Reduced tract integrity of the model for social communication is a neural substrate of social communication deficits in autism spectrum disorder.
BACKGROUND
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with social communication deficits as one of the core symptoms. Recently, a five-level model for the social communication has been proposed in which white matter tracts corresponding to each level of the model are identified. Given that the model for social communication subserves social language functions, we hypothesized that the tract integrity of the model for social communication may be reduced in ASD, and the reduction may be related to social communication deficits.


METHODS
Sixty-two right-handed boys with ASD and 55 typically developing (TD) boys received clinical evaluations, intelligence tests, the Social Communication Questionnaire (SCQ), and MRI scans. Generalized fractional anisotropy (GFA) was measured by diffusion spectrum imaging to indicate the microstructural integrity of the tracts for each level of the social communication model. Group difference in the tract integrity and its relationship with the SCQ subscales of social communication and social interaction were investigated.


RESULTS
We found that the GFA values of the superior longitudinal fasciculus III (SLF III, level 1) and the frontal aslant tracts (FAT, level 2) were decreased in ASD compared to TD. Moreover, the GFA values of the SLF III and the FAT were associated with the social interaction subscale in ASD.


CONCLUSIONS
The tract integrity of the model for social communication is reduced in ASD, and the reduction is associated with impaired social interaction. Our results support that reduced tract integrity of the model for social communication might be a neural substrate of social communication deficits in ASD.
Institute of Medical Device and Imaging, National Taiwan University College of Medicine, Taipei, Taiwan.|The Ph.D. Program for Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Yu-Chun
YC
Lo
Institute of Medical Device and Imaging, National Taiwan University College of Medicine, Taipei, Taiwan.
Yu-Jen
YJ
Chen
Institute of Medical Device and Imaging, National Taiwan University College of Medicine, Taipei, Taiwan.
Yung-Chin
YC
Hsu
Institute of Medical Device and Imaging, National Taiwan University College of Medicine, Taipei, Taiwan.|Institute of Brain and Mind Sciences, National Taiwan University, Taipei, Taiwan.|Neurobiology and Cognitive Science Center, National Taiwan University, Taipei, Taiwan.|Department of Medical Imaging, National Taiwan University Hospital, Taipei, Taiwan.|Molecular Imaging Center, National Taiwan University, Taipei, Taiwan.
Wen-Yih Isaac
WI
Tseng
Institute of Brain and Mind Sciences, National Taiwan University, Taipei, Taiwan.|Neurobiology and Cognitive Science Center, National Taiwan University, Taipei, Taiwan.|Department of Psychiatry, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan.
Susan Shur-Fen
SS
Gau
D000293:Adolescent; D000328:Adult; D000067877:Autism Spectrum Disorder / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D002648:Child; D003142:Communication; D056324:Diffusion Tensor Imaging; D006801:Humans; D007398:Interpersonal Relations; D008297:Male; D008959:Models, Neurological; D009434:Neural Pathways / Q000000981:diagnostic imaging; D066127:White Matter / Q000000981:diagnostic imaging*; D055815:Young Adult
Autism spectrum disorders; brain imaging; communication