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Documents disponibles écrits par cet auteur (3)
Faire une suggestion Affiner la rechercheAnalysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets / Merel C. POSTEMA in Journal of Child Psychology and Psychiatry, 62-10 (October 2021)
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[article]
Titre : Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets Type de document : texte imprimé Auteurs : Merel C. POSTEMA, Auteur ; Martine HOOGMAN, Auteur ; Sara AMBROSINO, Auteur ; Philip ASHERSON, Auteur ; Tobias BANASCHEWSKI, Auteur ; Cibele E. BANDEIRA, Auteur ; Alexandr BARANOV, Auteur ; Claiton H.D. BAU, Auteur ; Sarah BAUMEISTER, Auteur ; Ramona BAUR-STREUBEL, Auteur ; Mark A. BELLGROVE, Auteur ; Joseph BIEDERMAN, Auteur ; Janita B. BRALTEN, Auteur ; Daniel BRANDEIS, Auteur ; Silvia BREM, Auteur ; Jan K. BUITELAAR, Auteur ; Geraldo F. BUSATTO, Auteur ; Francisco Xavier CASTELLANOS, Auteur ; Mara CERCIGNANI, Auteur ; Tiffany M. CHAIM-AVANCINI, Auteur ; Kaylita C. CHANTILUKE, Auteur ; Anastasia CHRISTAKOU, Auteur ; David COGHILL, Auteur ; Annette CONZELMANN, Auteur ; Ana I. CUBILLO, Auteur ; Renata B. CUPERTINO, Auteur ; Patrick DE ZEEUW, Auteur ; Alysa E. DOYLE, Auteur ; Sarah DURSTON, Auteur ; Eric A. EARL, Auteur ; Jeffery N. EPSTEIN, Auteur ; Thomas ETHOFER, Auteur ; Damien A. FAIR, Auteur ; Andreas J. FALLGATTER, Auteur ; Stephen V. FARAONE, Auteur ; Thomas FRODL, Auteur ; Matt C. GABEL, Auteur ; Tinatin GOGBERASHVILI, Auteur ; Eugenio H. GREVET, Auteur ; Jan HAAVIK, Auteur ; Neil A. HARRISON, Auteur ; Catharina A. HARTMAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Sarah HOHMANN, Auteur ; Marie F. HØVIK, Auteur ; Terry L. JERNIGAN, Auteur ; Bernd KARDATZKI, Auteur ; Georgii KARKASHADZE, Auteur ; Clare KELLY, Auteur ; Gregor KOHLS, Auteur ; Kerstin KONRAD, Auteur ; Jonna KUNTSI, Auteur ; Luisa LÁZARO, Auteur ; Sara LERA-MIGUEL, Auteur ; Klaus-Peter LESCH, Auteur ; Mario R. LOUZA, Auteur ; Astri J. LUNDERVOLD, Auteur ; Charles B MALPAS, Auteur ; Paulo MATTOS, Auteur ; Hazel MCCARTHY, Auteur ; Leyla NAMAZOVA-BARANOVA, Auteur ; Rosa NICOLAU, Auteur ; Joel T. NIGG, Auteur ; Stephanie NOVOTNY, Auteur ; Eileen OBERWELLAND WEISS, Auteur ; Ruth L. O'GORMAN TUURA, Auteur ; Jaap OOSTERLAAN, Auteur ; Bob ORANJE, Auteur ; Yannis PALOYELIS, Auteur ; Paul PAULI, Auteur ; Felipe A. PICON, Auteur ; Kerstin J. PLESSEN, Auteur ; Josep Antoni RAMOS-QUIROGA, Auteur ; Andreas REIF, Auteur ; Liesbeth RENEMAN, Auteur ; Pedro G.P. ROSA, Auteur ; Katya RUBIA, Auteur ; Anouk SCHRANTEE, Auteur ; Lizanne SCHWEREN, Auteur ; Jochen SEITZ, Auteur ; Philip SHAW, Auteur ; Tim J. SILK, Auteur ; Norbert SKOKAUSKAS, Auteur ; Juan C. SOLIVA VILA, Auteur ; Michael C. STEVENS, Auteur ; Gustavo SUDRE, Auteur ; Leanne TAMM, Auteur ; Fernanda TOVAR-MOLL, Auteur ; Theo G.M. VAN ERP, Auteur ; Alasdair VANCE, Auteur ; Oscar VILARROYA, Auteur ; Yolanda VIVES-GILABERT, Auteur ; Georg G. VON POLIER, Auteur ; Susanne WALITZA, Auteur ; Yuliya N. YONCHEVA, Auteur ; Marcus V. ZANETTI, Auteur ; Georg C. ZIEGLER, Auteur ; David C. GLAHN, Auteur ; Neda JAHANSHAD, Auteur Année de publication : 2021 Article en page(s) : p.1202-1219 Langues : Anglais (eng) Mots-clés : Attention-deficit brain asymmetry brain laterality hyperactivity disorder large-scale data structural MRI Index. décimale : PER Périodiques Résumé : Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from −0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait. En ligne : https://doi.org/10.1111/jcpp.13396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=462
