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

Neuroanatomical underpinnings of autism symptomatology in carriers and non-carriers of the 22q11.2 microdeletion / Maria GUDBRANDSEN in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) . - 46 p. Titre : Neuroanatomical underpinnings of autism symptomatology in carriers and non-carriers of the 22q11.2 microdeletion Type de document : Texte imprimé et/ou numérique Auteurs : Maria GUDBRANDSEN, Auteur ; Anke BLETSCH, Auteur ; Caroline MANN, Auteur ; Eileen DALY, Auteur ; Clodagh M. MURPHY, Auteur ; Vladimira STOENCHEVA, Auteur ; Charlotte E. BLACKMORE, Auteur ; Maria ROGDAKI, Auteur ; Leila KUSHAN, Auteur ; Carrie E. BEARDEN, Auteur ; Declan G. M. MURPHY, Auteur ; Michael C. CRAIG, Auteur ; Christine ECKER, Auteur Article en page(s) : 46 p. Langues : Anglais (eng) Mots-clés : 22q11.2 deletion syndrome  Autism spectrum disorder  Brain anatomy  Neurodevelopment  Surface-based anatomy  authors reported any financial interests or conflicts of interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: A crucial step to understanding the mechanistic underpinnings of autism spectrum disorder (ASD), is to examine if the biological underpinnings of ASD in genetic high-risk conditions, like 22q11.2 deletion syndrome (22q11.2DS), are similar to those in idiopathic illness. This study aimed to examine if ASD symptomatology in 22q11.2DS is underpinned by the same-or distinct-neural systems that mediate these symptoms in non-deletion carriers. METHODS: We examined vertex-wise estimates of cortical volume (CV), surface area (SA), and cortical thickness across 131 individuals between 6 and 25?years of age including (1) 50 individuals with 22q11.2DS, out of which n = 25 had a diagnosis of ASD, (2) 40 non-carriers of the microdeletion with a diagnosis of ASD (i.e., idiopathic ASD), and (3) 41 typically developing (TD) controls. We employed a 2-by-2 factorial design to identify neuroanatomical variability associated with the main effects of 22q11.2DS and ASD, as well as their interaction. Further, using canonical correlation analysis (CCA), we compared neuroanatomical variability associated with the complex (i.e., multivariate) clinical phenotype of ASD between 22q11.2 deletion carriers and non-carriers. RESULTS: The set of brain regions associated with the main effect of 22q11.2DS was distinct from the neuroanatomical underpinnings of the main effect of ASD. Moreover, significant 22q11.2DS-by-ASD interactions were observed for CV and SA in the dorsolateral prefrontal cortex, precentral gyrus, and posterior cingulate cortex, suggesting that the neuroanatomy of ASD is significantly modulated by 22q11.2DS (p < 0.01). We further established that the multivariate patterns of neuroanatomical variability associated with differences in symptom profiles significantly differed between 22q11.2 deletion carriers and non-carriers. LIMITATIONS: We employed a multicenter design to overcome single-site recruitment limitations; however, FreeSurfer-derived measures of surface anatomy have been shown to be highly reliable across scanner platforms and field strengths. Further, we controlled for gender to address the differing distribution between idiopathic ASD individuals and the other groups. Nonetheless, the gender distribution in our sample reflects that of the respective populations, adding to the generalizability of our results. Last, we included individuals with a relatively wide age range (i.e., 6-25?years). CONCLUSIONS: Our findings indicate that neuroanatomical correlates of ASD symptomatology in carriers of the 22q11.2 microdeletion diverge from those in idiopathic ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00356-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 [article] Neuroanatomical underpinnings of autism symptomatology in carriers and non-carriers of the 22q11.2 microdeletion [Texte imprimé et/ou numérique] / Maria GUDBRANDSEN, Auteur ; Anke BLETSCH, Auteur ; Caroline MANN, Auteur ; Eileen DALY, Auteur ; Clodagh M. MURPHY, Auteur ; Vladimira STOENCHEVA, Auteur ; Charlotte E. BLACKMORE, Auteur ; Maria ROGDAKI, Auteur ; Leila KUSHAN, Auteur ; Carrie E. BEARDEN, Auteur ; Declan G. M. MURPHY, Auteur ; Michael C. CRAIG, Auteur ; Christine ECKER, Auteur . - 46 p. Langues : Anglais (eng) in Molecular Autism > 11 (2020) . - 46 p. Mots-clés : 22q11.2 deletion syndrome  