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SH3 and Multiple Ankyrin Repeat Domains 3 ( SHANK3 )-caused autism spectrum disorder (ASD) may present a unique opportunity to clarify the heterogeneous neuropathological mechanisms of ASD. However, the specificity and commonality of disrupted large-scale brain organization in  SHANK3- deficient children remain largely unknown. The present study combined genetic tests, neurobehavioral evaluations, and magnetic resonance imaging, aiming to explore the disruptions of both local and networked cortical structural organization in ASD children with and without  SHANK3  deficiency. Multiple surface morphological parameters such as cortical thickness (CT) and sulcus depth were estimated, and the graph theory was adopted to characterize the topological properties of structural covariance networks (SCNs). Finally, a correlation analysis between the alterations in brain morphological features and the neurobehavioral evaluations was performed. Compared with typically developed children, increased CT and reduced nodal degree were found in both ASD children with and without  SHANK3  defects mainly in the lateral temporal cortex, prefrontal cortex (PFC), temporo-parietal junction (TPJ), superior temporal gyrus (STG), and limbic/paralimbic regions. Besides commonality, our findings showed some distinct abnormalities in ASD children with  SHANK3  defects compared to those without. Locally, more changes in the STG and orbitofrontal cortex were exhibited in ASD children with  SHANK3  defects, while more changes in the TPJ and inferior parietal lobe (IPL) in those without  SHANK3  defects were observed. For the SCNs, a trend toward regular network topology was observed in ASD children with  SHANK3  defects, but not in those without. In addition, ASD children with  SHANK3  defects showed more alterations of nodal degrees in the anterior and posterior cingulate cortices and right insular, while there were more disruptions in the sensorimotor areas and the left insular and dorsomedial PFC in ASD without  SHANK3  defects. Our findings indicate dissociable disruptions of local and networked brain morphological features in ASD children with and without  SHANK3  deficiency. Moreover, this monogenic study may provide a valuable path for parsing the heterogeneity of brain disturbances in ASD.

Common and Distinct Disruptions of Cortical Surface Morphology Between Autism Spectrum Disorder Children With and Without SHANK3 Deficiency