in Journal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1202-1219[article] Analysis of structural brain asymmetries in attention-deficit/hyperactivity disorder in 39 datasets [texte imprimé] / Merel C. POSTEMA, Auteur ; Martine HOOGMAN, Auteur ; Sara AMBROSINO, Auteur ; Philip ASHERSON, Auteur ; Tobias BANASCHEWSKI, Auteur ; Cibele E. BANDEIRA, Auteur ; Alexandr BARANOV, Auteur ; Claiton H.D. BAU, Auteur ; Sarah BAUMEISTER, Auteur ; Ramona BAUR-STREUBEL, Auteur ; Mark A. BELLGROVE, Auteur ; Joseph BIEDERMAN, Auteur ; Janita B. BRALTEN, Auteur ; Daniel BRANDEIS, Auteur ; Silvia BREM, Auteur ; Jan K. BUITELAAR, Auteur ; Geraldo F. BUSATTO, Auteur ; Francisco Xavier CASTELLANOS, Auteur ; Mara CERCIGNANI, Auteur ; Tiffany M. CHAIM-AVANCINI, Auteur ; Kaylita C. CHANTILUKE, Auteur ; Anastasia CHRISTAKOU, Auteur ; David COGHILL, Auteur ; Annette CONZELMANN, Auteur ; Ana I. CUBILLO, Auteur ; Renata B. CUPERTINO, Auteur ; Patrick DE ZEEUW, Auteur ; Alysa E. DOYLE, Auteur ; Sarah DURSTON, Auteur ; Eric A. EARL, Auteur ; Jeffery N. EPSTEIN, Auteur ; Thomas ETHOFER, Auteur ; Damien A. FAIR, Auteur ; Andreas J. FALLGATTER, Auteur ; Stephen V. FARAONE, Auteur ; Thomas FRODL, Auteur ; Matt C. GABEL, Auteur ; Tinatin GOGBERASHVILI, Auteur ; Eugenio H. GREVET, Auteur ; Jan HAAVIK, Auteur ; Neil A. HARRISON, Auteur ; Catharina A. HARTMAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Pieter J. HOEKSTRA, Auteur ; Sarah HOHMANN, Auteur ; Marie F. HØVIK, Auteur ; Terry L. JERNIGAN, Auteur ; Bernd KARDATZKI, Auteur ; Georgii KARKASHADZE, Auteur ; Clare KELLY, Auteur ; Gregor KOHLS, Auteur ; Kerstin KONRAD, Auteur ; Jonna KUNTSI, Auteur ; Luisa LÁZARO, Auteur ; Sara LERA-MIGUEL, Auteur ; Klaus-Peter LESCH, Auteur ; Mario R. LOUZA, Auteur ; Astri J. LUNDERVOLD, Auteur ; Charles B MALPAS, Auteur ; Paulo MATTOS, Auteur ; Hazel MCCARTHY, Auteur ; Leyla NAMAZOVA-BARANOVA, Auteur ; Rosa NICOLAU, Auteur ; Joel T. NIGG, Auteur ; Stephanie NOVOTNY, Auteur ; Eileen OBERWELLAND WEISS, Auteur ; Ruth L. O'GORMAN TUURA, Auteur ; Jaap OOSTERLAAN, Auteur ; Bob ORANJE, Auteur ; Yannis PALOYELIS, Auteur ; Paul PAULI, Auteur ; Felipe A. PICON, Auteur ; Kerstin J. PLESSEN, Auteur ; Josep Antoni RAMOS-QUIROGA, Auteur ; Andreas REIF, Auteur ; Liesbeth RENEMAN, Auteur ; Pedro G.P. ROSA, Auteur ; Katya RUBIA, Auteur ; Anouk SCHRANTEE, Auteur ; Lizanne SCHWEREN, Auteur ; Jochen SEITZ, Auteur ; Philip SHAW, Auteur ; Tim J. SILK, Auteur ; Norbert SKOKAUSKAS, Auteur ; Juan C. SOLIVA VILA, Auteur ; Michael C. STEVENS, Auteur ; Gustavo SUDRE, Auteur ; Leanne TAMM, Auteur ; Fernanda TOVAR-MOLL, Auteur ; Theo G.M. VAN ERP, Auteur ; Alasdair VANCE, Auteur ; Oscar VILARROYA, Auteur ; Yolanda VIVES-GILABERT, Auteur ; Georg G. VON POLIER, Auteur ; Susanne WALITZA, Auteur ; Yuliya N. YONCHEVA, Auteur ; Marcus V. ZANETTI, Auteur ; Georg C. ZIEGLER, Auteur ; David C. GLAHN, Auteur ; Neda JAHANSHAD, Auteur . - 2021 . - p.1202-1219.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1202-1219
Mots-clés : Attention-deficit brain asymmetry brain laterality hyperactivity disorder large-scale data structural MRI Index. décimale : PER Périodiques Résumé : Objective Some studies have suggested alterations of structural brain asymmetry in attention-deficit/hyperactivity disorder (ADHD), but findings have been contradictory and based on small samples. Here, we performed the largest ever analysis of brain left-right asymmetry in ADHD, using 39 datasets of the ENIGMA consortium. Methods We analyzed asymmetry of subcortical and cerebral cortical structures in up to 1,933 people with ADHD and 1,829 unaffected controls. Asymmetry Indexes (AIs) were calculated per participant for each bilaterally paired measure, and linear mixed effects modeling was applied separately in children, adolescents, adults, and the total sample, to test exhaustively for potential associations of ADHD with structural brain asymmetries. Results There was no evidence for altered caudate nucleus asymmetry in ADHD, in contrast to prior literature. In children, there was less rightward asymmetry of the total hemispheric surface area compared to controls (t = 2.1, p = .04). Lower rightward asymmetry of medial orbitofrontal cortex surface area in ADHD (t = 2.7, p = .01) was similar to a recent finding for autism spectrum disorder. There were also some differences in cortical thickness asymmetry across age groups. In adults with ADHD, globus pallidus asymmetry was altered compared to those without ADHD. However, all effects were small (Cohen’s d from −0.18 to 0.18) and would not survive study-wide correction for multiple testing. Conclusion Prior studies of altered structural brain asymmetry in ADHD were likely underpowered to detect the small effects reported here. Altered structural asymmetry is unlikely to provide a useful biomarker for ADHD, but may provide neurobiological insights into the trait. En ligne : https://doi.org/10.1111/jcpp.13396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=462 Evidence of neurocognitive and resting state functional connectivity differences in carriers of NRXN1 deletions / Jacqueline FITZGERALD in Journal of Neurodevelopmental Disorders, 17 (2025)
