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Environmental stressors present negative consequences for development. However, their impact on relevant neurocognitive processes, particularly in underrepresented samples, is less clear. The current project aims to examine how adverse experiences influence efficiency of evidence accumulation and neural connectivity in adolescents. The study included 199 adolescents from the Future of Families and Child Wellbeing Study, a population-based longitudinal cohort study with substantial representation of youths from disadvantaged backgrounds. Participants completed an emotional-faces, gender-identification task while undergoing functional MRI. Reaction times (RT) and responses were recorded and fitted with a drift diffusion model. Parameters were estimated using the Dynamic Model of Choice software, which provides a better characterization of the underlying cognitive mechanisms compared with using RTs or cognitive batteries. Analyses investigating the impact of adverse experiences to drift rate and functional connectivity are underway. Results from this study will provide a better understanding of adversity on neurocognitive mechanisms in adolescents.

Abstract Efficiency of evidence accumulation (EEA), an individual’s ability to selectively gather goal-relevant information to make adaptive choices, is thought to be a key neurocomputational mechanism associated with cognitive functioning and transdiagnostic risk for psychopathology. However, the neural basis of individual differences in EEA is poorly understood, especially regarding the role of largescale brain network dynamics. We leverage data from 5198 participants from the Human Connectome Project and Adolescent Brain Cognitive Development Study to demonstrate a strong association between EEA and flexible adaptation to cognitive demand in the “task-positive” frontoparietal and dorsal attention networks. Notably, individuals with higher EEA displayed divergent task-positive network activation across n-back task conditions: higher activation under high cognitive demand (2-back) and lower activation under low demand (0-back). These findings suggest that brain networks’ flexible adaptation to cognitive demands is a key neural underpinning of EEA.

This study aimed to clarify the psychometric properties and development of Go/No-Go (GNG) task-related neural activation across critical periods of neurobiological maturation by examining its longitudinal stability, factor structure, developmental change, and associations with a computational index of task-general cognitive control. A longitudinal sample (N=289) of adolescents from the Michigan Longitudinal Study was assessed at four time-points (mean number of timepoints per participant=2.05; standard deviation=0.89) spanning early adolescence (ages 10−13) to young adulthood (22−25). Results suggested that regional neural activations from the “successful inhibition” (SI>GO) and “failed inhibition” (FI>GO; error-monitoring) contrasts are each described well by a single general factor. Neural activity across both contrasts showed developmental increases throughout adolescence that plateau in young adulthood. Neural activity metrics evidenced low temporal stability across this period of marked developmental change, and the SI>GO factor showed no relations with a behavioral index of cognitive control. The FI>GO factor displayed stronger criterion validity in the form of significant, positive associations with behaviorally measured cognitive control. Findings emphasize the utility of well-validated psychometric methods and longitudinal data for clarifying the measurement properties of functional neuroimaging metrics and improving measurement practices in developmental cognitive neuroscience.

Abstract Childhood attention-deficit/hyperactivity disorder (ADHD) symptoms are believed to result from disrupted neurocognitive development. However, evidence for the clinical and predictive value of neurocognitive assessments in this context has been mixed, and there have been no large-scale efforts to quantify their potential for use in generalizable models that predict individuals’ ADHD symptoms in new data. Using data drawn from the Adolescent Brain Cognitive Development Study (ABCD), a consortium that recruited a diverse sample of over 10,000 youth (ages 9–10 at baseline) across 21 U.S. sites, we develop and test cross-validated machine learning models for predicting youths’ ADHD symptoms using neurocognitive abilities, demographics, and child and family characteristics. Models used baseline demographic and biometric measures, geocoded neighborhood data, youth reports of child and family characteristics, and neurocognitive tests to predict parent- and teacher-reported ADHD symptoms at the 1-year and 2-year follow-up time points. Predictive models explained 15–20% of the variance in 1-year ADHD symptoms for ABCD Study sites that were left out of the model-fitting process and 12–13% of the variance in 2-year ADHD symptoms. Models displayed high generalizability across study sites and trivial loss of predictive power when transferred from training data to left-out data. Features from multiple domains contributed meaningfully to prediction, including neurocognition, sex, self-reported impulsivity, parental monitoring, and screen time. This work quantifies the information value of neurocognitive abilities and other child characteristics for predicting ADHD symptoms and provides a foundational method for predicting individual youths’ symptoms in new data across contexts.