Autism spectrum disorder  Brain anatomy  Neurodevelopment  Surface-based anatomy  authors reported any financial interests or conflicts of interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: A crucial step to understanding the mechanistic underpinnings of autism spectrum disorder (ASD), is to examine if the biological underpinnings of ASD in genetic high-risk conditions, like 22q11.2 deletion syndrome (22q11.2DS), are similar to those in idiopathic illness. This study aimed to examine if ASD symptomatology in 22q11.2DS is underpinned by the same-or distinct-neural systems that mediate these symptoms in non-deletion carriers. METHODS: We examined vertex-wise estimates of cortical volume (CV), surface area (SA), and cortical thickness across 131 individuals between 6 and 25?years of age including (1) 50 individuals with 22q11.2DS, out of which n = 25 had a diagnosis of ASD, (2) 40 non-carriers of the microdeletion with a diagnosis of ASD (i.e., idiopathic ASD), and (3) 41 typically developing (TD) controls. We employed a 2-by-2 factorial design to identify neuroanatomical variability associated with the main effects of 22q11.2DS and ASD, as well as their interaction. Further, using canonical correlation analysis (CCA), we compared neuroanatomical variability associated with the complex (i.e., multivariate) clinical phenotype of ASD between 22q11.2 deletion carriers and non-carriers. RESULTS: The set of brain regions associated with the main effect of 22q11.2DS was distinct from the neuroanatomical underpinnings of the main effect of ASD. Moreover, significant 22q11.2DS-by-ASD interactions were observed for CV and SA in the dorsolateral prefrontal cortex, precentral gyrus, and posterior cingulate cortex, suggesting that the neuroanatomy of ASD is significantly modulated by 22q11.2DS (p < 0.01). We further established that the multivariate patterns of neuroanatomical variability associated with differences in symptom profiles significantly differed between 22q11.2 deletion carriers and non-carriers. LIMITATIONS: We employed a multicenter design to overcome single-site recruitment limitations; however, FreeSurfer-derived measures of surface anatomy have been shown to be highly reliable across scanner platforms and field strengths. Further, we controlled for gender to address the differing distribution between idiopathic ASD individuals and the other groups. Nonetheless, the gender distribution in our sample reflects that of the respective populations, adding to the generalizability of our results. Last, we included individuals with a relatively wide age range (i.e., 6-25?years). CONCLUSIONS: Our findings indicate that neuroanatomical correlates of ASD symptomatology in carriers of the 22q11.2 microdeletion diverge from those in idiopathic ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00356-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427

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

Public ISBD [article]  inMolecular Autism > 11 (2020) . - 17 p. Titre : Social brain activation during mentalizing in a large autism cohort: the Longitudinal European Autism Project Type de document : Texte imprimé et/ou numérique Auteurs : Carolin MOESSNANG, Auteur ; Sarah BAUMEISTER, Auteur ; Julian TILLMANN, Auteur ; David GOYARD, Auteur ; Tony CHARMAN, Auteur ; Sara AMBROSINO, Auteur ; Simon BARON-COHEN, Auteur ; Christian F. BECKMANN, Auteur ; Sven BÖLTE, Auteur ; Carsten BOURS, Auteur ; Daisy CRAWLEY, Auteur ; Flavio DELL'ACQUA, Auteur ; Sarah DURSTON, Auteur ; Christine ECKER, Auteur ; Vincent FROUIN, Auteur ; Hannah HAYWARD, Auteur ; Rosemary HOLT, Auteur ; Mark H. JOHNSON, Auteur ; Emily JONES, Auteur ; Meng-Chuan LAI, Auteur ; Michael V. LOMBARDO, Auteur ; Luke MASON, Auteur ; Marianne OLDENHINKEL, Auteur ; Antonio PERSICO, Auteur ; Antonia SAN JOSE CACERES, Auteur ; Will SPOOREN, Auteur ; Eva LOTH, Auteur ; Declan G. M. MURPHY, Auteur ; Jan K. BUITELAAR, Auteur ; Tobias BANASCHEWSKI, Auteur ; Daniel BRANDEIS, Auteur ; Heike TOST, Auteur ; Andreas MEYER-LINDENBERG, Auteur Article en page(s) : 17 p. Langues : Anglais (eng) Mots-clés : Animated shapes  Autism  Autism spectrum disorder  Development  Mentalizing  Multi-site  Social brain  Theory of mind  fMRI  Science, Atheneum Partners, Blueprint Partnership, Boehringer Ingelheim, Daimler und  Benz Stiftung, Elsevier, F. Hoffmann-La Roche, ICARE