Aberrant local striatal functional connectivity in attention-deficit/hyperactivity disorder / Daniel VON RHEIN in Journal of Child Psychology and Psychiatry, 57-6 (June 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-6 (June 2016) . - p.697-705 Titre : Aberrant local striatal functional connectivity in attention-deficit/hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : Daniel VON RHEIN, Auteur ; Marianne OLDEHINKEL, Auteur ; Christian F. BECKMANN, Auteur ; Jaap OOSTERLAAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Catharina A. HARTMAN, Auteur ; Pieter J. HOEKSTRA, Auteur ; Barbara FRANKE, Auteur ; Roshan COOLS, Auteur ; Jan K. BUITELAAR, Auteur ; Maarten MENNES, Auteur Article en page(s) : p.697-705 Langues : Anglais (eng) Mots-clés : Resting-state fMRI  functional connectivity  attention-deficit/hyperactivity disorder  cortico-striatal networks  striatum  putamen Index. décimale : PER Périodiques Résumé : Background Task-based and resting-state functional Magnetic Resonance Imaging (fMRI) studies report attention-deficit/hyperactivity disorder (ADHD)-related alterations in brain regions implicated in cortico-striatal networks. We assessed whether ADHD is associated with changes in the brain's global cortico-striatal functional architecture, or whether ADHD-related alterations are limited to local, intrastriatal functional connections. Methods We included a cohort of adolescents with ADHD (N = 181) and healthy controls (N = 140) and assessed functional connectivity of nucleus accumbens, caudate nucleus, anterior putamen, and posterior putamen. To assess global cortico-striatal functional architecture we computed whole-brain functional connectivity by including all regions of interest in one multivariate analysis. We assessed local striatal functional connectivity using partial correlations between the time series of the striatal regions. Results Diagnostic status did not influence global cortico-striatal functional architecture. However, compared to controls, participants with ADHD exhibited significantly increased local functional connectivity between anterior and posterior putamen (p = .0003; ADHD: z = .30, controls: z = .24). Results were not affected by medication use or comorbid oppositional defiant disorder and conduct disorder. Conclusions Our results do not support hypotheses that ADHD is associated with alterations in cortico-striatal networks, but suggest changes in local striatal functional connectivity. We interpret our findings as aberrant development of local functional connectivity of the putamen, potentially leading to decreased functional segregation between anterior and posterior putamen in ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.12529 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=289 [article] Aberrant local striatal functional connectivity in attention-deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / Daniel VON RHEIN, Auteur ; Marianne OLDEHINKEL, Auteur ; Christian F. BECKMANN, Auteur ; Jaap OOSTERLAAN, Auteur ; Dirk J. HESLENFELD, Auteur ; Catharina A. HARTMAN, Auteur ; Pieter J. HOEKSTRA, Auteur ; Barbara FRANKE, Auteur ; Roshan COOLS, Auteur ; Jan K. BUITELAAR, Auteur ; Maarten MENNES, Auteur . - p.697-705. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-6 (June 2016) . - p.697-705 Mots-clés : Resting-state fMRI  functional connectivity  attention-deficit/hyperactivity disorder  cortico-striatal networks  striatum  putamen Index. décimale : PER Périodiques Résumé : Background Task-based and resting-state functional Magnetic Resonance Imaging (fMRI) studies report attention-deficit/hyperactivity disorder (ADHD)-related alterations in brain regions implicated in cortico-striatal networks. We assessed whether ADHD is associated with changes in the brain's global cortico-striatal functional architecture, or whether ADHD-related alterations are limited to local, intrastriatal functional connections. Methods We included a cohort of adolescents with ADHD (N = 181) and healthy controls (N = 140) and assessed functional connectivity of nucleus accumbens, caudate nucleus, anterior putamen, and posterior putamen. To assess global cortico-striatal functional architecture we computed whole-brain functional connectivity by including all regions