Alterations in plasma cytokine levels in chinese children with autism spectrum disorder / Chun-Chun HU in Autism Research, 11-7 (July 2018)  

Public ISBD [article]  inAutism Research > 11-7 (July 2018) . - p.989-999 Titre : Alterations in plasma cytokine levels in chinese children with autism spectrum disorder Type de document : texte imprimé Auteurs : Chun-Chun HU, Auteur ; Xiu XU, Auteur ; Guo-Liang XIONG, Auteur ; Qiong XU, Auteur ; Bing-Rui ZHOU, Auteur ; Chun-Yang LI, Auteur ; Qi QIN, Auteur ; Chun-Xue LIU, Auteur ; Hui-Ping LI, Auteur ; Yun-Jun SUN, Auteur ; Xiang YU, Auteur Article en page(s) : p.989-999 Langues : Anglais (eng) Mots-clés : TGF-beta1  TNF-alpha  cytokine  eotaxin  immune  neuroinflammation Index. décimale : PER Périodiques Résumé : Genetic alterations, together with environmental risk factors during infancy and childhood, contribute significantly to the etiology of autism spectrum disorder (ASD), a heterogeneous neurodevelopmental condition characterized by impairments in social interaction and restricted, repetitive behaviors. Mounting evidence points to a critical contribution of immunological risk factors to the development of ASD. By affecting multiple neurodevelopmental processes, immune system dysfunction could act as a point of convergence between genetics and environmental factors in ASD. Previous studies have shown altered cytokine levels in individuals with ASD, but research in Asian populations are limited. Here, we measured the plasma levels of 11 candidate cytokines in ASD and typically developing (TD) children. The cohort included 41 TD children and 87 children with ASD, aged 1-6 years. We found that as compared to the TD group, children with ASD had higher plasma levels of Eotaxin, TGF-beta1 and TNF-alpha. The increase in TGF-beta1 level was most significant in males, while the increase in Eotaxin was most significant in females. Eotaxin level negatively correlated with the social affect score (SA) in ADOS, while TNF-alpha level positively correlated with total development quotient (DQ), measured using GMDS. These pilot findings suggest potentially important roles of Eotaxin, TGF-beta1 and TNF-alpha in ASD in the Chinese population. Autism Res 2018, 11: 989-999. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Alteration of immune system function is an important risk factor for autism spectrum disorder (ASD). Here we found that the levels of cytokines, including Eotaxin, TGF-beta1 and TNF-alpha, are elevated in Chinese children with ASD, as compared to typically developing children. The change in TGF-beta1 level was most prominent in boys, while that of Eotaxin was more significant in girls. These results provide evidence for changes in cytokine profile in Chinese children with ASD. En ligne : http://dx.doi.org/10.1002/aur.1940 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Alterations in plasma cytokine levels in chinese children with autism spectrum disorder [texte imprimé] / Chun-Chun HU, Auteur ; Xiu XU, Auteur ; Guo-Liang XIONG, Auteur ; Qiong XU, Auteur ; Bing-Rui ZHOU, Auteur ; Chun-Yang LI, Auteur ; Qi QIN, Auteur ; Chun-Xue LIU, Auteur ; Hui-Ping LI, Auteur ; Yun-Jun SUN, Auteur ; Xiang YU, Auteur . - p.989-999. Langues : Anglais (eng) in Autism Research > 11-7 (July 2018) . - p.989-999 Mots-clés : TGF-beta1  TNF-alpha  cytokine  eotaxin  immune  neuroinflammation Index. décimale : PER Périodiques Résumé : Genetic alterations, together with environmental risk factors during infancy and childhood, contribute significantly to the etiology of autism spectrum disorder (ASD), a heterogeneous neurodevelopmental condition characterized by impairments in social interaction and restricted, repetitive behaviors. Mounting evidence points to a critical contribution of immunological risk factors to the development of ASD. By affecting multiple neurodevelopmental processes, immune system dysfunction could act as a point of convergence between genetics and environmental factors in ASD. Previous studies have shown altered cytokine levels in individuals with ASD, but research