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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.

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.

In this work, we expand the normative model repository introduced in Rutherford et al., 2022a to include normative models charting lifespan trajectories of structural surface area and brain functional connectivity, measured using two unique resting-state network atlases (Yeo-17 and Smith-10), and an updated online platform for transferring these models to new data sources. We showcase the value of these models with a head-to-head comparison between the features output by normative modeling and raw data features in several benchmarking tasks: mass univariate group difference testing (schizophrenia versus control), classification (schizophrenia versus control), and regression (predicting general cognitive ability). Across all benchmarks, we show the advantage of using normative modeling features, with the strongest statistically significant results demonstrated in the group difference testing and classification tasks. We intend for these accessible resources to facilitate the wider adoption of normative modeling across the neuroimaging community.

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

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.

Defining reference models for population variation, and the ability to study individual deviations is essential for understanding inter-individual variability and its relation to the onset and progression of medical conditions. In this work, we assembled a reference cohort of neuroimaging data from 82 sites (N=58,836; ages 2–100) and used normative modeling to characterize lifespan trajectories of cortical thickness and subcortical volume. Models are validated against a manually quality checked subset (N=24,354) and we provide an interface for transferring to new data sources. We showcase the clinical value by applying the models to a transdiagnostic psychiatric sample (N=1985), showing they can be used to quantify variability underlying multiple disorders whilst also refining case-control inferences. These models will be augmented with additional samples and imaging modalities as they become available. This provides a common reference platform to bind results from different studies and ultimately paves the way for personalized clinical decision-making.

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.

The problem of moral compliance is the problem of explaining how moral norms are sustained over extented stretches of time despite the existence of selfish evolutionary incentives that favor their violation. There are, broadly speaking, two kinds of solutions that have been offered to the problem of moral compliance, the reciprocity-based account and the punishment-based account. In this paper, I argue that though the reciprocity-based account has been widely endorsed by evolutionary theorists, the account is in fact deeply implausible. I provide three arguments that suggest that moral norms are sustained by punishment, not reciprocity. But in addition to solving the problem of moral compliance, the punishment-based account provides an additional important theoretical dividend. It points the way for how theorists might build an evolutionary account of a feature of human groups that has long fascinated and troubled social scientists and moral philosophers – the existence of moral diversity. [ABSTRACT FROM AUTHOR]