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Background: Suicide is the second-leading cause of death in youth. Understanding the neural correlates of suicide ideation (SI) in children is crucial to ongoing efforts to understand and prevent youth suicide. This study characterized key neural networks during rest and emotion task conditions in an epidemiologically informed sample of children who report current, past, or no SI., Methods: Data are from the adolescent brain cognitive development study, including 8248 children (ages 9-10; mean age = 119.2 months; 49.2% female) recruited from the community. Resting-state functional connectivity (RSFC) and activation to emotional stimuli in the salience (SN) and default mode (DMN) networks were measured through fMRI. Self-reported SI and clinical profiles were gathered. We examined the replicability of our model results through repeated sub-sample reliability analyses., Results: Children with current SI (2.0%), compared to those without any past SI, showed lower DMN RSFC ( B = -0.267, p < 0.001) and lower DMN activation in response to negative as compared to neutral faces ( B = -0.204, p = 0.010). These results were robust to the effects of MDD, ADHD, and medication use. Sub-sample analysis further supported the robustness of these results. We did not find support for differences in SN RSFC or in SN activation to positive or negative stimuli for children with or without SI., Conclusions: Results from a large brain imaging study using robust statistical approaches suggest aberrant DMN functioning in children with current suicide ideation. Findings suggest potential mechanisms that may be targeted in suicide prevention efforts.

Importance: Incidental findings (IFs) are unexpected abnormalities discovered during imaging and can range from normal anatomic variants to findings requiring urgent medical intervention. In the case of brain magnetic resonance imaging (MRI), reliable data about the prevalence and significance of IFs in the general population are limited, making it difficult to anticipate, communicate, and manage these findings., Objectives: To determine the overall prevalence of IFs in brain MRI in the nonclinical pediatric population as well as the rates of specific findings and findings for which clinical referral is recommended., Design, Setting, and Participants: This cohort study was based on the April 2019 release of baseline data from 11 810 children aged 9 to 10 years who were enrolled and completed baseline neuroimaging in the Adolescent Brain Cognitive Development (ABCD) study, the largest US population-based longitudinal observational study of brain development and child health, between September 1, 2016, and November 15, 2018. Participants were enrolled at 21 sites across the US designed to mirror the demographic characteristics of the US population. Baseline structural MRIs were centrally reviewed for IFs by board-certified neuroradiologists and findings were described and categorized (category 1, no abnormal findings; 2, no referral recommended; 3; consider referral; and 4, consider immediate referral). Children were enrolled through a broad school-based recruitment process in which all children of eligible age at selected schools were invited to participate. Exclusion criteria were severe sensory, intellectual, medical, or neurologic disorders that would preclude or interfere with study participation. During the enrollment process, demographic data were monitored to ensure that the study met targets for sex, socioeconomic, ethnic, and racial diversity. Data were analyzed from March 15, 2018, to November 20, 2020., Main Outcomes and Measures: Percentage of children with IFs in each category and prevalence of specific IFs., Results: A total of 11 679 children (52.1% boys, mean [SD] age, 9.9 [0.62] years) had interpretable baseline structural MRI results. Of these, 2464 participants (21.1%) had IFs, including 2013 children (17.2%) assigned to category 2, 431 (3.7%) assigned to category 3, and 20 (0.2%) assigned to category 4. Overall rates of IFs did not differ significantly between singleton and twin gestations or between monozygotic and dizygotic twins, but heritability analysis showed heritability for the presence or absence of IFs (h2 = 0.260; 95% CI, 0.135-0.387)., Conclusions and Relevance: Incidental findings in brain MRI and findings with potential clinical significance are both common in the general pediatric population. By assessing IFs and concurrent developmental and health measures and following these findings over the longitudinal study course, the ABCD study has the potential to determine the significance of many common IFs.