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Titre : Evidence of neurocognitive and resting state functional connectivity differences in carriers of NRXN1 deletions Type de document : texte imprimé Auteurs : Jacqueline FITZGERALD, Auteur ; Ciara J. MOLLOY, Auteur ; Thomas DINNEEN, Auteur ; Niamh E. FEERICK, Auteur ; Matthew O'SULLIVAN, Auteur ; Richard O'CONAILL, Auteur ; Maryam AL-SHEHHI, Auteur ; Richard REILLY, Auteur ; Sally Ann LYNCH, Auteur ; Eleisa A. HERON, Auteur ; Clare KELLY, Auteur ; Sanbing SHEN, Auteur ; Louise GALLAGHER, Auteur Langues : Anglais (eng) Mots-clés : Humans Female Male Magnetic Resonance Imaging Adult Young Adult Calcium-Binding Proteins/genetics Diffusion Tensor Imaging Brain/diagnostic imaging/physiopathology Neural Cell Adhesion Molecules/genetics Adolescent Cell Adhesion Molecules, Neuronal/genetics Cognition/physiology Neuropsychological Tests Gene Deletion Neural Pathways/diagnostic imaging/physiopathology Executive Function/physiology Cognition Copy number variant NRXN1 deletion Neuroimaging the study was obtained from St. James’s Hospital/Tallaght University Hospital Research Ethics Committee (REC reference: 2015/03/01). Participants over 18 years provided written consent and parental written consent was provided for those under 18 years. Consent for publication: All authors who contributed to the article have approved the submitted version. Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: NRXN1 deletion (NRXN1 del) is a rare copy number variant associated with several neurodevelopmental, neuropsychiatric, and cognitive outcomes. The NRXN1 gene encodes for a pre-synaptic cell adhesion molecule that is important for synapse formation, regulation and neurotransmission. We used a gene-first approach to investigate neurocognitive and brain phenotypes in NRXN1 del carriers. METHODS: Forty-two participants (21 NRXN1 del carriers and 21 neurotypical age and sex-matched comparisons) completed IQ assessments, and a neurocognitive battery, including, executive function, attention, and social cognition tasks. Magnetic resonance imaging (MRI) data, including T1-weighted anatomical scans, resting state functional MRI and diffusion tensor imaging, were acquired in 36 participants (17 NRXN1 del carriers and 19 comparisons). RESULTS: NRXN1 del carriers had lower mean IQ and poorer spatial working memory performance compared to comparisons (p ≤ 0.05). Neuroimaging results revealed group differences in visual and ventral attention resting state networks (p < 0.05). Network-based statistical analysis showed a significant effect of group status for 28/115 connections, with poorer segregation between visual and default networks in NRXN1 del carriers relative to comparisons. No differences in brain structural volume or cortical thickness, or diffusion measures of white matter structural architecture were observed between groups. CONCLUSIONS: This exploratory study provides evidence for neurocognitive impacts and brain functional differences related to underlying synaptic mechanisms. Brain functional differences in NRXN1 del carriers may support altered excitation/inhibition dynamics within the brain. Gene-first approaches may establish brain-based translational markers to identify neurobiologically informed subgroups within neurodevelopmental and neuropsychiatric conditions, and ultimately transdiagnostic therapeutic strategies. En ligne : https://dx.doi.org/10.1186/s11689-025-09625-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576