Studies of reward effects on behavior in adolescence typically rely on performance metrics that confound myriad cognitive and non-cognitive processes, making it challenging to determine which process is impacted by reward. The present longitudinal study applied the diffusion decision model to a reward task to isolate the influence of reward on response caution from influences of processing and motor speed. Participants completed three annual assessments from early to middle adolescence (N = 387, 55% female, M[subscript age] = 12.1 at Wave 1; M[subscript age] = 13.1 at Wave 2, M[subscript age] = 14.1 at Wave 3) and three annual assessments in late adolescence (M[subscript ages] = 17.8, 18.9, 19.9). At each assessment, participants completed a two-choice reaction time task under conditions of no-reward and a block in which points were awarded for speeded accuracy. Reward reduced response caution at all waves, as expected, but had a greater impact as teens moved from early to middle adolescence. Simulations to identify optimal response caution showed that teens were overly cautious in early adolescence but became too focused on speed over accuracy by middle adolescence. By late adolescence, participants adopted response styles that maximized reward. Further, response style was associated with both internalizing and externalizing symptoms in early-to-middle adolescence, providing evidence for the construct validity of a diffusion model approach in this developmental period.

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.

The Adolescent Brain Cognitive Development (ABCD) Study is a longitudinal neuroimaging study of unprecedented scale that is in the process of following over 11,000 youth from middle childhood though age 20. However, a design feature of the study's stop-signal task violates ''context independence'', an assumption critical to current non-parametric methods for estimating stop-signal reaction time (SSRT), a key measure of inhibitory ability in the study. This has led some experts to call for the task to be changed and for previously collected data to be used with caution. We present a cognitive process modeling framework, the RDEX-ABCD model, that provides a parsimonious explanation for the impact of this design feature on “go” stimulus processing and successfully accounts for key behavioral trends in the ABCD data. Simulation studies using this model suggest that failing to account for the context independence violations in the ABCD design can lead to erroneous inferences in several realistic scenarios. However, we demonstrate that RDEX-ABCD effectively addresses these violations and can be used to accurately measure SSRT along with an array of additional mechanistic parameters of interest (e.g., attention to the stop signal, cognitive efficiency), advancing investigators’ ability to draw valid and nuanced inferences from ABCD data. Availability of data and materials: Data from the ABCD Study are available through the NIH Data Archive (NDA): nda.nih.gov/abcd. Code for all analyses featured in this study is openly available on the Open Science Framework (OSF): osf.io/2h8a7/.

Little is known about how exposure to limited socioeconomic resources (SER) in childhood gets “under the skin” to shape brain development, especially using rigorous whole-brain multivariate methods in large, adequately powered samples. The present study examined resting state functional connectivity patterns from 5821 youth in the Adolescent Brain Cognitive Development (ABCD) study, employing multivariate methods across three levels: whole-brain, network-wise, and connection-wise. Across all three levels, SER was associated with widespread alterations across the connectome. However, critically, we found that parental education was the primary driver of neural associations with SER. These parental education associations with the developing connectome exhibited notable concentrations in somatosensory and subcortical regions, and they were partially accounted for by home enrichment activities, child’s cognitive abilities, and child’s grades, indicating interwoven links between parental education, child stimulation, and child cognitive performance. These results add a new data-driven, multivariate perspective on links between household SER and the child’s developing functional connectome.

