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Research has documented changes in parenting practices and in emotion regulation (ER) during adolescence. However, developmental trajectories of these constructs and how they may be linked are not clearly known. The present study examined longitudinal associations between developmental trajectories of negative parenting and developmental trajectories of ER (e.g., abilities and strategy use, including cognitive reappraisal and suppression). The sample included 167 adolescents (53% males) who were first recruited at age 13 or 14 years and assessed annually four times. Adolescents self-reported on the perceived degree of their parent's negative parenting and ER. Growth mixture modeling revealed two distinct trajectories of negative parenting across adolescence: Class 1 contained the majority of adolescents (84%), with moderate initial levels of negative parenting that decreased across adolescence; Class 2 contained a smaller group of adolescents (16%), reporting moderate initial levels of negative parenting that increased across adolescence. Though growth curve modeling did not reveal significant growth in ER across time in the sample as a whole, results from a two-group model demonstrated that ER development significantly differs depending on adolescents' experiences of negative parenting trajectories. Adolescents experiencing decreases in negative parenting showed significant increases in ER abilities and no significant changes in suppression. Adolescents experiencing increases in negative parenting exhibited significant decreases in ER abilities. Adolescent's cognitive reappraisal was unaffected by negative parenting. The findings underscore the significant role of differential parenting environments in the development of ER abilities during adolescence. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

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.

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. National Institute on Drug AbuseUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute on Drug Abuse (NIDA)European Commission [R01 DA036017] Published version This work was supported by grants from the National Institute on Drug Abuse (R01 DA036017 to Jungmeen KimSpoon and Brooks KingCasas. We thank the former and current JK Lifespan Development Lab members for their help with data collection. We are grateful to the adolescents and parents who participated in our study.

OBJECTIVE: Male adolescents exhibit greater impulsivity and externalizing symptomatology relative to female adolescents. Furthermore, externalizing symptomatology has been associated with greater alcohol use and differential anterior insula functioning. The current longitudinal study on adolescents examined whether activity in the anterior insula, when processing uncertain outcomes and representing risk, is directly associated with gender differences in later adolescent alcohol use frequency, as well as indirectly through externalizing symptomatology. METHOD: Using functional magnetic resonance imaging, we examined whether gender moderated these associations in a sample of 161 adolescents (53% male) with repeated annual measurements over 3 years. We monitored responding of a region implicated in risk processing during an economic lottery choice task involving uncertain outcomes. Self-reported externalizing symptomatology and alcohol use frequency were collected at all time points. RESULTS: Results indicated that there was a significant indirect effect of anterior insula processing during the task at Time 1 on alcohol use at Time 3 through externalizing symptomatology at Time 2 for male, but not female, adolescents. Externalizing symptomatology predicted alcohol use for both male and female adolescents. CONCLUSIONS: The findings suggest gender differences in vulnerability to later alcohol use, specifically in terms of how a neurobiological susceptibility to risk insensitivity may disproportionately influence male adolescents’ externalizing symptomatology. Male adolescents who do not effectively integrate risk-related signals are likely to engage in externalizing behaviors, which in turn are related to later alcohol use. Findings also suggest differential roles of risk-related brain function that contribute to gendered pathways to adolescent health-risk behaviors.

Existing literature has demonstrated an association between higher adolescent religiousness and lower risk taking via higher self-regulation. The present 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.

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.

Hedonic dysregulation is evident in addiction and substance use disorders, but it is not clearly understood how hedonic processes may interact with brain development related to cognitive control to influence risky decision making and substance use during adolescence. The present study used prospective longitudinal data to clarify the role of cognitive control in the link between hedonic experiences and the development of substance use during adolescence. Participants included 167 adolescents (53% male) assessed at four time points, annually. Adolescents participated in a functional magnetic resonance imaging (fMRI) session where blood-oxygen level dependent (BOLD) response was monitored during the Multi-Source- Interference Task to assess cognitive control. Substance use and hedonia were assessed using self-report. A two-group growth curve model of substance use with hedonia as a time-varying covariate indicated that higher levels of hedonia predicted higher substance use, but only in adolescents with higher activation in the frontoparietal regions and in the rostral anterior cingulate cortex during cognitive control. Results elucidate the moderating effects of neural cognitive control on associations between hedonia and adolescent substance use, suggesting that lower cognitive control functioning in the brain may exacerbate risk for substance use promoted by hedonia. Published version