in Journal of Neurodevelopmental Disorders > 17 (2025)[article] Evidence of neurocognitive and resting state functional connectivity differences in carriers of NRXN1 deletions [texte imprimé] / Jacqueline FITZGERALD, Auteur ; Ciara J. MOLLOY, Auteur ; Thomas DINNEEN, Auteur ; Niamh E. FEERICK, Auteur ; Matthew O'SULLIVAN, Auteur ; Richard O'CONAILL, Auteur ; Maryam AL-SHEHHI, Auteur ; Richard REILLY, Auteur ; Sally Ann LYNCH, Auteur ; Eleisa A. HERON, Auteur ; Clare KELLY, Auteur ; Sanbing SHEN, Auteur ; Louise GALLAGHER, Auteur.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 17 (2025)
Mots-clés : Humans Female Male Magnetic Resonance Imaging Adult Young Adult Calcium-Binding Proteins/genetics Diffusion Tensor Imaging Brain/diagnostic imaging/physiopathology Neural Cell Adhesion Molecules/genetics Adolescent Cell Adhesion Molecules, Neuronal/genetics Cognition/physiology Neuropsychological Tests Gene Deletion Neural Pathways/diagnostic imaging/physiopathology Executive Function/physiology Cognition Copy number variant NRXN1 deletion Neuroimaging the study was obtained from St. James’s Hospital/Tallaght University Hospital Research Ethics Committee (REC reference: 2015/03/01). Participants over 18 years provided written consent and parental written consent was provided for those under 18 years. Consent for publication: All authors who contributed to the article have approved the submitted version. Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: NRXN1 deletion (NRXN1 del) is a rare copy number variant associated with several neurodevelopmental, neuropsychiatric, and cognitive outcomes. The NRXN1 gene encodes for a pre-synaptic cell adhesion molecule that is important for synapse formation, regulation and neurotransmission. We used a gene-first approach to investigate neurocognitive and brain phenotypes in NRXN1 del carriers. METHODS: Forty-two participants (21 NRXN1 del carriers and 21 neurotypical age and sex-matched comparisons) completed IQ assessments, and a neurocognitive battery, including, executive function, attention, and social cognition tasks. Magnetic resonance imaging (MRI) data, including T1-weighted anatomical scans, resting state functional MRI and diffusion tensor imaging, were acquired in 36 participants (17 NRXN1 del carriers and 19 comparisons). RESULTS: NRXN1 del carriers had lower mean IQ and poorer spatial working memory performance compared to comparisons (p ≤ 0.05). Neuroimaging results revealed group differences in visual and ventral attention resting state networks (p < 0.05). Network-based statistical analysis showed a significant effect of group status for 28/115 connections, with poorer segregation between visual and default networks in NRXN1 del carriers relative to comparisons. No differences in brain structural volume or cortical thickness, or diffusion measures of white matter structural architecture were observed between groups. CONCLUSIONS: This exploratory study provides evidence for neurocognitive impacts and brain functional differences related to underlying synaptic mechanisms. Brain functional differences in NRXN1 del carriers may support altered excitation/inhibition dynamics within the brain. Gene-first approaches may establish brain-based translational markers to identify neurobiologically informed subgroups within neurodevelopmental and neuropsychiatric conditions, and ultimately transdiagnostic therapeutic strategies. En ligne : https://dx.doi.org/10.1186/s11689-025-09625-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=576 He said, she said: Autism spectrum diagnosis and gender differentially affect relationships between executive functions and social communication / Brea CHOUINARD in Autism, 23-7 (October 2019)
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[article]
