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Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children

Functional pathology of the default mode network is posited to be central to social-cognitive impairment in autism spectrum disorders (ASD). Altered functional connectivity of the default mode network's midline core may be a potential endophenotype for social deficits in ASD. Generalizability f...

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Autores principales: Yerys, Benjamin E., Gordon, Evan M., Abrams, Danielle N., Satterthwaite, Theodore D., Weinblatt, Rachel, Jankowski, Kathryn F., Strang, John, Kenworthy, Lauren, Gaillard, William D., Vaidya, Chandan J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573091/
https://www.ncbi.nlm.nih.gov/pubmed/26484047
http://dx.doi.org/10.1016/j.nicl.2015.07.018
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author Yerys, Benjamin E.
Gordon, Evan M.
Abrams, Danielle N.
Satterthwaite, Theodore D.
Weinblatt, Rachel
Jankowski, Kathryn F.
Strang, John
Kenworthy, Lauren
Gaillard, William D.
Vaidya, Chandan J.
author_facet Yerys, Benjamin E.
Gordon, Evan M.
Abrams, Danielle N.
Satterthwaite, Theodore D.
Weinblatt, Rachel
Jankowski, Kathryn F.
Strang, John
Kenworthy, Lauren
Gaillard, William D.
Vaidya, Chandan J.
author_sort Yerys, Benjamin E.
collection PubMed
description Functional pathology of the default mode network is posited to be central to social-cognitive impairment in autism spectrum disorders (ASD). Altered functional connectivity of the default mode network's midline core may be a potential endophenotype for social deficits in ASD. Generalizability from prior studies is limited by inclusion of medicated participants and by methods favoring restricted examination of network function. This study measured resting-state functional connectivity in 22 8–13 year-old non-medicated children with ASD and 22 typically developing controls using seed-based and network segregation functional connectivity methods. Relative to controls the ASD group showed both under- and over-functional connectivity within default mode and non-default mode regions, respectively. ASD symptoms correlated negatively with the connection strength of the default mode midline core—medial prefrontal cortex–posterior cingulate cortex. Network segregation analysis with the participation coefficient showed a higher area under the curve for the ASD group. Our findings demonstrate that the default mode network in ASD shows a pattern of poor segregation with both functional connectivity metrics. This study confirms the potential for the functional connection of the midline core as an endophenotype for social deficits. Poor segregation of the default mode network is consistent with an excitation/inhibition imbalance model of ASD.
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spelling pubmed-45730912015-10-19 Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children Yerys, Benjamin E. Gordon, Evan M. Abrams, Danielle N. Satterthwaite, Theodore D. Weinblatt, Rachel Jankowski, Kathryn F. Strang, John Kenworthy, Lauren Gaillard, William D. Vaidya, Chandan J. Neuroimage Clin Regular Article Functional pathology of the default mode network is posited to be central to social-cognitive impairment in autism spectrum disorders (ASD). Altered functional connectivity of the default mode network's midline core may be a potential endophenotype for social deficits in ASD. Generalizability from prior studies is limited by inclusion of medicated participants and by methods favoring restricted examination of network function. This study measured resting-state functional connectivity in 22 8–13 year-old non-medicated children with ASD and 22 typically developing controls using seed-based and network segregation functional connectivity methods. Relative to controls the ASD group showed both under- and over-functional connectivity within default mode and non-default mode regions, respectively. ASD symptoms correlated negatively with the connection strength of the default mode midline core—medial prefrontal cortex–posterior cingulate cortex. Network segregation analysis with the participation coefficient showed a higher area under the curve for the ASD group. Our findings demonstrate that the default mode network in ASD shows a pattern of poor segregation with both functional connectivity metrics. This study confirms the potential for the functional connection of the midline core as an endophenotype for social deficits. Poor segregation of the default mode network is consistent with an excitation/inhibition imbalance model of ASD. Elsevier 2015-08-18 /pmc/articles/PMC4573091/ /pubmed/26484047 http://dx.doi.org/10.1016/j.nicl.2015.07.018 Text en © 2015 The Authors. Published by Elsevier Inc. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Regular Article
Yerys, Benjamin E.
Gordon, Evan M.
Abrams, Danielle N.
Satterthwaite, Theodore D.
Weinblatt, Rachel
Jankowski, Kathryn F.
Strang, John
Kenworthy, Lauren
Gaillard, William D.
Vaidya, Chandan J.
Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children
title Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children
title_full Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children
title_fullStr Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children
title_full_unstemmed Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children
title_short Default mode network segregation and social deficits in autism spectrum disorder: Evidence from non-medicated children
title_sort default mode network segregation and social deficits in autism spectrum disorder: evidence from non-medicated children
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573091/
https://www.ncbi.nlm.nih.gov/pubmed/26484047
http://dx.doi.org/10.1016/j.nicl.2015.07.018
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