Difficulties with higher-order cognitive functions in youth are a potentially important vulnerability factor for the emergence of problematic behaviors and a range of psychopathologies. This study examined 2013 9-10 year olds in the first data release from the Adolescent Brain Cognitive Development 21-site consortium study in order to identify resting state functional connectivity patterns that predict individual-differences in three domains of higher-order cognitive functions: General Ability, Speed/Flexibility, and Learning/Memory. For General Ability scores in particular, we observed consistent cross-site generalizability, with statistically significant predictions in 14 out of 15 held-out sites. These results survived several tests for robustness including replication in split-half analysis and in a low head motion subsample. We additionally found that connectivity patterns involving task control networks and default mode network were prominently implicated in predicting differences in General Ability across participants. These findings demonstrate that resting state connectivity can be leveraged to produce generalizable markers of neurocognitive functioning. Additionally, they highlight the importance of task control-default mode network interconnections as a major locus of individual differences in cognitive functioning in early adolescence.

Psychosocial acceleration theory suggests that pubertal maturation is accelerated in response to adversity. In addition, suboptimal caregiving accelerates development of the amygdala-medial prefrontal cortex circuit. These findings may be related. Here, we assess whether associations between family environment and measures of the amygdala-medial prefrontal cortex circuit are mediated by pubertal development in more than 2000 9- and 10-year-old children from the Adolescent Brain Cognitive Development Study (http://dx.doi.org/10.15154/1412097). Using structural equation modeling, demographic, child-reported, and parent-reported data on family dynamics were compiled into a higher level family environment latent variable. Magnetic resonance imaging preprocessing and compilations were performed by the Adolescent Brain Cognitive Development Study's data analysis core. Anterior cingulate cortex (ACC) thickness, area, white matter fractional anisotropy, amygdala volume, and cingulo-opercular network-amygdala resting-state functional connectivity were assessed. For ACC cortical thickness and ACC fractional anisotropy, significant indirect effects indicated that a stressful family environment relates to more advanced pubertal stage and more mature brain structure. For cingulo-opercular network-amygdala functional connectivity, results indicated a trend in the expected direction. For ACC area, evidence for quadratic mediation by pubertal stage was found. Sex-stratified analyses suggest stronger results for girls. Despite small effect sizes, structural measures of circuits important for emotional behavior are associated with family environment and show initial evidence of accelerated pubertal development.

The Minnesota Center for Twin and Family Research (MCTFR) comprises multiple longitudinal, community-representative investigations of twin and adoptive families that focus on psychological adjustment, personality, cognitive ability and brain function, with a special emphasis on substance use and related psychopathology. The MCTFR includes the Minnesota Twin Registry (MTR), a cohort of twins who have completed assessments in middle and older adulthood; the Minnesota Twin Family Study (MTFS) of twins assessed from childhood and adolescence into middle adulthood; the Enrichment Study (ES) of twins oversampled for high risk for substance-use disorders assessed from childhood into young adulthood; the Adolescent Brain (AdBrain) study, a neuroimaging study of adolescent twins; and the Siblings Interaction and Behavior Study (SIBS), a study of adoptive and nonadoptive families assessed from adolescence into young adulthood. Here we provide a brief overview of key features of these established studies and describe new MCTFR investigations that follow up and expand upon existing studies or recruit and assess new samples, including the MTR Study of Relationships, Personality, and Health (MTR-RPH); the Colorado-Minnesota (COMN) Marijuana Study; the Adolescent Brain Cognitive Development (ABCD) study; the Colorado Online Twins (CoTwins) study and the Children of Twins (CoT) study.

The Adolescent Brain Cognitive Development (ABCD) Study is an ongoing, nationwide study of the effects of environmental influences on behavioral and brain development in adolescents. The main objective of the study is to recruit and assess over eleven thousand 9-10-year-olds and follow them over the course of 10 years to characterize normative brain and cognitive development, the many factors that influence brain development, and the effects of those factors on mental health and other outcomes. The study employs state-of-the-art multimodal brain imaging, cognitive and clinical assessments, bioassays, and careful assessment of substance use, environment, psychopathological symptoms, and social functioning. The data is a resource of unprecedented scale and depth for studying typical and atypical development. The aim of this manuscript is to describe the baseline neuroimaging processing and subject-level analysis methods used by ABCD. Processing and analyses include modality-specific corrections for distortions and motion, brain segmentation and cortical surface reconstruction derived from structural magnetic resonance imaging (sMRI), analysis of brain microstructure using diffusion MRI (dMRI), task-related analysis of functional MRI (fMRI), and functional connectivity analysis of resting-state fMRI. This manuscript serves as a methodological reference for users of publicly shared neuroimaging data from the ABCD Study., (Copyright © 2019 Elsevier Inc. All rights reserved.)