of interest in one multivariate analysis. We assessed local striatal functional connectivity using partial correlations between the time series of the striatal regions. Results Diagnostic status did not influence global cortico-striatal functional architecture. However, compared to controls, participants with ADHD exhibited significantly increased local functional connectivity between anterior and posterior putamen (p = .0003; ADHD: z = .30, controls: z = .24). Results were not affected by medication use or comorbid oppositional defiant disorder and conduct disorder. Conclusions Our results do not support hypotheses that ADHD is associated with alterations in cortico-striatal networks, but suggest changes in local striatal functional connectivity. We interpret our findings as aberrant development of local functional connectivity of the putamen, potentially leading to decreased functional segregation between anterior and posterior putamen in ADHD. En ligne : http://dx.doi.org/10.1111/jcpp.12529 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=289

Altered functional connectivity of the amygdaloid input nuclei in adolescents and young adults with autism spectrum disorder: a resting state fMRI study / A. RAUSCH in Molecular Autism, 7 (2016)  

Public ISBD [article]  inMolecular Autism > 7 (2016) . - 13p. Titre : Altered functional connectivity of the amygdaloid input nuclei in adolescents and young adults with autism spectrum disorder: a resting state fMRI study Type de document : Texte imprimé et/ou numérique Auteurs : A. RAUSCH, Auteur ; W. ZHANG, Auteur ; K. V. HAAK, Auteur ; M. MENNES, Auteur ; E. J. HERMANS, Auteur ; E. VAN OORT, Auteur ; G. VAN WINGEN, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur ; W. B. GROEN, Auteur Article en page(s) : 13p. Langues : Anglais (eng) Mots-clés : Adolescent  Afferent Pathways/pathology/physiopathology  Amygdala/pathology/physiopathology  Autism Spectrum Disorder/pathology/physiopathology  Basolateral Nuclear Complex/pathology/physiopathology  Central Amygdaloid Nucleus/pathology/physiopathology  Connectome  Efferent Pathways/pathology/physiopathology  Emotions  Female  Humans  Image Processing, Computer-Assisted  Magnetic Resonance Imaging  Male  Models, Neurological  Models, Psychological  Neocortex/pathology/physiopathology  Nerve Net/pathology/physiopathology  Signal-To-Noise Ratio  Social Perception  Surveys and Questionnaires  Temporal Lobe/pathology/physiopathology  Young Adult  Amygdala  Autism spectrum disorder  Centromedial  Connectivity  Input-output  Laterobasal  Nuclei  Superficial Index. décimale : PER Périodiques Résumé : BACKGROUND: Amygdala dysfunction is hypothesized to underlie the social deficits observed in autism spectrum disorders (ASD). However, the neurobiological basis of this hypothesis is underspecified because it is unknown whether ASD relates to abnormalities of the amygdaloid input or output nuclei. Here, we investigated the functional connectivity of the amygdaloid social-perceptual input nuclei and emotion-regulation output nuclei in ASD versus controls. METHODS: We collected resting state functional magnetic resonance imaging (fMRI) data, tailored to provide optimal sensitivity in the amygdala as well as the neocortex, in 20 adolescents and young adults with ASD and 25 matched controls. We performed a regular correlation analysis between the entire amygdala (EA) and the whole brain and used a partial correlation analysis to investigate whole-brain functional connectivity uniquely related to each of the amygdaloid subregions. RESULTS: Between-group comparison of regular EA correlations showed significantly reduced connectivity in visuospatial and superior parietal areas in ASD compared to controls. Partial correlation analysis revealed that this effect was driven by the left superficial and right laterobasal input subregions, but not the centromedial output nuclei. CONCLUSIONS: These results indicate reduced connectivity of specifically the amygdaloid sensory input channels in ASD, suggesting that abnormal amygdalo-cortical connectivity can be traced down to the socio-perceptual pathways. En ligne : http://dx.doi.org/10.1186/s13229-015-0060-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329 [article] Altered functional