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Cortical gradient perturbation in attention deficit hyperactivity disorder correlates with neurotransmitter‐, cell type‐specific and chromosome‐ transcriptomic signatures.

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Title: Cortical gradient perturbation in attention deficit hyperactivity disorder correlates with neurotransmitter‐, cell type‐specific and chromosome‐ transcriptomic signatures.
Authors: Chen, Zhiyi (AUTHOR), Xu, Ting (AUTHOR), Liu, Xuerong (AUTHOR), Becker, Benjamin (AUTHOR), Li, Wei (AUTHOR), Xia, Lei (AUTHOR), Zhao, Wenqi (AUTHOR), Zhang, Rong (AUTHOR), Huo, Zhenzhen (AUTHOR), Hu, Bowen (AUTHOR), Tang, Yancheng (AUTHOR), Xiao, Zhibing (AUTHOR), Feng, Zhengzhi (AUTHOR), Chen, Ji (AUTHOR), Feng, Tingyong (AUTHOR)
Source: Psychiatry & Clinical Neurosciences. May2024, Vol. 78 Issue 5, p309-321. 13p.
Subjects: Attention-deficit hyperactivity disorder, Gene expression, Episodic memory, Transcriptomes, Genetic variation, Least squares
Abstract: Aims: This study aimed to illuminate the neuropathological landscape of attention deficit hyperactivity disorder (ADHD) by a multiscale macro–micro‐molecular perspective from in vivo neuroimaging data. Methods: The "ADHD‐200 initiative" repository provided multi‐site high‐quality resting‐state functional connectivity (rsfc‐) neuroimaging for ADHD children and matched typically developing (TD) cohort. Diffusion mapping embedding model to derive the functional connectome gradient detecting biologically plausible neural pattern was built, and the multivariate partial least square method to uncover the enrichment of neurotransmitomic, cellular and chromosomal gradient‐transcriptional signatures of AHBA enrichment and meta‐analytic decoding. Results: Compared to TD, ADHD children presented connectopic cortical gradient perturbations in almost all the cognition‐involved brain macroscale networks (all pBH <0.001), but not in the brain global topology. As an intermediate phenotypic variant, such gradient perturbation was spatially enriched into distributions of GABAA/BZ and 5‐HT2A receptors (all pBH <0.01) and co‐varied with genetic transcriptional expressions (e.g. DYDC2, ATOH7, all pBH <0.01), associated with phenotypic variants in episodic memory and emotional regulations. Enrichment models demonstrated such gradient‐transcriptional variants indicated the risk of both cell‐specific and chromosome‐ dysfunctions, especially in enriched expression of oligodendrocyte precursors and endothelial cells (all pperm <0.05) as well enrichment into chromosome 18, 19 and X (pperm <0.05). Conclusions: Our findings bridged brain macroscale neuropathological patterns to microscale/cellular biological architectures for ADHD children, demonstrating the neurobiologically pathological mechanism of ADHD into the genetic and molecular variants in GABA and 5‐HT systems as well brain‐derived enrichment of specific cellular/chromosomal expressions. [ABSTRACT FROM AUTHOR]
Copyright of Psychiatry & Clinical Neurosciences is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Cortical gradient perturbation in attention deficit hyperactivity disorder correlates with neurotransmitter‐, cell type‐specific and chromosome‐ transcriptomic signatures.