The Adolescent Brain Cognitive Development (ABCD) study is poised to be the largest single-cohort long-term longitudinal study of neurodevelopment and child health in the United States. Baseline data on N= 4521 children aged 9-10 were released for public access on November 2, 2018. In this paper we performed principal component analyses of the neurocognitive assessments administered to the baseline sample. The neurocognitive battery included seven measures from the NIH Toolbox as well as five other tasks. We implemented a Bayesian Probabilistic Principal Components Analysis (BPPCA) model that incorporated nesting of subjects within families and within data collection sites. We extracted varimax-rotated component scores from a three-component model and associated these scores with parent-rated Child Behavior Checklist (CBCL) internalizing, externalizing, and stress reactivity. We found evidence for three broad components that encompass general cognitive ability, executive function, and learning/memory. These were significantly associated with CBCL scores in a differential manner but with small effect sizes. These findings set the stage for longitudinal analysis of neurocognitive and psychopathological data from the ABCD cohort as they age into the period of maximal adolescent risk-taking., (Copyright © 2018. Published by Elsevier Ltd.)

The ABCD twin study will elucidate the genetic and environmental contributions to a wide range of mental and physical health outcomes in children, including substance use, brain and behavioral development, and their interrelationship. Comparisons within and between monozygotic and dizygotic twin pairs, further powered by multiple assessments, provide information about genetic and environmental contributions to developmental associations, and enable stronger tests of causal hypotheses, than do comparisons involving unrelated children. Thus a sub-study of 800 pairs of same-sex twins was embedded within the overall Adolescent Brain and Cognitive Development (ABCD) design. The ABCD Twin Hub comprises four leading centers for twin research in Minnesota, Colorado, Virginia, and Missouri. Each site is enrolling 200 twin pairs, as well as singletons. The twins are recruited from registries of all twin births in each State during 2006-2008. Singletons at each site are recruited following the same school-based procedures as the rest of the ABCD study. This paper describes the background and rationale for the ABCD twin study, the ascertainment of twin pairs and implementation strategy at each site, and the details of the proposed analytic strategies to quantify genetic and environmental influences and test hypotheses critical to the aims of the ABCD study., (Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The Adolescent Brain Cognitive Development Study (ABCD) will capture a breadth of multi-faceted biobehavioral, environmental, familial, and genetic longitudinal developmental open-access data from over 11,000 9-10 year olds throughout the United States of America (USA) for an envisioned ten-year span. This will subsequently represent the largest study ever attempted with this level of brain phenotypic detail. This study holds the opportunity for exciting advances in the understanding of typical adolescent neurodevelopment, discovery of neurodevelopmental underpinnings of mental illness, as well as the neurodevelopmental influences of (and on) social factors, substance use, and critically - their interaction. This project will certainly take unprecedented steps in informing the nature of adolescence and the developing brain. The scale and open-access features of ABCD also necessarily entail areas for consideration to enhance the integrity of the ABCD study, and protect against potential misuse and misinterpretation of ABCD data. Ultimately, with the open-source data, all scientists in the broader community have as much responsibility as the investigators within the Consortium to treat these data with care. It will be fascinating to see what dynamic data these paths generate. ABCD is poised to exemplify how large-scale longitudinal developmental neuroscientific studies can be designed and efficiently conducted., (Copyright © 2018 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Adolescent substance abuse is a major public health problem, particularly given the negative brain and behavioral consequences that often occur during and following acute intoxication. Negative outcomes appear to be especially pronounced when substance use is initiated in the early adolescent years, perhaps due to neural adaptations that