in Asian populations are limited. Here, we measured the plasma levels of 11 candidate cytokines in ASD and typically developing (TD) children. The cohort included 41 TD children and 87 children with ASD, aged 1-6 years. We found that as compared to the TD group, children with ASD had higher plasma levels of Eotaxin, TGF-beta1 and TNF-alpha. The increase in TGF-beta1 level was most significant in males, while the increase in Eotaxin was most significant in females. Eotaxin level negatively correlated with the social affect score (SA) in ADOS, while TNF-alpha level positively correlated with total development quotient (DQ), measured using GMDS. These pilot findings suggest potentially important roles of Eotaxin, TGF-beta1 and TNF-alpha in ASD in the Chinese population. Autism Res 2018, 11: 989-999. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Alteration of immune system function is an important risk factor for autism spectrum disorder (ASD). Here we found that the levels of cytokines, including Eotaxin, TGF-beta1 and TNF-alpha, are elevated in Chinese children with ASD, as compared to typically developing children. The change in TGF-beta1 level was most prominent in boys, while that of Eotaxin was more significant in girls. These results provide evidence for changes in cytokine profile in Chinese children with ASD. En ligne : http://dx.doi.org/10.1002/aur.1940 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons / Qiong XU in Molecular Autism, 9 (2018)  

Public ISBD [article]  inMolecular Autism > 9 (2018) . - 65 p. Titre : Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons Type de document : texte imprimé Auteurs : Qiong XU, Auteur ; Yuan-Yuan LIU, Auteur ; Xiaoming WANG, Auteur ; Guo-he TAN, Auteur ; Hui-Ping LI, Auteur ; Samuel W. HULBERT, Auteur ; Chun-Yang LI, Auteur ; Chun-Chun HU, Auteur ; Z.Q. XIONG, Auteur ; Xiu XU, Auteur ; Yong-hui JIANG, Auteur Article en page(s) : 65 p. Langues : Anglais (eng) Mots-clés : Animals  Autistic Disorder/*genetics/pathology  Cells, Cultured  Cerebral Cortex/cytology/growth & development  DNA-Binding Proteins/*genetics/metabolism  Humans  Mice  Mice, Inbred C57BL  *Neurogenesis  Neurons/cytology/*metabolism/physiology  *Autism spectrum disorder (ASD)  *chd8  *Chromatin remodeling  *Neurite growth  *Neurodevelopment  Animal Care and Use Committee-approved protocols both at Children's Hospital of  Fudan University ethics approval ID: 2015-87 and Duke University. Human  postmortem brain tissues: The use of archived human postmortem brain tissues is  approved by Institute Review Board at Duke University.Not applicableThe authors  declare that they have no competing interests.Springer Nature remains neutral  with regard to jurisdictional claims in published maps and institutional  affiliations. Index. décimale : PER Périodiques Résumé : Background: Mutations in CHD8, chromodomain helicase DNA-binding protein 8, are among the most replicated and common findings in genetic studies of autism spectrum disorder (ASD). The CHD8 protein is believed to act as a transcriptional regulator by remodeling chromatin structure and recruiting histone H1 to target genes. The mechanism by which deficiency of CHD8 causes ASD has not been fully elucidated. Methods: We examined the expression of CHD8 in human and mouse brains using both immunohistochemistry and RNA in situ hybridization. We performed in utero electroporation, neuronal culture, and biochemical analysis using RNAi to examine the functional consequences of CHD8 deficiency. Results: We discovered that CHD8 is expressed highly in neurons and at low levels in glia cells in both humans and mice. Specifically, CHD8 is localized predominately in the nucleus of both MAP2 and parvalbumin-positive neurons. In the developing mouse brain, expression of Chd8 peaks from E16 to E18 and then decreases significantly at P14 to adulthood. Knockdown of Chd8 results in reduced axon and dendritic growth, disruption of axon projections to the contralateral cortex, and delayed neuronal migration at E18.5 which recovers by P3 and P7. Conclusion: Our