who participated in a longitudinal study across four time points (approximately one year between assessments). At Time 1 (Mage = 14 years), we measured seven indicators of adversity: socioeconomic disadvantage, abuse, neglect, household chaos, parent substance use, parent depression, and negative life events. At Times 2-4, adolescents' behavioral performance and functional activation during a cognitive control task were measured. At Time 5, adolescents and their caregiver reported on adolescent internalizing and externalizing symptomatology. Using latent profile analysis, we identified four distinct adversity subgroups: a low exposure group, a neglect group, a household instability group, and a poly-adversity group. These groups significantly differed on subsequent levels of psychopathology, but not cognitive control. Specifically, the poly-adversity group reported significantly higher levels of both internalizing and externalizing symptomatology relative to the low exposure group, and the household instability group demonstrated elevated risk for externalizing symptomatology. When using a cumulative risk approach, higher levels of adversity exposure were associated with significantly worse cognitive control performance (but not neural activation). These results suggest that psychopathology outcomes may be differentially predicted by distinct patterns of risk, and that cognitive control impairment may be more strongly predicted by cumulative risk.

Characterizing the dimensional structure of early-life adversity in the Adolescent Brain Cognitive Development (ABCD) Study.

Early-life adversity has profound consequences for youth neurodevelopment and adjustment; however, experiences of adversity are heterogeneous and interrelated in complex ways that can be difficult to operationalize and organize in developmental research. We sought to characterize the underlying dimensional structure of co-occurring adverse experiences among a subset of youth (ages 9-10) from the Adolescent Brain Cognitive Development (ABCD) Study (N = 7115), a community sample of youth in the United States. We identified 60 environmental and experiential variables that reflect adverse experiences. Exploratory factor analysis identified 10 robust dimensions of early-life adversity co-occurrence, corresponding to conceptual domains such as caregiver substance use and biological caregiver separation, caregiver psychopathology, caregiver lack of support, and socioeconomic disadvantage / neighborhood lack of safety. These dimensions demonstrated distinct associations with internalizing problems, externalizing problems, cognitive flexibility, and inhibitory control. Non-metric multidimensional scaling characterized qualitative similarity among the 10 identified dimensions. Results supported a nonlinear three-dimensional structure representing early-life adversity, including continuous gradients of "perspective", "environmental uncertainty", and "acts of omission/commission". Our findings suggest that there are distinct dimensions of early-life adversity co-occurrence in the ABCD sample at baseline, and the resulting dimensions may have unique implications for neurodevelopment and youth behavior.