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 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.
Center for Autism Research, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA ; Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA ; Center for Autism Spectrum Disorders, Children's National Health System, USA ; Center for Neuroscience, Children's National Health System, Washington, DC, USA.
Benjamin E
BE
Yerys
Neurology Department, Washington University School of Medicine, Washington, DC, USA.
Evan M
EM
Gordon
Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA ; Psychology Department, Georgia State University, Atlanta, GA, USA.
Danielle N
DN
Abrams
Brain Behavior Laboratory, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Theodore D
TD
Satterthwaite
Center for Autism Spectrum Disorders, Children's National Health System, USA.
Rachel
R
Weinblatt
Center for Autism Spectrum Disorders, Children's National Health System, USA ; Psychology Department, University of Oregon, Eugene, OR, USA.
Kathryn F
KF
Jankowski
Center for Autism Spectrum Disorders, Children's National Health System, USA ; Center for Neuroscience, Children's National Health System, Washington, DC, USA.
John
J
Strang
Center for Autism Spectrum Disorders, Children's National Health System, USA ; Center for Neuroscience, Children's National Health System, Washington, DC, USA.
Lauren
L
Kenworthy
Center for Neuroscience, Children's National Health System, Washington, DC, USA.
William D
WD
Gaillard
Center for Neuroscience, Children's National Health System, Washington, DC, USA ; Psychology Department, University of Oregon, Eugene, OR, USA.
Chandan J
CJ
Vaidya
D000293:Adolescent; D000067877:Autism Spectrum Disorder / Q000150:complications* / Q000473:pathology*; D001921:Brain / Q000098:blood supply / Q000473:pathology*; D001931:Brain Mapping; D016022:Case-Control Studies; D002648:Child; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008959:Models, Neurological; D009415:Nerve Net / Q000473:pathology; D009434:Neural Pathways / Q000098:blood supply / Q000473:pathology; D010100:Oxygen / Q000097:blood; D012920:Social Behavior Disorders / Q000209:etiology*
D010100:Oxygen
Autism spectrum disorders; Default mode network; Functional connectivity; Resting state