Abstract General cognitive ability (GCA) is an individual difference dimension linked to important academic, occupational, and health-related outcomes and its development is strongly linked to differences in socioeconomic status (SES). Complex abilities of the human brain are realized through interconnections among distributed brain regions, but brain-wide connectivity patterns associated with GCA in youth, and the influence of SES on these connectivity patterns, are poorly understood. The present study examined functional connectomes from 5937 9- and 10-year-olds in the Adolescent Brain Cognitive Development (ABCD) multi-site study. Using multivariate predictive modeling methods, we identified whole-brain functional connectivity patterns linked to GCA. In leave-one-site-out cross-validation, we found these connectivity patterns exhibited strong and statistically reliable generalization at 19 out of 19 held-out sites accounting for 18.0% of the variance in GCA scores (cross-validated partial η 2). GCA-related connections were remarkably dispersed across brain networks: across 120 sets of connections linking pairs of large-scale networks, significantly elevated GCA-related connectivity was found in 110 of them, and differences in levels of GCA-related connectivity across brain networks were notably modest. Consistent with prior work, socioeconomic status was a strong predictor of GCA in this sample, and we found that distributed GCA-related brain connectivity patterns significantly statistically mediated this relationship (mean proportion mediated: 15.6%, p

Abstract Convergent research identifies a general factor (“P factor”) that confers transdiagnostic risk for psychopathology. Large-scale networks are key organizational units of the human brain. However, studies of altered network connectivity patterns associated with the P factor are limited, especially in early adolescence when most mental disorders are first emerging. We studied 11,875 9- and 10-year olds from the Adolescent Brain and Cognitive Development (ABCD) study, of whom 6593 had high-quality resting-state scans. Network contingency analysis was used to identify altered interconnections associated with the P factor among 16 large-scale networks. These connectivity changes were then further characterized with quadrant analysis that quantified the directionality of P factor effects in relation to neurotypical patterns of positive versus negative connectivity across connections. The results showed that the P factor was associated with altered connectivity across 28 network cells (i.e., sets of connections linking pairs of networks); p PERMUTATION values

Abstract Women were historically excluded from research participation partly due to the assumption that ovarian hormone fluctuations lead to variation, especially in emotion, that could not be experimentally controlled. Although challenged in principle and practice, relevant empirical data are limited by single measurement occasions. The current paper fills this knowledge gap using data from a 75-day intensive longitudinal study. Three indices of daily affective variability—volatility, emotional inertia, and cyclicity—were evaluated using Bayesian inferential methods in 142 men, naturally cycling women, and women using three different oral contraceptive formulations (that “stabilize” hormone fluctuations). Results provided more evidence for similarities between men and women—and between naturally cycling women and oral contraceptive users—than for differences. Even if differences exist, effects are likely small. Thus, there is little indication that ovarian hormones influence affective variability in women to a greater extent than the biopsychosocial factors that influence daily emotion in men.

Quantifying individual differences in higher-order cognitive functions is a foundational area of cognitive science that also has profound implications for research on psychopathology. For the past 2 decades, the dominant approach in these fields has been to attempt to fractionate higher-order functions into hypothesized components (e.g., inhibition, updating) through a combination of experimental manipulation and factor analysis. However, the putative constructs obtained through this paradigm have recently been met with substantial criticism on both theoretical and empirical grounds. Concurrently, an alternative approach has emerged focusing on parameters of formal computational models of cognition that have been developed in mathematical psychology. These models posit biologically plausible and experimentally validated explanations of the data-generating process for cognitive tasks, allowing them to be used to measure the latent mechanisms that underlie performance. One of the primary insights provided by recent applications of this approach is that individual and clinical differences in performance on a wide variety of cognitive tasks, ranging from simple choice tasks to complex executive paradigms, are largely driven by efficiency of evidence accumulation, a computational mechanism defined by sequential sampling models. This review assembles evidence for the hypothesis that efficiency of evidence accumulation is a central individual difference dimension that explains neurocognitive deficits in multiple clinical disorders and identifies ways in which this insight can advance clinical neuroscience research. We propose that recognition of efficiency of evidence accumulation as a major driver of neurocognitive differences will allow the field to make clearer inferences about cognitive abnormalities in psychopathology and their links to neurobiology.

