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We developed a novel Proactive Reactive and Attentional Dynamics (PRAD) computational model designed to dissect the latent mechanisms of inhibitory control in human cognition. Leveraging data from over 7,500 participants in the NIH Adolescent Brain Cognitive Development study, we demonstrate that PRAD surpasses traditional models by integrating proactive, reactive, and attentional components of inhibitory control. Employing a hierarchical Bayesian framework, PRAD offers a granular view of the dynamics underpinning action execution and inhibition, provides debiased estimates of stop-signal reaction times, and elucidates individual and temporal variability in cognitive control processes. Our findings reveal significant intra-individual variability, challenging conventional assumptions of random variability across trials. By addressing nonergodicity and systematically accounting for the multi-componential nature of cognitive control, PRAD advances our understanding of the cognitive mechanisms driving individual differences in cognitive control and provides a sophisticated computational framework for dissecting dynamic cognitive processes across diverse populations. 

Nonergodicity and Simpson’s paradox present significant, yet underappreciated challenges in neuroscience. Leveraging brain imaging and behavioral data from over 4,000 children and a Bayesian computational model of cognitive dynamics, we investigated brain-behavior relationships underlying cognitive control at both between-subjects and within-subjects levels. Strikingly, we observed a reversal of associations of inhibitory control brain activations with dynamic behavioral measures when comparing between-subjects and within-subjects analyses, revealing the nonergodic nature of these processes. This nonergodicity was pervasive throughout the brain but most pronounced in the salience network. Additionally, within-subjects analysis uncovered dissociated brain representations of reactive and proactive control processes, as well as distinct brain-behavior associations for individuals who adaptively versus maladaptively regulated cognitive control. Our findings offer insights into dynamic neural mechanisms of cognitive control during a critical developmental period. This work highlights the importance of embracing nonergodicity in human neuroscience, with implications for both theoretical understanding and applications to AI and psychopathology. 

Learning disabilities affect a significant proportion of children worldwide, with far-reaching consequences for their academic, professional, and personal lives. Here we develop digital twins – biologically plausible personalized Deep Neural Networks (pDNNs) – to investigate the neurophysiological mechanisms underlying learning disabilities in children. Our pDNN reproduces behavioral and neural activity patterns observed in affected children, including lower performance accuracy, slower learning rates, neural hyper-excitability, and reduced neural differentiation of numerical problems. Crucially, pDNN models reveal aberrancies in the geometry of manifold structure, providing a comprehensive view of how neural excitability influences both learning performance and the internal structure of neural representations. Our findings not only advance knowledge of the neurophysiological underpinnings of learning differences but also open avenues for targeted, personalized strategies designed to bridge cognitive gaps in affected children. This work reveals the power of digital twins integrating AI and neuroscience to uncover mechanisms underlying neurodevelopmental disorders. 

Abstract Number sense, the ability to decipher quantity, forms the foundation for mathematical cognition. How number sense emerges with learning is, however, not known. Here we use a biologically-inspired neural architecture comprising cortical layers V1, V2, V3, and intraparietal sulcus (IPS) to investigate how neural representations change with numerosity training. Learning dramatically reorganized neuronal tuning properties at both the single unit and population levels, resulting in the emergence of sharply-tuned representations of numerosity in the IPS layer. Ablation analysis revealed that spontaneous number neurons observed prior to learning were not critical to formation of number representations post-learning. Crucially, multidimensional scaling of population responses revealed the emergence of absolute and relative magnitude representations of quantity, including mid-point anchoring. These learnt representations may underlie changes from logarithmic to cyclic and linear mental number lines that are characteristic of number sense development in humans. Our findings elucidate mechanisms by which learning builds novel representations supporting number sense. 

Abstract Efficient memory-based problem-solving strategies are a cardinal feature of expertise across a wide range of cognitive domains in childhood. However, little is known about the neurocognitive mechanisms that underlie the acquisition of efficient memory-based problem-solving strategies. Here we develop, to the best of our knowledge, a novel neurocognitive process model of latent memory processes to investigate how cognitive training designed to improve children’s problem-solving skills alters brain network organization and leads to increased use and efficiency of memory retrieval-based strategies. We found that training increased both the use and efficiency of memory retrieval. Functional brain network analysis revealed training-induced changes in modular network organization, characterized by increase in network modules and reorganization of hippocampal-cortical circuits. Critically, training-related changes in modular network organization predicted performance gains, with emergent hippocampal, rather than parietal cortex, circuitry driving gains in efficiency of memory retrieval. Our findings elucidate a neurocognitive process model of brain network mechanisms that drive learning and gains in children’s efficient problem-solving strategies.