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  Data: &lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Chen%2C+Zhiyi%22&quot;&gt;Chen, Zhiyi&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Xu%2C+Ting%22&quot;&gt;Xu, Ting&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Liu%2C+Xuerong%22&quot;&gt;Liu, Xuerong&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Becker%2C+Benjamin%22&quot;&gt;Becker, Benjamin&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Li%2C+Wei%22&quot;&gt;Li, Wei&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Xia%2C+Lei%22&quot;&gt;Xia, Lei&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Zhao%2C+Wenqi%22&quot;&gt;Zhao, Wenqi&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Zhang%2C+Rong%22&quot;&gt;Zhang, Rong&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Huo%2C+Zhenzhen%22&quot;&gt;Huo, Zhenzhen&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Hu%2C+Bowen%22&quot;&gt;Hu, Bowen&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Tang%2C+Yancheng%22&quot;&gt;Tang, Yancheng&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Xiao%2C+Zhibing%22&quot;&gt;Xiao, Zhibing&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Feng%2C+Zhengzhi%22&quot;&gt;Feng, Zhengzhi&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Chen%2C+Ji%22&quot;&gt;Chen, Ji&lt;/searchLink&gt; (AUTHOR)&lt;br /&gt;&lt;searchLink fieldCode=&quot;AR&quot; term=&quot;%22Feng%2C+Tingyong%22&quot;&gt;Feng, Tingyong&lt;/searchLink&gt; (AUTHOR)
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22Psychiatry+%26+Clinical+Neurosciences%22&quot;&gt;Psychiatry &amp; Clinical Neurosciences&lt;/searchLink&gt;. May2024, Vol. 78 Issue 5, p309-321. 13p.
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  Data: &lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Attention-deficit+hyperactivity+disorder%22&quot;&gt;Attention-deficit hyperactivity disorder&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Gene+expression%22&quot;&gt;Gene expression&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Episodic+memory%22&quot;&gt;Episodic memory&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Transcriptomes%22&quot;&gt;Transcriptomes&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Genetic+variation%22&quot;&gt;Genetic variation&lt;/searchLink&gt;&lt;br /&gt;&lt;searchLink fieldCode=&quot;DE&quot; term=&quot;%22Least+squares%22&quot;&gt;Least squares&lt;/searchLink&gt;
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Aims: This study aimed to illuminate the neuropathological landscape of attention deficit hyperactivity disorder (ADHD) by a multiscale macro–micro‐molecular perspective from in vivo neuroimaging data. Methods: The &quot;ADHD‐200 initiative&quot; repository provided multi‐site high‐quality resting‐state functional connectivity (rsfc‐) neuroimaging for ADHD children and matched typically developing (TD) cohort. Diffusion mapping embedding model to derive the functional connectome gradient detecting biologically plausible neural pattern was built, and the multivariate partial least square method to uncover the enrichment of neurotransmitomic, cellular and chromosomal gradient‐transcriptional signatures of AHBA enrichment and meta‐analytic decoding. Results: Compared to TD, ADHD children presented connectopic cortical gradient perturbations in almost all the cognition‐involved brain macroscale networks (all pBH &lt;0.001), but not in the brain global topology. As an intermediate phenotypic variant, such gradient perturbation was spatially enriched into distributions of GABAA/BZ and 5‐HT2A receptors (all pBH &lt;0.01) and co‐varied with genetic transcriptional expressions (e.g. DYDC2, ATOH7, all pBH &lt;0.01), associated with phenotypic variants in episodic memory and emotional regulations. Enrichment models demonstrated such gradient‐transcriptional variants indicated the risk of both cell‐specific and chromosome‐ dysfunctions, especially in enriched expression of oligodendrocyte precursors and endothelial cells (all pperm &lt;0.05) as well enrichment into chromosome 18, 19 and X (pperm &lt;0.05). Conclusions: Our findings bridged brain macroscale neuropathological patterns to microscale/cellular biological architectures for ADHD children, demonstrating the neurobiologically pathological mechanism of ADHD into the genetic and molecular variants in GABA and 5‐HT systems as well brain‐derived enrichment of specific cellular/chromosomal expressions. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: &lt;i&gt;Copyright of Psychiatry &amp; Clinical Neurosciences is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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        Value: 10.1111/pcn.13649
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        Text: English
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        PageCount: 13
        StartPage: 309
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      – SubjectFull: Attention-deficit hyperactivity disorder
        Type: general
      – SubjectFull: Gene expression
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      – SubjectFull: Episodic memory
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      – SubjectFull: Transcriptomes
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      – SubjectFull: Genetic variation
        Type: general
      – SubjectFull: Least squares
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    Titles:
      – TitleFull: Cortical gradient perturbation in attention deficit hyperactivity disorder correlates with neurotransmitter‐, cell type‐specific and chromosome‐ transcriptomic signatures.
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            – D: 01
              M: 05
              Text: May2024
              Type: published
              Y: 2024
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