increase risk for substance use disorders into adulthood. Recent models to explain these epidemiological trends have focused on brain-based vulnerabilities to use as well as neurodevelopmental aberrations associated with initiation of use in substance naïve samples or through the description of case-control differences between heavy users and controls. Within this research, adolescent alcohol and marijuana users have shown relative decreases in regional gray matter volumes, substance-specific alterations in white matter volumes, deviations in microstructural integrity in white matter tracts that regulate communication between subcortical areas and higher level regulatory control regions, and deficits in functional connectivity. How these brain anomalies map onto other types of youth risk behavior and later vulnerabilities represent major questions for continued research. This special issue addresses these compelling and timely questions by introducing new methodologies, empirical relationships, and perspectives from major leaders in this field., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Behavioral responses to, and the neural processing of, rewards change dramatically during adolescence and may contribute to observed increases in risk-taking during this developmental period. Functional MRI (fMRI) studies suggest differences between adolescents and adults in neural activation during reward processing, but findings are contradictory, and effects have been found in non-predicted directions. The current study uses an activation likelihood estimation (ALE) approach for quantitative meta-analysis of functional neuroimaging studies to: (1) confirm the network of brain regions involved in adolescents' reward processing, (2) identify regions involved in specific stages (anticipation, outcome) and valence (positive, negative) of reward processing, and (3) identify differences in activation likelihood between adolescent and adult reward-related brain activation. Results reveal a subcortical network of brain regions involved in adolescent reward processing similar to that found in adults with major hubs including the ventral and dorsal striatum, insula, and posterior cingulate cortex (PCC). Contrast analyses find that adolescents exhibit greater likelihood of activation in the insula while processing anticipation relative to outcome and greater likelihood of activation in the putamen and amygdala during outcome relative to anticipation. While processing positive compared to negative valence, adolescents show increased likelihood for activation in the posterior cingulate cortex (PCC) and ventral striatum. Contrasting adolescent reward processing with the existing ALE of adult reward processing reveals increased likelihood for activation in limbic, frontolimbic, and striatal regions in adolescents compared with adults. Unlike adolescents, adults also activate executive control regions of the frontal and parietal lobes. These findings support hypothesized elevations in motivated activity during adolescence., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Adolescence is characterized by heightened risk-taking, including substance misuse. These behavioral patterns are influenced by ontogenic changes in neurotransmitter systems, particularly the dopamine system, which is fundamentally involved in the neural coding of reward and motivated approach behavior. During adolescence, this system evidences a peak in activity. At the same time, the dopamine (DA) system is neuroplastically altered by substance abuse, impacting subsequent function. Here, we describe properties of the dopamine system that change with typical adolescent development and that are altered with substance abuse. Much of this work has been gleaned from animal models due to limitations in measuring dopamine in pediatric samples. Structural and functional neuroimaging techniques have been used to examine structures that are heavily DA-innervated; they measure morphological and functional changes with age and with drug exposure. Presenting marijuana abuse as an exemplar, we consider recent findings that support an adolescent peak in DA-driven reward-seeking behavior and related deviations in motivational systems that are associated with marijuana abuse/dependence. Clinicians are advised that (1) chronic adolescent marijuana use may lead to deficiencies in incentive motivation, (2) that this state is due to marijuana's interactions with the developing DA system, and (3) that treatment strategies should be directed to remediating resultant deficiencies in goal-directed activity.