findings indicate an important role for CHD8 in dendritic and axon development and neuronal migration and thus offer novel insights to further dissect the underlying molecular and circuit mechanisms of ASD caused by CHD8 deficiency. En ligne : https://dx.doi.org/10.1186/s13229-018-0244-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389 [article] Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons [texte imprimé] / Qiong XU, Auteur ; Yuan-Yuan LIU, Auteur ; Xiaoming WANG, Auteur ; Guo-he TAN, Auteur ; Hui-Ping LI, Auteur ; Samuel W. HULBERT, Auteur ; Chun-Yang LI, Auteur ; Chun-Chun HU, Auteur ; Z.Q. XIONG, Auteur ; Xiu XU, Auteur ; Yong-hui JIANG, Auteur . - 65 p. Langues : Anglais (eng) in Molecular Autism > 9 (2018) . - 65 p. Mots-clés : Animals  Autistic Disorder/*genetics/pathology  Cells, Cultured  Cerebral Cortex/cytology/growth & development  DNA-Binding Proteins/*genetics/metabolism  Humans  Mice  Mice, Inbred C57BL  *Neurogenesis  Neurons/cytology/*metabolism/physiology  *Autism spectrum disorder (ASD)  *chd8  *Chromatin remodeling  *Neurite growth  *Neurodevelopment  Animal Care and Use Committee-approved protocols both at Children's Hospital of  Fudan University ethics approval ID: 2015-87 and Duke University. Human  postmortem brain tissues: The use of archived human postmortem brain tissues is  approved by Institute Review Board at Duke University.Not applicableThe authors  declare that they have no competing interests.Springer Nature remains neutral  with regard to jurisdictional claims in published maps and institutional  affiliations. Index. décimale : PER Périodiques Résumé : Background: Mutations in CHD8, chromodomain helicase DNA-binding protein 8, are among the most replicated and common findings in genetic studies of autism spectrum disorder (ASD). The CHD8 protein is believed to act as a transcriptional regulator by remodeling chromatin structure and recruiting histone H1 to target genes. The mechanism by which deficiency of CHD8 causes ASD has not been fully elucidated. Methods: We examined the expression of CHD8 in human and mouse brains using both immunohistochemistry and RNA in situ hybridization. We performed in utero electroporation, neuronal culture, and biochemical analysis using RNAi to examine the functional consequences of CHD8 deficiency. Results: We discovered that CHD8 is expressed highly in neurons and at low levels in glia cells in both humans and mice. Specifically, CHD8 is localized predominately in the nucleus of both MAP2 and parvalbumin-positive neurons. In the developing mouse brain, expression of Chd8 peaks from E16 to E18 and then decreases significantly at P14 to adulthood. Knockdown of Chd8 results in reduced axon and dendritic growth, disruption of axon projections to the contralateral cortex, and delayed neuronal migration at E18.5 which recovers by P3 and P7. Conclusion: Our findings indicate an important role for CHD8 in dendritic and axon development and neuronal migration and thus offer novel insights to further dissect the underlying molecular and circuit mechanisms of ASD caused by CHD8 deficiency. En ligne : https://dx.doi.org/10.1186/s13229-018-0244-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389

Clinical impact and in vitro characterization of ADNP variants in pediatric patients / Chuanhui GE in Molecular Autism, 15 (2024)  

Public ISBD [article]  inMolecular Autism > 15 (2024) . - 5p. Titre : Clinical impact and in vitro characterization of ADNP variants in pediatric patients Type de document : texte imprimé Auteurs : Chuanhui GE, Auteur ; Yuxin TIAN, Auteur ; Chunchun HU, Auteur ; Lianni MEI, Auteur ; Dongyun LI, Auteur ; Ping DONG, Auteur ; Ying ZHANG, Auteur ; Huiping LI, Auteur ; Daijing SUN, Auteur ; Wenzhu PENG, Auteur ; Xiu XU, Auteur ; Yan JIANG, Auteur ; Qiong XU, Auteur Article en page(s) : 5p. Langues : Anglais (eng) Mots-clés : Humans  Child  Intellectual Disability/genetics  Autism Spectrum Disorder/genetics  HEK293 Cells  Neuroblastoma  Transcription Factors  Nerve Tissue Proteins  Homeodomain Proteins/genetics  ADNP syndrome  