connectivity of the amygdaloid input nuclei in adolescents and young adults with autism spectrum disorder: a resting state fMRI study [Texte imprimé et/ou numérique] / A. RAUSCH, Auteur ; W. ZHANG, Auteur ; K. V. HAAK, Auteur ; M. MENNES, Auteur ; E. J. HERMANS, Auteur ; E. VAN OORT, Auteur ; G. VAN WINGEN, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur ; W. B. GROEN, Auteur . - 13p. Langues : Anglais (eng) in Molecular Autism > 7 (2016) . - 13p. Mots-clés : Adolescent  Afferent Pathways/pathology/physiopathology  Amygdala/pathology/physiopathology  Autism Spectrum Disorder/pathology/physiopathology  Basolateral Nuclear Complex/pathology/physiopathology  Central Amygdaloid Nucleus/pathology/physiopathology  Connectome  Efferent Pathways/pathology/physiopathology  Emotions  Female  Humans  Image Processing, Computer-Assisted  Magnetic Resonance Imaging  Male  Models, Neurological  Models, Psychological  Neocortex/pathology/physiopathology  Nerve Net/pathology/physiopathology  Signal-To-Noise Ratio  Social Perception  Surveys and Questionnaires  Temporal Lobe/pathology/physiopathology  Young Adult  Amygdala  Autism spectrum disorder  Centromedial  Connectivity  Input-output  Laterobasal  Nuclei  Superficial Index. décimale : PER Périodiques Résumé : BACKGROUND: Amygdala dysfunction is hypothesized to underlie the social deficits observed in autism spectrum disorders (ASD). However, the neurobiological basis of this hypothesis is underspecified because it is unknown whether ASD relates to abnormalities of the amygdaloid input or output nuclei. Here, we investigated the functional connectivity of the amygdaloid social-perceptual input nuclei and emotion-regulation output nuclei in ASD versus controls. METHODS: We collected resting state functional magnetic resonance imaging (fMRI) data, tailored to provide optimal sensitivity in the amygdala as well as the neocortex, in 20 adolescents and young adults with ASD and 25 matched controls. We performed a regular correlation analysis between the entire amygdala (EA) and the whole brain and used a partial correlation analysis to investigate whole-brain functional connectivity uniquely related to each of the amygdaloid subregions. RESULTS: Between-group comparison of regular EA correlations showed significantly reduced connectivity in visuospatial and superior parietal areas in ASD compared to controls. Partial correlation analysis revealed that this effect was driven by the left superficial and right laterobasal input subregions, but not the centromedial output nuclei. CONCLUSIONS: These results indicate reduced connectivity of specifically the amygdaloid sensory input channels in ASD, suggesting that abnormal amygdalo-cortical connectivity can be traced down to the socio-perceptual pathways. En ligne : http://dx.doi.org/10.1186/s13229-015-0060-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329

Connectivity-Based Parcellation of the Amygdala Predicts Social Skills in Adolescents with Autism Spectrum Disorder / A. RAUSCH in Journal of Autism and Developmental Disorders, 48-2 (February 2018)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 48-2 (February 2018) . - p.572-582 Titre : Connectivity-Based Parcellation of the Amygdala Predicts Social Skills in Adolescents with Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : A. RAUSCH, Auteur ; W. ZHANG, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur ; W. B. GROEN, Auteur ; K. V. HAAK, Auteur Article en page(s) : p.572-582 Langues : Anglais (eng) Mots-clés : Amygdala  Autism spectrum disorder  Functional connectivity  Parcellation  Prefrontal Index. décimale : PER Périodiques Résumé : Amygdala dysfunction plays a role in the social impairments in autism spectrum disorders (ASD), but it is unclear which of its subregions are abnormal in ASD. This study compared the volume and functional connectivity (FC) strength of three FC-defined amygdala subregions between ASD and controls, and assessed their relation to social skills in ASD. A subregion associated with the social perception network was enlarged in ASD (F1 = 7.842, p = .008) and its volume correlated significantly with symptom severity (social skills: r = .548, p = .009). Posthoc analysis revealed that the enlargement was driven by the vmPFC amygdala network. These findings refine our understanding of abnormal amygdala connectivity in ASD and may inform future strategies for therapeutic interventions targeting the amygdalofrontal pathway. En ligne : https://doi.org/10.1007/s10803-017-3370-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=338 [article] Connectivity-Based Parcellation of the Amygdala Predicts Social Skills in Adolescents with Autism Spectrum Disorder [Texte imprimé et/ou numérique] / A. RAUSCH, Auteur ; W. ZHANG, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur ; W. B. GROEN, Auteur ; K. V. HAAK, Auteur . - p.572-582. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 48-2 (February 2018) . - p.572-582 Mots-clés : Amygdala  Autism spectrum disorder  Functional connectivity  Parcellation  Prefrontal Index. décimale : PER Périodiques Résumé : Amygdala dysfunction plays a role in the social impairments in autism spectrum disorders (ASD), but it is unclear which of its subregions are abnormal in ASD. This study compared the volume and functional connectivity (FC) strength of three FC-defined amygdala subregions between ASD and controls, and assessed their relation to social skills in ASD. A subregion associated with the social perception network was enlarged in ASD (F1 = 7.842, p = .008) and its volume correlated significantly with symptom severity (social skills: r = .548, p = .009). Posthoc analysis revealed that the enlargement was driven by the vmPFC amygdala network. These findings refine our understanding of abnormal amygdala connectivity in ASD and may inform future strategies for therapeutic interventions targeting the amygdalofrontal pathway. En ligne : https://doi.org/10.1007/s10803-017-3370-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=338

Gray matter covariations and core symptoms of autism: the EU-AIMS Longitudinal European Autism Project / Ting MEI in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) Titre : Gray matter covariations and core symptoms of autism: the EU-AIMS Longitudinal European Autism Project Type de document : Texte imprimé et/ou numérique Auteurs : Ting MEI, Auteur ; Alberto LLERA, Auteur ; Dorothea L. FLORIS, Auteur ; Natalie J. FORDE, Auteur ; Julian TILLMANN, Auteur ; Sarah DURSTON, Auteur ; Carolin MOESSNANG, Auteur ; Tobias BANASCHEWSKI, Auteur ; Rosemary J. HOLT, Auteur ; Simon BARON-COHEN, Auteur ; Annika RAUSCH, Auteur ; Eva LOTH, Auteur ; Flavio DELL'ACQUA, Auteur ; Tony CHARMAN, Auteur ; Declan G. M. MURPHY, Auteur ; Christine ECKER, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur Langues : Anglais (eng) Mots-clés : Autism  Canonical correlation analysis  Independent component analysis  Magnetic resonance imaging  Voxel-based morphometry  Cilag BV, Eli Lilly, Shire, Lundbeck, Roche, and Servier. He is not an employee of  any of these companies, and not a stock shareholder of any of these companies. He  has no other financial or material support, including expert testimony, patents or  royalties. CFB is director and shareholder in SBGNeuro Ltd. TB served in an advisory  or consultancy role for Lundbeck, Medice, Neurim Pharmaceuticals, Oberberg GmbH,  Shire, and Infectopharm. He received conference support or speaker’s fee by Lilly,  Medice, and Shire. He received royalties from Hogrefe, Kohlhammer, CIP Medien, and  Oxford University Press. TC has received consultancy from Roche and received book  royalties from Guildford Press and Sage. DGM has been a consultant to, and advisory  board member, for Roche and Servier. He is not an employee of any of these  companies, and not a stock shareholder of any of these companies. The present work  is unrelated to the above grants and relationships. The other authors report no  biomedical financial interests or potential conflicts of interest. Index. décimale : PER Périodiques Résumé : BACKGROUND: Voxel-based morphometry (VBM) studies in autism spectrum disorder (autism) have yielded diverging results. This might partly be attributed to structural alterations being associating with the combined influence of several regions rather than with a single region. Further, these structural covariation differences may relate to continuous measures of autism rather than with categorical case-control contrasts. The current study