Titre : He said, she said: Autism spectrum diagnosis and gender differentially affect relationships between executive functions and social communication Type de document : texte imprimé Auteurs : Brea CHOUINARD, Auteur ; Louise GALLAGHER, Auteur ; Clare KELLY, Auteur Article en page(s) : p.1793-1804 Langues : Anglais (eng) Mots-clés : autism executive functions metacognition social communication working memory Index. décimale : PER Périodiques Résumé : Autism spectrum disorder is characterized by difficulties with social communication, with a preponderance in males. Evidence supports a relationship between metacognitive executive functions (e.g. planning, working memory) and social communication in autism spectrum disorder, yet relationships with specific metacognitive executive functions and how gender alters the expression of these relationships require further study. We used multiple regression to examine relationships between informant-based measures of metacognitive executive function and social communication in intellectually able (IQ 85) female (n = 111; mean age = 10.2 +/- 2.8; 31 autism spectrum disorder) and male youth (n = 310; mean age = 10.5 +/- 1.9; 146 autism spectrum disorder) with and without autism spectrum disorder from the Autism Brain Imaging Data Exchange-II database. Executive function-social communication relationships were different in females and males with autism spectrum disorder. Relationships between the entire metacognitive index and social communication were stronger in males with autism spectrum disorder than without; this pattern was also observed for metacognitive sub-indices 'monitor' and 'working memory'. These patterns were not observed in females. Relationships between executive function and social communication appear different for female and male youth with an autism spectrum disorder diagnosis. To better understand the nature of metacognitive contributions to social communication in autism spectrum disorder, future work should investigate the co-development of monitoring, working memory and social communication, while taking gender into account. En ligne : http://dx.doi.org/10.1177/1362361318815639 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=406
in Autism > 23-7 (October 2019) . - p.1793-1804[article] He said, she said: Autism spectrum diagnosis and gender differentially affect relationships between executive functions and social communication [texte imprimé] / Brea CHOUINARD, Auteur ; Louise GALLAGHER, Auteur ; Clare KELLY, Auteur . - p.1793-1804.
Langues : Anglais (eng)
in Autism > 23-7 (October 2019) . - p.1793-1804
Mots-clés : autism executive functions metacognition social communication working memory Index. décimale : PER Périodiques Résumé : Autism spectrum disorder is characterized by difficulties with social communication, with a preponderance in males. Evidence supports a relationship between metacognitive executive functions (e.g. planning, working memory) and social communication in autism spectrum disorder, yet relationships with specific metacognitive executive functions and how gender alters the expression of these relationships require further study. We used multiple regression to examine relationships between informant-based measures of metacognitive executive function and social communication in intellectually able (IQ 85) female (n = 111; mean age = 10.2 +/- 2.8; 31 autism spectrum disorder) and male youth (n = 310; mean age = 10.5 +/- 1.9; 146 autism spectrum disorder) with and without autism spectrum disorder from the Autism Brain Imaging Data Exchange-II database. Executive function-social communication relationships were different in females and males with autism spectrum disorder. Relationships between the entire metacognitive index and social communication were stronger in males with autism spectrum disorder than without; this pattern was also observed for metacognitive sub-indices 'monitor' and 'working memory'. These patterns were not observed in females. Relationships between executive function and social communication appear different for female and male youth with an autism spectrum disorder diagnosis. To better understand the nature of metacognitive contributions to social communication in autism spectrum disorder, future work should investigate the co-development of monitoring, working memory and social communication, while taking gender into account. En ligne : http://dx.doi.org/10.1177/1362361318815639 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=406