Adversity exposure is a risk factor for psychopathology, which most frequently onsets during adolescence, and prior research has demonstrated that alterations in cortico-limbic connectivity may account in part for this association. In a sample of youth from the Adolescent Brain Cognitive Development (ABCD) Study (N = 4006), we tested a longitudinal structural equation model to examine the indirect effect of adversity exposure (negative life events) on later psychopathology via changes in cortico-limbic resting-state functional connectivity (rsFC). We also examined the potential protective effects of parental acceptance. Generally, cortico-limbic connectivity became more strongly negative between baseline and year 2 follow-up, suggesting that stronger negative correlations within these cortico-limbic networks may reflect a more mature phenotype. Exposure to a greater number of negative life events was associated with stronger negative cortico-limbic rsFC which, in turn, was associated with lower internalizing (but not externalizing) symptoms. The indirect effect of negative life events on internalizing symptoms via cortico-limbic rsFC was significant. Parental acceptance did not moderate the association between negative life events and rsFC. Our findings highlight how stressful childhood experiences may accelerate neurobiological maturation in specific cortico-limbic connections, potentially reflecting an adaptive process that protects against internalizing problems in the context of adversity., Highlights • Childhood adversity shapes cortico-limbic connectivity and mental health. • In the ABCD Study, cortico-limbic functional connectivity changed over time. • These changes explain the association between adversity and internalizing symptoms. • Adversity exposure may accelerate corticolimbic development.

Socioeconomic status (SES) is broadly associated with self-regulatory abilities across childhood and adolescence. However, there is limited understanding of the mechanisms underlying this association, especially during adolescence when individuals are particularly sensitive to environmental influences. The current study tested perceived stress, household chaos, parent cognitive control, and parent-adolescent relationship quality as potential proximal mediators of the association between family SES and neural correlates of cognitive control. A sample of 167 adolescents and their primary caregivers participated in a longitudinal study across four years. SES was indexed by caregivers’ education and income-to-needs ratio at Time 1. At Time 2, adolescents reported on their perceived stress, household chaos, and relationship with parents, and parents completed a cognitive control task. Two years later, adolescents completed the same cognitive control task while blood-oxygenation-level-dependent (BOLD) response was monitored with functional magnetic resonance imaging (fMRI). A parallel mediation model indicated that parent cognitive control, but not other proximal factors, explained the relation between SES and adolescents’ activation in the middle frontal gyrus during a cognitive control task. The results suggest potential targets for intervention and prevention efforts that may positively alter neurocognitive outcomes related to socioeconomic disadvantage. Published version

Highlights • Maltreatment and brain development related to risky decision making were studied. • Neglect predicted slower increases in risk-related insula and dACC activation. • Abuse predicted steeper decreases in control-related fronto-parietal activation. • Abuse predicted accelerated development of risk- and control-related brain regions. • Abuse and neglect had differential effects on adolescent brain development., The profound effects of child maltreatment on brain functioning have been documented. Yet, little is known about whether distinct maltreatment experiences are differentially related to underlying neural processes of risky decision making: valuation and control. Using conditional growth curve modeling, we compared a cumulative approach versus a dimensional approach (relative effects of abuse and neglect) to examine the link between child maltreatment and brain development. The sample included 167 adolescents (13–14 years at Time 1, 53 % male), assessed annually four times. Risk processing was assessed by blood-oxygen-level-dependent responses (BOLD) during a lottery choice task, and cognitive control by BOLD responses during the Multi-Source Interference Task. Cumulative maltreatment effects on insula and dorsolateral anterior cingulate cortex (dACC) activation during risk processing were not significant. However, neglect (but not abuse) was associated with slower developmental increases in insula and dACC activation. In contrast, cumulative maltreatment effects on fronto-parietal activation during cognitive control were significant, and abuse (but not neglect) was associated with steeper developmental decreases in fronto-parietal activation. The results suggest neglect effects on detrimental neurodevelopment of the valuation system and abuse effects on accelerated neurodevelopment of the control system, highlighting differential effects of distinct neglect versus abuse adverse experiences on neurodevelopment.

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.

Contains fulltext : 226836.pdf (Publisher’s version ) (Closed access) 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. 16 p.

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 1,083 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 through 11.5. In turn, maladaptive self-control trajectories at ages 8.5 through 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.

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.

We used a social developmental perspective to identify how prominent social contexts influence adolescent substance use during adolescence. Longitudinal data were collected 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.

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.

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 four 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 (fMRI) 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.

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 (NA) 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 (one 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.