한빛사 논문
Bo-yong Park1,2,*, Seok-Jun Hong1,3,4,5, Sofie L. Valk6,7, Casey Paquola1, Oualid Benkarim1, Richard A. I. Bethlehem8,9, Adriana Di Martino3, Michael P. Milham3, Alessandro Gozzi10, B. T. Thomas Yeo11,12,13,14,15, Jonathan Smallwood16,17 & Boris C. Bernhardt1,*
1McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada. 2Department of Data Science, Inha University, Incheon, South Korea. 3Center for the Developing Brain, Child Mind Institute, New York City, NY, USA. 4Center for Neuroscience Imaging Research, Institute for Basic Science, Sungkyunkwan University, Suwon, South Korea. 5Department of Biomedical Engineering, Sungkyunkwan University, Suwon, South Korea. 6Forschungszentrum, Julich, Germany. 7Max Planck Institute for Cognitive and Brain Sciences, Leipzig, Germany. 8Autism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge, UK. 9Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Cambridge, UK. 10Istituto Italiano di Tecnologia, Centre for Neuroscience and Cognitive Systems @ UNITN, Rovereto, Italy. 11Department of Electrical and Computer Engineering, National University of Singapore, Singapore, Singapore. 12Centre for Sleep and Cognition (CSC) & Centre for Translational Magnetic Resonance Research (TMR), National University of Singapore, Singapore, Singapore. 13N.1 Institute for Health & Institute for Digital Medicine (WisDM), National University of Singapore, Singapore, Singapore. 14Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA. 15Integrative Sciences and Engineering Programme (ISEP), National University of Singapore, Singapore, Singapore. 16Department of Psychology, York Neuroimaging Centre, University of York, York, UK. 17Department of Psychology, Queen’s University, Kingston, ON, Canada.
*Corresponding author
Abstract
The pathophysiology of autism has been suggested to involve a combination of both macroscale connectome miswiring and microcircuit anomalies. Here, we combine connectome-wide manifold learning with biophysical simulation models to understand associations between global network perturbations and microcircuit dysfunctions in autism. We studied neuroimaging and phenotypic data in 47 individuals with autism and 37 typically developing controls obtained from the Autism Brain Imaging Data Exchange initiative. Our analysis establishes significant differences in structural connectome organization in individuals with autism relative to controls, with strong between-group effects in low-level somatosensory regions and moderate effects in high-level association cortices. Computational models reveal that the degree of macroscale anomalies is related to atypical increases of recurrent excitation/inhibition, as well as subcortical inputs into cortical microcircuits, especially in sensory and motor areas. Transcriptomic association analysis based on postmortem datasets identifies genes expressed in cortical and thalamic areas from childhood to young adulthood. Finally, supervised machine learning finds that the macroscale perturbations are associated with symptom severity scores on the Autism Diagnostic Observation Schedule. Together, our analyses suggest that atypical subcortico-cortical interactions are associated with both microcircuit and macroscale connectome differences in autism.
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