aimed to identify structural covariation alterations in autism, and assessed canonical correlations between brain covariation patterns and core autism symptoms. METHODS: We studied 347 individuals with autism and 252 typically developing individuals, aged between 6 and 30 years, who have been deeply phenotyped in the Longitudinal European Autism Project. All participants' VBM maps were decomposed into spatially independent components using independent component analysis. A generalized linear model (GLM) was used to examine case-control differences. Next, canonical correlation analysis (CCA) was performed to separately explore the integrated effects between all the brain sources of gray matter variation and two sets of core autism symptoms. RESULTS: GLM analyses showed significant case-control differences for two independent components. The first component was primarily associated with decreased density of bilateral insula, inferior frontal gyrus, orbitofrontal cortex, and increased density of caudate nucleus in the autism group relative to typically developing individuals. The second component was related to decreased densities of the bilateral amygdala, hippocampus, and parahippocampal gyrus in the autism group relative to typically developing individuals. The CCA results showed significant correlations between components that involved variation of thalamus, putamen, precentral gyrus, frontal, parietal, and occipital lobes, and the cerebellum, and repetitive, rigid and stereotyped behaviors and abnormal sensory behaviors in autism individuals. LIMITATIONS: Only 55.9% of the participants with autism had complete questionnaire data on continuous parent-reported symptom measures. CONCLUSIONS: Covaried areas associated with autism diagnosis and/or symptoms are scattered across the whole brain and include the limbic system, basal ganglia, thalamus, cerebellum, precentral gyrus, and parts of the frontal, parietal, and occipital lobes. Some of these areas potentially subserve social-communicative behavior, whereas others may underpin sensory processing and integration, and motor behavior. En ligne : http://dx.doi.org/10.1186/s13229-020-00389-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 [article] Gray matter covariations and core symptoms of autism: the EU-AIMS Longitudinal European Autism Project [Texte imprimé et/ou numérique] / Ting MEI, Auteur ; Alberto LLERA, Auteur ; Dorothea L. FLORIS, Auteur ; Natalie J. FORDE, Auteur ; Julian TILLMANN, Auteur ; Sarah DURSTON, Auteur ; Carolin MOESSNANG, Auteur ; Tobias BANASCHEWSKI, Auteur ; Rosemary J. HOLT, Auteur ; Simon BARON-COHEN, Auteur ; Annika RAUSCH, Auteur ; Eva LOTH, Auteur ; Flavio DELL'ACQUA, Auteur ; Tony CHARMAN, Auteur ; Declan G. M. MURPHY, Auteur ; Christine ECKER, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur. Langues : Anglais (eng) in Molecular Autism > 11 (2020) Mots-clés : Autism  Canonical correlation analysis  Independent component analysis  Magnetic resonance imaging  Voxel-based morphometry  Cilag BV, Eli Lilly, Shire, Lundbeck, Roche, and Servier. He is not an employee of  any of these companies, and not a stock shareholder of any of these companies. He  has no other financial or material support, including expert testimony, patents or  royalties. CFB is director and shareholder in SBGNeuro Ltd. TB served in an advisory  or consultancy role for Lundbeck, Medice, Neurim Pharmaceuticals, Oberberg GmbH,  Shire, and Infectopharm. He received conference support or speaker’s fee by Lilly,  Medice, and Shire. He received royalties from Hogrefe, Kohlhammer, CIP Medien, and  Oxford University Press. TC has received consultancy from Roche and received book  royalties from Guildford Press and Sage. DGM has been a consultant to, and advisory  board member, for Roche and Servier. He is not an employee of any of these  companies, and not a stock shareholder of any of these companies. The present work  is unrelated to the above grants and relationships. The other authors report no  biomedical financial interests or potential conflicts of interest. Index. décimale : PER Périodiques Résumé : BACKGROUND: Voxel-based morphometry (VBM) studies in autism spectrum disorder (autism) have yielded diverging results. This might partly be attributed to