Schizophrenia, K. G. Jebsen  Foundation, L.E.K Consulting, Lundbeck International Foundation (LINF), R. Adamczak,  Roche Pharma, Science Foundation, Sumitomo Dainippon Pharma, Synapsis  Foundation–Alzheimer Research Switzerland, and System Analytics, and has received  lectures fees including travel fees from Boehringer Ingelheim, Fama Public  Relations, Institut d’investigacions Biomèdiques August Pi i Sunyer (IDIBAPS),  Janssen-Cilag, Klinikum Christophsbad, Göppingen, Lilly Deutschland, Luzerner  Psychiatrie, LVR Klinikum Düsseldorf, LWL Psychiatrie Verbund Westfalen-Lippe,  Otsuka Pharmaceuticals, Reunions i Ciencia S. L., Spanish Society of Psychiatry,  Südwestrundfunk Fernsehen, Stern TV, and Vitos Klinikum Kurhessen. WM has received  lecture or travel fees from Pfizer, Grünenthal, University of Zürich, International  Association for the Study on Pain (IASP), and European Federation of IASP Chapters  (EFIC). SB discloses that he has in the last 5?years acted as an author, consultant  or lecturer for Shire, Medice, Roche, Eli Lilly, Prima Psychiatry, GLGroup, System  Analytic, Ability Partner, Kompetento, Expo Medica, Clarion Healthcare, and  Prophase. He receives royalties for textbooks and diagnostic tools from  Huber/Hogrefe, Kohlhammer, and UTB. The other authors declare that they have no  competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental condition with key deficits in social functioning. It is widely assumed that the biological underpinnings of social impairment are neurofunctional alterations in the "social brain," a neural circuitry involved in inferring the mental state of a social partner. However, previous evidence comes from small-scale studies and findings have been mixed. We therefore carried out the to-date largest study on neural correlates of mentalizing in ASD. METHODS: As part of the Longitudinal European Autism Project, we performed functional magnetic resonance imaging at six European sites in a large, well-powered, and deeply phenotyped sample of individuals with ASD (N = 205) and typically developing (TD) individuals (N = 189) aged 6 to 30?years. We presented an animated shapes task to assess and comprehensively characterize social brain activation during mentalizing. We tested for effects of age, diagnosis, and their association with symptom measures, including a continuous measure of autistic traits. RESULTS: We observed robust effects of task. Within the ASD sample, autistic traits were moderately associated with functional activation in one of the key regions of the social brain, the dorsomedial prefrontal cortex. However, there were no significant effects of diagnosis on task performance and no effects of age and diagnosis on social brain responses. Besides a lack of mean group differences, our data provide no evidence for meaningful differences in the distribution of brain response measures. Extensive control analyses suggest that the lack of case-control differences was not due to a variety of potential confounders. CONCLUSIONS: Contrary to prior reports, this large-scale study does not support the assumption that altered social brain activation during mentalizing forms a common neural marker of ASD, at least with the paradigm we employed. Yet, autistic individuals show socio-behavioral deficits. Our work therefore highlights the need to interrogate social brain function with other brain measures, such as connectivity and network-based approaches, using other paradigms, or applying complementary analysis approaches to assess individual differences in this heterogeneous condition. En ligne : http://dx.doi.org/10.1186/s13229-020-0317-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 [article] Social brain activation during mentalizing in a large autism cohort: the Longitudinal European Autism Project [Texte imprimé et/ou numérique] / Carolin MOESSNANG, Auteur ; Sarah BAUMEISTER, Auteur ; Julian TILLMANN, Auteur ; David GOYARD, Auteur ; Tony CHARMAN, Auteur ; Sara AMBROSINO, Auteur ; Simon BARON-COHEN, Auteur ; Christian F. BECKMANN, Auteur ; Sven BÖLTE, Auteur ; Carsten BOURS, Auteur ; Daisy CRAWLEY, Auteur ; Flavio DELL'ACQUA, Auteur ; Sarah DURSTON, Auteur ; Christine ECKER, Auteur ; Vincent FROUIN, Auteur ; Hannah HAYWARD, Auteur ; Rosemary HOLT, Auteur ; Mark H. JOHNSON, Auteur ; Emily JONES, Auteur ; Meng-Chuan LAI, Auteur ; Michael V. LOMBARDO, Auteur ; Luke