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Different Brain Networks Underlying Intelligence In Autism Spectrum Disorders And Typically Developing Children

By Emmanuel P. K. Pua, Charles B Malpas, Stephen C Bowden, Marc L Seal

Posted 30 May 2017
bioRxiv DOI: 10.1101/143891 (published DOI: 10.1002/hbm.24074)

Background: There has been sustained clinical and cognitive neuroscience research interest in how network correlates of brain-behaviour relationships might be altered in Autism Spectrum Disorders (ASD) and other neurodevelopmental disorders. As previous work has mostly focused on adults, the nature of whole-brain connectivity networks underlying intelligence in pediatric cohorts with abnormal neurodevelopment requires further investigation. Methods: We used network-based statistics (NBS) to examine the association between resting-state functional Magnetic Resonance Imaging (fMRI) connectivity and fluid intelligence ability in male children (n=50) with Autism Spectrum Disorders (ASD; M=10.45, SD=1.58 years and in controls (M=10.38, SD=0.96 years) matched on fluid intelligence performance, age and sex. Repeat analyses were performed in independent sites for validation and replication. Results: Despite being equivalent on fluid intelligence ability to strictly matched neurotypical controls, boys with ASD displayed a subnetwork of significantly increased associations between functional connectivity and fluid intelligence. Between-group differences remained significant at higher edge thresholding, and results were validated in independent-site replication analyses in an equivalent age and sex-matched cohort with ASD. Regions consistently implicated in atypical connectivity correlates of fluid intelligence in ASD were the angular gyrus, posterior middle temporal gyrus, occipital and temporo-occipital regions. Conclusion: Development of fluid intelligence neural correlates in young ASD males is aberrant, with an increased strength in intrinsic connectivity association during childhood. Alterations in whole-brain network correlates of fluid intelligence in ASD may be a compensatory mechanism that allows equal task performance to neurotypical peers.

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