This longitudinal study examines associations between baseline individual differences and developmental changes in reward [i.e. behavioral approach system (BAS)] sensitivity and relevant brain structures' volumes to prospective substance use initiation during adolescence. A community sample of adolescents ages 15-18 with no prior substance use was assessed for substance use initiation (i.e. initiation of regular alcohol use and/or any use of other substances) during a 2-year follow-up period and for alcohol use frequency in the last year of the follow-up. Longitudinal 'increases' in BAS sensitivity were associated with substance use initiation and increased alcohol use frequency during the follow-up. Moreover, adolescents with smaller left nucleus accumbens at baseline were more likely to initiate substance use during the follow-up period. This study provides support for the link between developmental increases in reward sensitivity and substance use initiation in adolescence. The study also emphasizes the potential importance of individual differences in volumes of subcortical regions and their structural development for substance use initiation during adolescence., (© The Author (2014). Published by Oxford University Press. For Permissions, please email: journals.permissions@oup.com.)

Within this special issue, Ernst has provided a comprehensive overview of the triadic neural systems model and its explanatory power for the conceptualization of adolescent development. Within this commentary, we encourage further consideration of several issues as this valuable model is expanded and articulated. These issues include the extent of functional distinctions among the three proposed neural nodes that comprise the triadic framework, the proposed dichotomy between motivation and emotion as linked to approach versus avoidance, the extent to which approach and avoidance can be dissociated on behavioral and neural levels during adolescent development, and how individual difference factors mechanistically interact with broader age-based developmental trends., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Since this journal's inception, the field of adolescent brain development has flourished, as researchers have investigated the underpinnings of adolescent risk-taking behaviors. Explanations based on translational models initially attributed such behaviors to executive control deficiencies and poor frontal lobe function. This conclusion was bolstered by evidence that the prefrontal cortex and its interconnections are among the last brain regions to structurally and functionally mature. As substantial heterogeneity of prefrontal function was revealed, applications of neuroeconomic theory to adolescent development led to dual systems models of behavior. Current epidemiological trends, behavioral observations, and functional magnetic resonance imaging based brain activity patterns suggest a quadratic increase in limbically mediated incentive motivation from childhood to adolescence and a decline thereafter. This elevation occurs in the context of immature prefrontal function, so motivational strivings may be difficult to regulate. Theoretical models explain this patterning through brain-based accounts of subcortical-cortical integration, puberty-based models of adolescent sensation seeking, and neurochemical dynamics. Empirically sound tests of these mechanisms, as well as investigations of biology-context interactions, represent the field's most challenging future goals, so that applications to psychopathology can be refined and so that developmental cascades that incorporate neurobiological variables can be modeled.

Background: Alcohol use in excessive quantities has deleterious effects on brain structure and behavior in adults and during periods of rapid neurodevelopment, such as prenatally. Whether similar outcomes characterize other developmental periods, such as adolescence, and in the context of less extensive use is unknown. Recent cross-sectional studies suggest that binge drinking as well as alcohol use disorders in adolescence are associated with disruptions in white matter microstructure and gray matter volumes., Objectives: The current study followed typically developing adolescents from a baseline assessment, where no experience with alcohol was present, through two years, after which some individuals transitioned into regular use., Methods: Participants (n = 55) completed MRI scans and behavioral assessments., Results: Alcohol initiators (n = 30; mean baseline age 16.7 ± 1.3 years), compared to non-users (n = 25; mean baseline age 17.1 ± 1.2 years), showed altered patterns of neurodevelopment. They showed greater-than-expected decreases in cortical thickness in the right middle frontal gyrus from baseline to follow-up as well as blunted development of white matter in the right hemisphere precentral gyrus, lingual gyrus, middle temporal gyrus and anterior cingulate. Diffusion tensor imaging revealed a relative decrease over time in fractional anisotropy in the left caudate/thalamic region as well as in the right inferior frontal occipital fasciculus. Alcohol initiators did not differ from non-users at the baseline assessment; the groups were largely similar in other premorbid characteristics., Conclusions: Subclinical alcohol use during mid-to-late adolescence is associated with deviations in neurodevelopment across several brain tissue classes. Implications for continued development and behavior are discussed.

Figure 2 was distorted in production. The correct version is presented in the erratum.] Adolescence is a period of radical normative changes and increased risk for substance use, mood disorders, and physical injury. Researchers have proposed that increases in reward sensitivity (i.e., sensitivity of the behavioral approach system [BAS]) and/or increases in reactivity to all emotional stimuli (i.e., reward and threat sensitivities) lead to these phenomena. The present study is the first longitudinal investigation of changes in reward (i.e., BAS) sensitivity in 9- to 23-year-olds across a 2-year follow-up. Support was found for increased reward sensitivity from early to late adolescence, and evidence was found for decline in the early 20s. This decline is combined with a decrease in left nucleus accumbens (Nacc) volume, a key structure for reward processing, from the late teens into the early 20s. Furthermore, we found longitudinal increases in sensitivity to reward to be predicted by individual differences in the Nacc and medial orbitofrontal cortex (OFC) volumes at baseline in this developmental sample. Similarly, increases in sensitivity to threat (i.e., behavioral inhibition system sensitivity) were qualified by sex, with only females participants experiencing this increase, and predicted by individual differences in lateral OFC volumes at baseline., (PsycINFO Database Record (c) 2012 APA, all rights reserved.)