Abstract To what extent does gender expression vary day-to-day? Are daily changes related to psychological adjustment in the same way for all individuals? A person-specific approach was used to answer these questions in a 75-day intensive longitudinal study. Fifty-seven cisgender adults (27 women) provided over 4000 reports of daily masculinity and femininity and of three indices of internalizing problems. Results revealed: (a) substantial daily fluctuations in gender expression, especially in women; (b) sample-level links between daily increases in femininity or reductions in masculinity and heightened anxiety, depression, and self-reproach for men, but no apparent links for women; and (c) person-specific links between gender expression and psychological adjustment, such that some women reported internalizing problems with reduced masculinity (average male pattern) and some men reported problems with heightened masculinity (opposite the average male pattern). Findings highlight how intensive longitudinal research can illuminate the uniqueness of gender-related daily experiences, and their implications for the wellbeing of individuals.

The purpose of this study was to examine if personality traits can be used to characterize subgroups of youth diagnosed with childhood-onset conduct disorder (CD). Participants were 11,552 youth from the Adolescent Brain Cognitive Development study. Data used in this report came from doi: 10.15154/1504041 (M age 9.92; 45.3% female, 49.6% white, 19.0% Hispanic). A subset of this sample (n = 365) met criteria for CD. Latent profile analyses (LPA) were performed on this subgroup (n = 365) to define profiles of individuals with CD based on self-report measures of impulsivity, punishment sensitivity, reward response, and callous-unemotional traits. Follow up analyses determined if these groups differed on clinically relevant variables including psychopathology, environmental risk factors, social risk factors, and neurocognitive functioning. Participants with a CD diagnosis scored significantly higher on psychological, environmental, social, and neurocognitive risk factors. The LPA revealed three unique profiles, which differed significantly on liability for broad psychopathology and domain-specific liability for externalizing psychopathology but were largely matched on environmental and social risk factors. These unique configurations provide a useful way to further parse clinically relevant subgroups within youth who meet criteria for childhood-onset CD, setting the stage for prospective longitudinal research using these latent profiles to better understand the development of youth with childhood-onset CD.

Abstract Introduction Phenomena related to reward responsiveness have been extensively studied in their associations with substance use and socioemotional functioning. One important task in this literature is the Monetary Incentive Delay (MID) task. By cueing and delivering performance‐contingent reward, the MID task has been demonstrated to elicit robust activation of neural circuits involved in different phases of reward responsiveness. However, systematic evaluations of common MID task contrasts have been limited to between‐study comparisons of group‐level activation maps, limiting their ability to directly evaluate how researchers’ choice of contrasts impacts conclusions about individual differences in reward responsiveness or brain‐behavior associations. Methods In a sample of 104 participants (Age Mean = 19.3, SD = 1.3), we evaluate similarities and differences between contrasts in: group‐ and individual‐level activation maps using Jaccard's similarity index, region of interest (ROI) mean signal intensities using Pearson's r, and associations between ROI mean signal intensity and psychological measures using Bayesian correlation. Results Our findings demonstrate more similarities than differences between win and loss cues during the anticipation contrast, dissimilarity between some win anticipation contrasts, an apparent deactivation effect in the outcome phase, likely stemming from the blood oxygen level‐dependent undershoot, and behavioral associations that are less robust than previously reported. Conclusion Consistent with recent empirical findings, this work has practical implications for helping researchers interpret prior MID studies and make more informed a priori decisions about how their contrast choices may modify results.

There is substantial interest in identifying biobehavioral dimensions of individual variation that cut across heterogenous disorder categories, and computational models can play a major role in advancing this goal. In this report, we focused on efficiency of evidence accumulation (EEA), a computationally characterized variable derived from sequential sampling models of choice tasks. We created an EEA factor from three behavioral tasks in the UCLA Phenomics dataset (n = 272), which includes healthy participants (n = 130) as well-participants with schizophrenia (n = 50), bipolar disorder (n = 49), and attention-deficit/hyperactivity disorder (n = 43). We found that the EEA factor was significantly reduced in all three disorders, and that it correlated with an overall severity score for psychopathology as well as self-report measures of impulsivity. Although EEA was significantly correlated with general intelligence, it remained associated with psychopathology and symptom scales even after controlling for intelligence scores. Taken together, these findings suggest EEA is a promising computationally-characterized dimension of neurocognitive variation, with diminished EEA conferring transdiagnostic vulnerability to psychopathology.