developmental maturation of dynamic causal control signals in higher-order cognition a neurocognitive network model发育成熟的动态因果控制信号高阶认知神经认知网络模型.pdfVIP

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developmental maturation of dynamic causal control signals in higher-order cognition a neurocognitive network model发育成熟的动态因果控制信号高阶认知神经认知网络模型.pdf

developmental maturation of dynamic causal control signals in higher-order cognition a neurocognitive network model发育成熟的动态因果控制信号高阶认知神经认知网络模型

Developmental Maturation of Dynamic Causal Control Signals in Higher-Order Cognition: A Neurocognitive Network Model 1 1,2,3 Kaustubh Supekar *, Vinod Menon * 1 Department of Psychiatry Behavioral Sciences, Stanford University School of Medicine, Stanford, California, United States of America, 2 Department of Neurology Neurological Sciences, Stanford University School of Medicine, Stanford, California, United States of America, 3 Program in Neuroscience, Stanford University School of Medicine, Stanford, California, United States of America Abstract Cognitive skills undergo protracted developmental changes resulting in proficiencies that are a hallmark of human cognition. One skill that develops over time is the ability to problem solve, which in turn relies on cognitive control and attention abilities. Here we use a novel multimodal neurocognitive network-based approach combining task-related fMRI, resting-state fMRI and diffusion tensor imaging (DTI) to investigate the maturation of control processes underlying problem solving skills in 7–9 year-old children. Our analysis focused on two key neurocognitive networks implicated in a wide range of cognitive tasks including control: the insula-cingulate salience network, anchored in anterior insula (AI), ventrolateral prefrontal cortex and anterior cingulate cortex, and the fronto-parietal central executive network, anchored in dorsolateral prefrontal cortex and posterior parietal cortex (PPC). We found that, by age 9, the AI node of the salience network is a major causal hub initiating control signals during problem solving. Critically, despite stronger AI activation, the strength of causal regulatory influences from AI to the PPC node of the central executive network was significantly weaker and contributed to

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