structural alterations being associating with the combined influence of several regions rather than with a single region. Further, these structural covariation differences may relate to continuous measures of autism rather than with categorical case-control contrasts. The current study aimed to identify structural covariation alterations in autism, and assessed canonical correlations between brain covariation patterns and core autism symptoms. METHODS: We studied 347 individuals with autism and 252 typically developing individuals, aged between 6 and 30 years, who have been deeply phenotyped in the Longitudinal European Autism Project. All participants' VBM maps were decomposed into spatially independent components using independent component analysis. A generalized linear model (GLM) was used to examine case-control differences. Next, canonical correlation analysis (CCA) was performed to separately explore the integrated effects between all the brain sources of gray matter variation and two sets of core autism symptoms. RESULTS: GLM analyses showed significant case-control differences for two independent components. The first component was primarily associated with decreased density of bilateral insula, inferior frontal gyrus, orbitofrontal cortex, and increased density of caudate nucleus in the autism group relative to typically developing individuals. The second component was related to decreased densities of the bilateral amygdala, hippocampus, and parahippocampal gyrus in the autism group relative to typically developing individuals. The CCA results showed significant correlations between components that involved variation of thalamus, putamen, precentral gyrus, frontal, parietal, and occipital lobes, and the cerebellum, and repetitive, rigid and stereotyped behaviors and abnormal sensory behaviors in autism individuals. LIMITATIONS: Only 55.9% of the participants with autism had complete questionnaire data on continuous parent-reported symptom measures. CONCLUSIONS: Covaried areas associated with autism diagnosis and/or symptoms are scattered across the whole brain and include the limbic system, basal ganglia, thalamus, cerebellum, precentral gyrus, and parts of the frontal, parietal, and occipital lobes. Some of these areas potentially subserve social-communicative behavior, whereas others may underpin sensory processing and integration, and motor behavior. En ligne : http://dx.doi.org/10.1186/s13229-020-00389-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438

Gray matter covariations in autism: out-of-sample replication using the ENIGMA autism cohort / Ting MEI in Molecular Autism, 15 (2024)  

Public ISBD [article]  inMolecular Autism > 15 (2024) . - 3p. Titre : Gray matter covariations in autism: out-of-sample replication using the ENIGMA autism cohort Type de document : Texte imprimé et/ou numérique Auteurs : Ting MEI, Auteur ; Alberto LLERA, Auteur ; Natalie J. FORDE, Auteur ; Daan VAN ROOIJ, Auteur ; Dorothea L. FLORIS, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur Article en page(s) : 3p. Langues : Anglais (eng) Mots-clés : Humans  Gray Matter/diagnostic imaging  Autistic Disorder/diagnostic imaging  Autism Spectrum Disorder/diagnostic imaging  Retrospective Studies  Magnetic Resonance Imaging/methods  Brain/diagnostic imaging  Autism  Gray matter volume covariation  Replication  advisory board member of, and a speaker for Janssen Cilag BV, Eli Lilly, Shire,  Lundbeck, Roche, and Servier. He is not an employee of any of these companies,  and not a stock shareholder of any of these companies. He has no other financial  or material support, including expert testimony, patents or royalties. The  present work is unrelated to the above grants and relationships. The other  authors report no biomedical financial interests or potential conflicts of  interest. Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (henceforth autism) is a complex neurodevelopmental condition associated with differences in gray matter (GM) volume covariations, as reported in our previous study of the Longitudinal European Autism Project (LEAP) data. To make progress on the identification of potential neural markers and to validate the robustness of our previous findings, we aimed to replicate our results using data from the Enhancing Neuroimaging Genetics Through Meta-Analysis (ENIGMA) autism working group. METHODS: We studied 781 autistic and 927 non-autistic individuals (6-30 years, IQ???50), across 37 sites. Voxel-based morphometry was used to quantify GM volume as before. Subsequently, we used spatial maps of the two autism-related independent components (ICs) previously identified in the LEAP sample as templates for regression analyses to separately estimate the ENIGMA-participant loadings to each of these two ICs. Between-group differences in participants' loadings on each component were examined, and we additionally investigated the relation between participant loadings and autistic behaviors within the autism group. RESULTS: The two components of interest, previously identified in the LEAP dataset, showed significant between-group differences upon regressions into the ENIGMA cohort. The associated brain patterns were consistent with those found in the initial identification study. The first IC was primarily associated with increased volumes of bilateral insula, inferior frontal gyrus, orbitofrontal cortex, and caudate in the autism group relative to the control group (? = 0.129, p = 0.013). The second IC was related to increased volumes of the bilateral amygdala, hippocampus, and parahippocampal gyrus in the autism group relative to non-autistic individuals (? = 0.116, p = 0.024). However, when accounting for the site-by-group interaction effect, no significant main effect of the group can be identified (p > 0.590). We did not find significant univariate association between the brain measures and behavior in autism (p > 0.085). LIMITATIONS: The distributions of age, IQ, and sex between LEAP and ENIGMA are statistically different from each other. Owing to limited access to the behavioral data of the autism group, we were unable to further our understanding of the neural basis of behavioral dimensions of the sample. CONCLUSIONS: The current study is unable to fully replicate the autism-related brain patterns from LEAP in the ENIGMA cohort. The diverse group effects across ENIGMA sites demonstrate the challenges of generalizing the average findings of the GM covariation patterns to a large-scale cohort integrated retrospectively from multiple studies. Further analyses need to be conducted to gain additional insights into the generalizability of these two GM covariation patterns. En ligne : https://dx.doi.org/10.1186/s13229-024-00583-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=537 [article] Gray matter covariations in autism: out-of-sample replication using the ENIGMA autism cohort [Texte imprimé et/ou numérique] / Ting MEI, Auteur ; Alberto LLERA, Auteur ; Natalie J. FORDE, Auteur ; Daan VAN ROOIJ, Auteur ; Dorothea L. FLORIS, Auteur ; Christian F. BECKMANN, Auteur ; Jan K. BUITELAAR, Auteur . - 3p. Langues : Anglais (eng) in Molecular Autism > 15 (2024) . - 3p. Mots-clés : Humans  Gray Matter/diagnostic imaging  Autistic Disorder/diagnostic imaging  Autism Spectrum Disorder/diagnostic imaging  Retrospective Studies  Magnetic Resonance Imaging/methods  Brain/diagnostic imaging  Autism  Gray matter volume covariation  Replication  advisory board member of, and a speaker for Janssen Cilag BV, Eli Lilly, Shire,  Lundbeck, Roche, and Servier. He is not an employee of any of these companies,  and not a stock shareholder of any of these companies. He has no other financial  or material support, including expert testimony, patents or royalties. The  present work is unrelated to the above grants and relationships. The other  authors report no biomedical financial interests or potential conflicts of  interest. Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (henceforth autism) is a complex neurodevelopmental condition associated with differences in gray matter (GM) volume covariations, as reported in our previous study of the Longitudinal European Autism Project (LEAP) data. To make progress on the identification of potential neural markers and to validate the robustness of our previous findings, we aimed to replicate our results using data from the Enhancing Neuroimaging Genetics Through Meta-Analysis (ENIGMA) autism working group. METHODS: We studied 781 autistic and 927 non-autistic individuals (6-30 years, IQ???50), across 37 sites. Voxel-based morphometry was used to quantify GM volume as before. Subsequently, we used spatial maps of the two autism-related independent components (ICs) previously identified in the LEAP sample as templates for regression analyses to separately estimate the ENIGMA-participant loadings to each of these two ICs. Between-group differences in participants' loadings on each component were examined, and we additionally investigated the relation between participant loadings and autistic behaviors within the autism group. RESULTS: The two components of interest, previously identified in the LEAP dataset, showed significant between-group differences upon regressions into the ENIGMA cohort. The associated brain patterns were consistent with those found in the initial identification study. The first IC was primarily associated with increased volumes of bilateral insula, inferior frontal gyrus, orbitofrontal cortex, and caudate in the autism group relative to the control group (? = 0.129, p = 0.013). The second IC was related to increased volumes of the bilateral amygdala, hippocampus, and parahippocampal gyrus in the autism group relative to non-autistic individuals (? = 0.116, p = 0.024). However, when accounting for the site-by-group interaction effect, no significant main effect of the group can be identified (p > 0.590). We did not find significant univariate association between the brain measures and behavior in autism (p > 0.085). LIMITATIONS: The distributions of age, IQ, and sex between LEAP and ENIGMA are statistically different from each other. Owing to limited access to the behavioral data of the autism group, we were unable to further our understanding of the neural basis of behavioral dimensions of the sample. CONCLUSIONS: The current study is unable to fully replicate the autism-related brain patterns from LEAP in the ENIGMA cohort. The diverse group effects across ENIGMA sites demonstrate the challenges of generalizing the average findings of the GM covariation patterns to a large-scale cohort integrated retrospectively from multiple studies. Further analyses need to be conducted to gain additional insights into the generalizability of these two GM covariation patterns. En ligne : https://dx.doi.org/10.1186/s13229-024-00583-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=537

Linking functional and structural brain organisation with behaviour in autism: a multimodal EU-AIMS Longitudinal European Autism Project (LEAP) study / Alberto LLERA ; Ting MEI ; Koen HAAK ; Christina ISAKOGLOU ; Dorothea L. FLORIS ; Sarah DURSTON ; Carolin MOESSNANG ; Tobias BANASCHEWSKI ; Simon BARON-COHEN ; Eva LOTH ; Flavio DELL'ACQUA ; Tony CHARMAN ; Declan G. M. MURPHY ; Christine ECKER ; Jan K. BUITELAAR ; Christian F. BECKMANN in Molecular Autism, 14 (2023)  

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Patterns of connectome variability in autism across five functional activation tasks: findings from the LEAP project / Tristan LOODEN in Molecular Autism, 13 (2022)  

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Resting state EEG power spectrum and functional connectivity in autism: a cross-sectional analysis / Pilar GARCES in Molecular Autism, 13 (2022)  

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Social brain activation during mentalizing in a large autism cohort: the Longitudinal European Autism Project / Carolin MOESSNANG in Molecular Autism, 11 (2020)  

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The neuroanatomical substrates of autism and ADHD and their link to putative genomic underpinnings / Caroline GURR ; Johanna LEYHAUSEN ; Hanna SEELEMEYER ; Anke BLETSCH ; Tim SCHAEFER ; Charlotte M. PRETZSCH ; Bethany OAKLEY ; Eva LOTH ; Dorothea L. FLORIS ; Jan K. BUITELAAR ; Christian F. BECKMANN ; Tobias BANASCHEWSKI ; Tony CHARMAN ; Emily J. H. JONES ; Julian TILLMANN ; Chris H CHATHAM ; Thomas BOURGERON ; EU-AIMS LEAP Group ; Declan G. M. MURPHY ; Christine ECKER in Molecular Autism, 14 (2023)  

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Towards robust and replicable sex differences in the intrinsic brain function of autism / D. L. FLORIS in Molecular Autism, 12 (2021)  

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