Healthy participants (n = 79), ages 9-23, completed a delay discounting task assessing the extent to which the value of a monetary reward declines as the delay to its receipt increases. Diffusion tensor imaging (DTI) was used to evaluate how individual differences in delay discounting relate to variation in fractional anisotropy (FA) and mean diffusivity (MD) within whole-brain white matter using voxel-based regressions. Given that rapid prefrontal lobe development is occurring during this age range and that functional imaging studies have implicated the prefrontal cortex in discounting behavior, we hypothesized that differences in FA and MD would be associated with alterations in the discounting rate. The analyses revealed a number of clusters where less impulsive performance on the delay discounting task was associated with higher FA and lower MD. The clusters were located primarily in bilateral frontal and temporal lobes and were localized within white matter tracts, including portions of the inferior and superior longitudinal fasciculi, anterior thalamic radiation, uncinate fasciculus, inferior fronto-occipital fasciculus, corticospinal tract, and splenium of the corpus callosum. FA increased and MD decreased with age in the majority of these regions. Some, but not all, of the discounting/DTI associations remained significant after controlling for age. Findings are discussed in terms of both developmental and age-independent effects of white matter organization on discounting behavior.

Studies of adults with schizophrenia provide converging evidence for abnormalities in the limbic system. Limbic structures that show consistent patient/control differences in both postmortem and neuroimaging studies include the anterior cingulate and hippocampus, although differences in the amygdala, parahippocampal gyrus, and fornix have also been observed. Studies of white matter in children and adolescents with schizophrenia tend to show findings that are more focal than those seen in adults. Interestingly, these focal abnormalities in early-onset schizophrenia tend to be more localized to limbic regions. While it is unclear if these early limbic abnormalities are primary in the etiology of schizophrenia, there is evidence that supports a developmental progression with early limbic abnormalities evolving over time to match the neuroimaging profiles seen in adults with schizophrenia. Alternatively, the aberrations in limbic structures may be secondary to a more widespread or global pathological processes occurring with the brain that disrupt neural transmission. The goal of this article is to provide a review of the limbic system and limbic network abnormalities reported in children and adolescents with schizophrenia. These findings are compared with the adult literature and placed within a developmental context. These observations from neuroimaging studies enrich our current understanding of the neurodevelopmental model of schizophrenia and raise further questions about primary vs secondary processes. Additional research within a developmental framework is necessary to determine the putative etiologic roles for limbic and other brain abnormalities in early-onset schizophrenia.

Background: Use of MDMA (ecstasy), a serotonin neurotoxin, has been associated with memory impairment and psychological dysfunction. This study examined cognitive functioning in abstinent MDMA users and MDMA-naive controls., Method: Participants completed measures of intelligence, motor function, attention, memory span, verbal fluency, immediate and delayed verbal memory, and working memory. They were also assessed for the presence of psychopathology. In addition to comparing cognitive function in MDMA users relative to controls, the possibility that clinically dysfunctional MDMA use increases the risk of cognitive impairment was examined., Results: MDMA users exhibited relative deficits in mnemonic and executive functions. Additionally, users that met DSM-IV substance use disorder criteria for lifetime MDMA abuse or dependence exhibited a number of additional deficits relative to those who did not meet these criteria., Conclusion: These findings suggest that clinically dysfunctional, rather than purely recreational, MDMA use is associated with cognitive impairment. Future research studies of diverse samples of users may shed light on the mechanisms that underlie these differences.

The prefrontal cortex modulates executive control processes and structurally matures throughout adolescence. Consistent with these events, prefrontal functions that demand high levels of executive control may mature later than those that require working memory but decreased control. To test this hypothesis, adolescents (9 to 20 years old) completed nonverbal working memory tasks with varying levels of executive demands. Findings suggest that recall-guided action for single units of spatial information develops until 11 to 12 years. The ability to maintain and manipulate multiple spatial units develops until 13 to 15 years. Strategic self-organization develops until ages 16 to 17 years. Recognition memory did not appear to develop over this age range. Implications for prefrontal cortex organization by level of processing are discussed.

Healthy adolescents (79 girls, 66 boys), ages 9-17, completed the Iowa Gambling Task (IGT; A. Bechara, A. R. Damasio, H. Damasio, & S. W. Anderson, 1994) as well as working memory (digit span) and behavioral inhibition (go/no-go) tasks. Cross-sectional age-related changes were seen on all 3 tasks. Gender differences were seen in IGT deck preference and attentional variables (i.e., go/no-go hit rate and forward digit span). After age, gender, and general intellectual abilities were controlled for, IGT performance was not predicted by working memory or behavioral inhibition scores. Findings suggest that the ventromedial prefrontal cortex or its connections are functionally maturing during adolescence in a manner that can be distinguished from maturation of other prefrontal regions. Development of these functions may continue into young adulthood.

