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Article: Decreased homotopic interhemispheric functional connectivity in children with autism spectrum disorder

TitleDecreased homotopic interhemispheric functional connectivity in children with autism spectrum disorder
Authors
Keywordsautism spectrum disorder
children
corpus callosum
homotopic interhemispheric functional connectivity
resting-state
Issue Date2021
Citation
Autism Research, 2021, v. 14, n. 8, p. 1609-1620 How to Cite?
AbstractWhile several functional and structural changes occur in large-scale brain networks in autism spectrum disorder (ASD), reduced interhemispheric resting-state functional connectivity (rsFC) between homotopic regions may be of particular importance as a biomarker. ASD is an early-onset developmental disorder and neural alterations are often age-dependent. Although there is some evidence for homotopic interhemispheric rsFC alterations in language processing regions in ASD children, wider analyses using large data sets have not been performed. The present study, therefore, conducted a voxel-based homotopic interhemispheric rsFC analysis in 146 ASD and 175 typically developing children under-age 10 and examined associations with symptom severity in the autism brain imaging data exchange data sets. Given the role of corpus callosum (CC) in interhemispheric connectivity and reported CC volume changes in ASD we additionally examined whether there were parallel volumetric changes. Results demonstrated decreased homotopic rsFC in ASD children in the posterior cingulate cortex (PCC) and precuneus of the default mode network, the precentral gyrus of the mirror neuron system, and the caudate of the reward system. Homotopic rsFC of the PCC was associated with symptom severity. Furthermore, although no significant CC volume changes were found in ASD children, there was a significant negative correlation between the anterior CC volumes and homotopic rsFC strengths in the caudate. The present study shows that a reduced pattern of homotopic interhemispheric rsFC in ASD adults/adolescents is already present in children of 5–10 years old and further supports their potential use as a general ASD biomarker. Lay summary: Homotopic interhemispheric functional connectivity plays an important role in synchronizing activity between the two hemispheres and is altered in adults and adolescents with autism spectrum disorder (ASD). In the present study focused on children with ASD, we have observed a similar pattern of decreased homotopic connectivity, suggesting that alterations in homotopic interhemispheric connectivity may occur early in ASD and be a useful general biomarker across ages.
Persistent Identifierhttp://hdl.handle.net/10722/330718
ISSN
2023 Impact Factor: 5.3
2023 SCImago Journal Rankings: 1.686
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYao, Shuxia-
dc.contributor.authorZhou, Menghan-
dc.contributor.authorZhang, Yuan-
dc.contributor.authorZhou, Feng-
dc.contributor.authorZhang, Qianqian-
dc.contributor.authorZhao, Zhongbo-
dc.contributor.authorJiang, Xi-
dc.contributor.authorXu, Xiaolei-
dc.contributor.authorBecker, Benjamin-
dc.contributor.authorKendrick, Keith M.-
dc.date.accessioned2023-09-05T12:13:33Z-
dc.date.available2023-09-05T12:13:33Z-
dc.date.issued2021-
dc.identifier.citationAutism Research, 2021, v. 14, n. 8, p. 1609-1620-
dc.identifier.issn1939-3792-
dc.identifier.urihttp://hdl.handle.net/10722/330718-
dc.description.abstractWhile several functional and structural changes occur in large-scale brain networks in autism spectrum disorder (ASD), reduced interhemispheric resting-state functional connectivity (rsFC) between homotopic regions may be of particular importance as a biomarker. ASD is an early-onset developmental disorder and neural alterations are often age-dependent. Although there is some evidence for homotopic interhemispheric rsFC alterations in language processing regions in ASD children, wider analyses using large data sets have not been performed. The present study, therefore, conducted a voxel-based homotopic interhemispheric rsFC analysis in 146 ASD and 175 typically developing children under-age 10 and examined associations with symptom severity in the autism brain imaging data exchange data sets. Given the role of corpus callosum (CC) in interhemispheric connectivity and reported CC volume changes in ASD we additionally examined whether there were parallel volumetric changes. Results demonstrated decreased homotopic rsFC in ASD children in the posterior cingulate cortex (PCC) and precuneus of the default mode network, the precentral gyrus of the mirror neuron system, and the caudate of the reward system. Homotopic rsFC of the PCC was associated with symptom severity. Furthermore, although no significant CC volume changes were found in ASD children, there was a significant negative correlation between the anterior CC volumes and homotopic rsFC strengths in the caudate. The present study shows that a reduced pattern of homotopic interhemispheric rsFC in ASD adults/adolescents is already present in children of 5–10 years old and further supports their potential use as a general ASD biomarker. Lay summary: Homotopic interhemispheric functional connectivity plays an important role in synchronizing activity between the two hemispheres and is altered in adults and adolescents with autism spectrum disorder (ASD). In the present study focused on children with ASD, we have observed a similar pattern of decreased homotopic connectivity, suggesting that alterations in homotopic interhemispheric connectivity may occur early in ASD and be a useful general biomarker across ages.-
dc.languageeng-
dc.relation.ispartofAutism Research-
dc.subjectautism spectrum disorder-
dc.subjectchildren-
dc.subjectcorpus callosum-
dc.subjecthomotopic interhemispheric functional connectivity-
dc.subjectresting-state-
dc.titleDecreased homotopic interhemispheric functional connectivity in children with autism spectrum disorder-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/aur.2523-
dc.identifier.pmid33908177-
dc.identifier.scopuseid_2-s2.0-85111608854-
dc.identifier.volume14-
dc.identifier.issue8-
dc.identifier.spage1609-
dc.identifier.epage1620-
dc.identifier.eissn1939-3806-
dc.identifier.isiWOS:000644814300001-

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