MASON, Auteur ; Marianne OLDENHINKEL, Auteur ; Antonio PERSICO, Auteur ; Antonia SAN JOSE CACERES, Auteur ; Will SPOOREN, Auteur ; Eva LOTH, Auteur ; Declan G. M. MURPHY, Auteur ; Jan K. BUITELAAR, Auteur ; Tobias BANASCHEWSKI, Auteur ; Daniel BRANDEIS, Auteur ; Heike TOST, Auteur ; Andreas MEYER-LINDENBERG, Auteur . - 17 p. Langues : Anglais (eng) in Molecular Autism > 11 (2020) . - 17 p. Mots-clés : Animated shapes  Autism  Autism spectrum disorder  Development  Mentalizing  Multi-site  Social brain  Theory of mind  fMRI  Science, Atheneum Partners, Blueprint Partnership, Boehringer Ingelheim, Daimler und  Benz Stiftung, Elsevier, F. Hoffmann-La Roche, ICARE Schizophrenia, K. G. Jebsen  Foundation, L.E.K Consulting, Lundbeck International Foundation (LINF), R. Adamczak,  Roche Pharma, Science Foundation, Sumitomo Dainippon Pharma, Synapsis  Foundation–Alzheimer Research Switzerland, and System Analytics, and has received  lectures fees including travel fees from Boehringer Ingelheim, Fama Public  Relations, Institut d’investigacions Biomèdiques August Pi i Sunyer (IDIBAPS),  Janssen-Cilag, Klinikum Christophsbad, Göppingen, Lilly Deutschland, Luzerner  Psychiatrie, LVR Klinikum Düsseldorf, LWL Psychiatrie Verbund Westfalen-Lippe,  Otsuka Pharmaceuticals, Reunions i Ciencia S. L., Spanish Society of Psychiatry,  Südwestrundfunk Fernsehen, Stern TV, and Vitos Klinikum Kurhessen. WM has received  lecture or travel fees from Pfizer, Grünenthal, University of Zürich, International  Association for the Study on Pain (IASP), and European Federation of IASP Chapters  (EFIC). SB discloses that he has in the last 5?years acted as an author, consultant  or lecturer for Shire, Medice, Roche, Eli Lilly, Prima Psychiatry, GLGroup, System  Analytic, Ability Partner, Kompetento, Expo Medica, Clarion Healthcare, and  Prophase. He receives royalties for textbooks and diagnostic tools from  Huber/Hogrefe, Kohlhammer, and UTB. The other authors declare that they have no  competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental condition with key deficits in social functioning. It is widely assumed that the biological underpinnings of social impairment are neurofunctional alterations in the "social brain," a neural circuitry involved in inferring the mental state of a social partner. However, previous evidence comes from small-scale studies and findings have been mixed. We therefore carried out the to-date largest study on neural correlates of mentalizing in ASD. METHODS: As part of the Longitudinal European Autism Project, we performed functional magnetic resonance imaging at six European sites in a large, well-powered, and deeply phenotyped sample of individuals with ASD (N = 205) and typically developing (TD) individuals (N = 189) aged 6 to 30?years. We presented an animated shapes task to assess and comprehensively characterize social brain activation during mentalizing. We tested for effects of age, diagnosis, and their association with symptom measures, including a continuous measure of autistic traits. RESULTS: We observed robust effects of task. Within the ASD sample, autistic traits were moderately associated with functional activation in one of the key regions of the social brain, the dorsomedial prefrontal cortex. However, there were no significant effects of diagnosis on task performance and no effects of age and diagnosis on social brain responses. Besides a lack of mean group differences, our data provide no evidence for meaningful differences in the distribution of brain response measures. Extensive control analyses suggest that the lack of case-control differences was not due to a variety of potential confounders. CONCLUSIONS: Contrary to prior reports, this large-scale study does not support the assumption that altered social brain activation during mentalizing forms a common neural marker of ASD, at least with the paradigm we employed. Yet, autistic individuals show socio-behavioral deficits. Our work therefore highlights the need to interrogate social brain function with other brain measures, such as connectivity and network-based approaches, using other paradigms, or applying complementary analysis approaches to assess individual differences in this heterogeneous condition. En ligne : http://dx.doi.org/10.1186/s13229-020-0317-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427

---

1 (1 - 3 / 3)