Temporal stability of individual differences is an important prerequisite for accurate tracking of prospective relationships between neurocognition and real-world behavioral outcomes such as substance abuse and psychopathology. Here we report age-related changes and longitudinal test-retest stability (TRS) for the Neurocognition battery of the Adolescent Brain and Cognitive Development (ABCD) study, which included the NIH Toolbox (TB) Cognitive Domain and additional memory and visuospatial processing tests administered at baseline (ages 9-11) and two-year follow-up. As expected, performance improved significantly with age, but the effect size varied broadly, with Pattern Comparison and the Crystallized Cognition Composite showing the largest age-related gain (Cohen's d:.99 and.97, respectively). TRS ranged from fair (Flanker test: r = 0.44) to excellent (Crystallized Cognition Composite: r = 0.82). A comparison of longitudinal changes and cross-sectional age-related differences within baseline and follow-up assessments suggested that, for some measures, longitudinal changes may be confounded by practice effects and differences in task stimuli or procedure between baseline and follow-up. In conclusion, a subset of measures showed good stability of individual differences despite significant age-related changes, warranting their use as prospective predictors. However, caution is needed in the interpretation of observed longitudinal changes as indicators of neurocognitive development.

The Adolescent Brain Cognitive Development (ABCD) study is poised to be the largest single-cohort long-term longitudinal study of neurodevelopment and child health in the United States. Baseline data on N= 4521 children aged 9-10 were released for public access on November 2, 2018. In this paper we performed principal component analyses of the neurocognitive assessments administered to the baseline sample. The neurocognitive battery included seven measures from the NIH Toolbox as well as five other tasks. We implemented a Bayesian Probabilistic Principal Components Analysis (BPPCA) model that incorporated nesting of subjects within families and within data collection sites. We extracted varimax-rotated component scores from a three-component model and associated these scores with parent-rated Child Behavior Checklist (CBCL) internalizing, externalizing, and stress reactivity. We found evidence for three broad components that encompass general cognitive ability, executive function, and learning/memory. These were significantly associated with CBCL scores in a differential manner but with small effect sizes. These findings set the stage for longitudinal analysis of neurocognitive and psychopathological data from the ABCD cohort as they age into the period of maximal adolescent risk-taking.

Background: Cannabis is increasingly perceived as a harmless drug by recreational users, yet chronic use may impact brain changes into adulthood. Repeated cannabis exposure has been associated with enduring synaptic changes in executive control and reward networks. It is important to determine whether there are brain functional alterations within these networks in individuals that do not seek treatment for chronic cannabis abuse. Methods: This longitudinal study compared resting-state functional connectivity changes in executive control and reward networks between 23 non-treatment-seeking young adults with cannabis use disorder (6 females; baseline age M = 19.3 ± 1.18) and 21 age-matched controls (10 females; baseline age M = 19.4 ± 0.65) to determine group differences in the temporal trajectories of resting-state functional connectivity across a 2-year span. Results: Results showed i) significant increases in resting-state functional connectivity between the caudal anterior cingulate cortex and precentral and parietal regions over time in the control group, but not in the cannabis use disorder group, and ii) sustained lower resting-state functional connectivity of anterior cingulate cortex seeds with frontal and thalamic regions in the cannabis use disorder group vs. the age-matched controls. Resting-state functional connectivity strength was correlated with cannabis use patterns in the cannabis use disorder sample. Conclusion: Longitudinal alterations in intrinsic functional organization of executive control networks found in non-treatment-seeking young adults with cannabis use disorder (when compared to age-matched controls) may impact regulatory control over substance use behavior. Current findings were limited to examining executive control and reward networks seeded in ACC and NAcc, respectively. Future studies with larger sample sizes and enough power are needed to conduct exploratory analyses examining rsFC of other networks beyond those within the scope of the current study. [ABSTRACT FROM AUTHOR]