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Dysmaturation of the default mode network in autism

Authors

  • Stuart D. Washington,

    Corresponding author
    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
    3. Children's National Medical Center, Northwest, Washington, District of Columbia
    • Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of ColumbiaRoom LM14, Preclinical Sciences Building, Georgetown University Medical Center, 3900 Reservoir Rd NW, Washington, DC 20057, USA. E-mail: jwv5@georgetown.edu

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  • Evan M. Gordon,

    1. Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, District of Columbia
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  • Jasmit Brar,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Samantha Warburton,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Alice T. Sawyer,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Amanda Wolfe,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Erin R. Mease-Ference,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Laura Girton,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Ayichew Hailu,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • Juma Mbwana,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
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  • William D. Gaillard,

    1. Children's National Medical Center, Northwest, Washington, District of Columbia
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  • M. Layne Kalbfleisch,

    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Krasnow Investigation of Developmental Learning and Behavior, Fairfax, Virginia
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  • John W. VanMeter

    Corresponding author
    1. Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of Columbia
    2. Department of Neurology, Georgetown University Medical Center, Washington, District of Columbia
    • Center for Functional and Molecular Imaging, Georgetown University Medical Center, Washington, District of ColumbiaRoom LM14, Preclinical Sciences Building, Georgetown University Medical Center, 3900 Reservoir Rd NW, Washington, DC 20057, USA. E-mail: jwv5@georgetown.edu

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Abstract

Two hypotheses of autism spectrum disorder (ASD) propose that this condition is characterized by deficits in Theory of Mind and by hypoconnectivity between remote cortical regions with hyperconnectivity locally. The default mode network (DMN) is a set of remote, functionally connected cortical nodes less active during executive tasks than at rest and is implicated in Theory of Mind, episodic memory, and other self-reflective processes. We show that children with ASD have reduced connectivity between DMN nodes and increased local connectivity within DMN nodes and the visual and motor resting-state networks. We show that, like the trajectory of synaptogenesis, internodal DMN functional connectivity increased as a quadratic function of age in typically developing children, peaking between, 11 and 13 years. In children with ASD, these long-distance connections fail to develop during adolescence. These findings support the “developmental disconnection model” of ASD, provide a possible mechanistic explanation for the Theory-of-Mind hypothesis of ASD, and show that the window for effectively treating ASD could be wider than previously thought. Hum Brain Mapp 35:1284–1296, 2014. © 2013 Wiley Periodicals, Inc.

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