Interference of default mode on attention networks in adults with attention-deficit/hyperactivity disorder and its association with genetic variants and treatment outcomes.

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  • Additional Information
    • Source:
      Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101473265 Publication Model: Print Cited Medium: Internet ISSN: 1755-5949 (Electronic) Linking ISSN: 17555930 NLM ISO Abbreviation: CNS Neurosci Ther Subsets: MEDLINE
    • Publication Information:
      Original Publication: Oxford, UK : Wiley-Blackwell, c2008-
    • Subject Terms:
      Attention Deficit Disorder with Hyperactivity*/genetics ; Attention Deficit Disorder with Hyperactivity*/physiopathology ; Attention Deficit Disorder with Hyperactivity*/diagnostic imaging ; Magnetic Resonance Imaging* ; Connectome* ; Default Mode Network*/diagnostic imaging ; Default Mode Network*/physiopathology; Humans ; Male ; Female ; Adult ; Treatment Outcome ; Young Adult ; Brain/diagnostic imaging ; Brain/physiopathology ; Attention/physiology ; Genetic Variation/genetics ; Nerve Net/diagnostic imaging ; Nerve Net/physiopathology ; Cognitive Behavioral Therapy/methods
    • Abstract:
      Aims: Altered brain functional connectivity has been proposed as the neurobiological underpinnings of attention-deficit/hyperactivity disorder (ADHD), and the default mode interference hypothesis is one of the most popular neuropsychological models. Here, we explored whether this hypothesis is supported in adults with ADHD and the association with high-risk genetic variants and treatment outcomes.
      Methods: Voxel-based whole-brain connectome analysis was conducted on resting-state functional MRI data from 84 adults with ADHD and 89 healthy controls to identify functional connectivity substrates corresponding to ADHD-related alterations. The candidate genetic variants and 12-week cognitive behavioral therapy data were leveraged from the same population to assess these associations.
      Results: We detected breakdowns of functional connectivity in the precuneus and left middle temporal gyrus in adults with ADHD, with exact contributions from decreased connectivity within the default mode, dorsal and ventral attention networks, as well as increased connectivity among them with the middle temporal gyrus serving as a crucial 'bridge'. Additionally, significant associations between the altered functional connectivity and genetic variants in both MAOA and MAOB were detected. Treatment restored brain function, with the amelioration of connectivity of the middle temporal gyrus, accompanied by improvements in ADHD core symptoms.
      Conclusions: These findings support the interference of default mode on attention in adults with ADHD and its association with genetic risk variants and clinical management, providing insights into the underlying pathogenesis of ADHD and potential biomarkers for treatment evaluation.
      (© 2024 The Author(s). CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)
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    • Grant Information:
      82271575 National Natural Science Foundation of China; 81571340 National Natural Science Foundation of China; 81901826 National Natural Science Foundation of China; 61932008 National Natural Science Foundation of China; CFH: 2024-2-4114 Capital's Funds for Health Improvement and Research; CFH: 2020-2-4112 Capital's Funds for Health Improvement and Research; 20220484061 Beijing Nova Program; 20230484444 Beijing Nova Program; PKU2023LCXQ043 Clinical Medicine Plus X-Young Scholars Project, Peking University, the Fundamental Research Funds for the Central Universities; 19ZR1405600 Natural Science Foundation of Shanghai; 20ZR1404900 Natural Science Foundation of Shanghai; 973 program 2014CB846104 National Key Basic Research Program of China; 2018SHZDZX01 Shanghai Municipal Science and Technology Major Project; ZJLab and Shanghai Center for Brain Science and Brain-inspired Technology
    • Contributed Indexing:
      Keywords: MAO genotype; adults with ADHD; cognitive behavioral therapy; connectome analysis; functional connectivity
    • Publication Date:
      Date Created: 20240815 Date Completed: 20240815 Latest Revision: 20240817
    • Publication Date:
      20240817
    • Accession Number:
      PMC11325164
    • Accession Number:
      10.1111/cns.14900
    • Accession Number:
      39145420