ADNP variants  Autism spectrum disorder  Global developmental delay  Hvdas  Helsmoortel-Van der Aa syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Helsmoortel-Van der Aa syndrome (HVDAS) is a rare genetic disorder caused by variants in the activity-dependent neuroprotector homeobox (ADNP) gene; hence, it is also called ADNP syndrome. ADNP is a multitasking protein with the function as a transcription factor, playing a critical role in brain development. Furthermore, ADNP variants have been identified as one of the most common single-gene causes of autism spectrum disorder (ASD) and intellectual disability. METHODS: We assembled a cohort of 15 Chinese pediatric patients, identified 13 variants in the coding region of ADNP gene, and evaluated their clinical phenotypes. Additionally, we constructed the corresponding ADNP variants and performed western blotting and immunofluorescence analysis to examine their protein expression and subcellular localization in human HEK293T and SH-SY5Y cells. RESULTS: Our study conducted a thorough characterization of the clinical manifestations in 15 children with ADNP variants, and revealed a broad spectrum of symptoms including global developmental delay, intellectual disability, ASD, facial abnormalities, and other features. In vitro studies were carried out to check the expression of ADNP with identified variants. Two cases presented missense variants, while the remainder exhibited nonsense or frameshift variants, leading to truncated mutants in in vitro overexpression systems. Both overexpressed wildtype ADNP and all the different mutants were found to be confined to the nuclei in HEK293T cells; however, the distinctive pattern of nuclear bodies formed by the wildtype ADNP was either partially or entirely disrupted by the mutant proteins. Moreover, two variants of p.Y719* on the nuclear localization signal (NLS) of ADNP disrupted the nuclear expression pattern, predominantly manifesting in the cytoplasm in SH-SY5Y cells. LIMITATIONS: Our study was limited by a relatively small sample size and the absence of a longitudinal framework to monitor the progression of patient conditions over time. Additionally, we lacked in vivo evidence to further indicate the causal implications of the identified ADNP variants. CONCLUSIONS: Our study reported the first cohort of HVDAS patients in the Chinese population and provided systematic clinical presentations and laboratory examinations. Furthermore, we identified multiple genetic variants and validated them in vitro. Our findings offered valuable insights into the diverse genetic variants associated with HVDAS. En ligne : https://dx.doi.org/10.1186/s13229-024-00584-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538 [article] Clinical impact and in vitro characterization of ADNP variants in pediatric patients [texte imprimé] / Chuanhui GE, Auteur ; Yuxin TIAN, Auteur ; Chunchun HU, Auteur ; Lianni MEI, Auteur ; Dongyun LI, Auteur ; Ping DONG, Auteur ; Ying ZHANG, Auteur ; Huiping LI, Auteur ; Daijing SUN, Auteur ; Wenzhu PENG, Auteur ; Xiu XU, Auteur ; Yan JIANG, Auteur ; Qiong XU, Auteur . - 5p. Langues : Anglais (eng) in Molecular Autism > 15 (2024) . - 5p. Mots-clés : Humans  Child  Intellectual Disability/genetics  Autism Spectrum Disorder/genetics  HEK293 Cells  Neuroblastoma  Transcription Factors  Nerve Tissue Proteins  Homeodomain Proteins/genetics  ADNP syndrome  ADNP variants  Autism spectrum disorder  Global developmental delay  Hvdas  Helsmoortel-Van der Aa syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Helsmoortel-Van der Aa syndrome (HVDAS) is a rare genetic disorder caused by variants in the activity-dependent neuroprotector homeobox (ADNP) gene; hence, it is also called ADNP syndrome. ADNP is a multitasking protein with the function as a transcription factor, playing a critical role in brain development. Furthermore, ADNP variants have been identified as one of the most common single-gene causes of autism spectrum disorder (ASD) and intellectual disability. METHODS: We assembled a cohort of 15 Chinese pediatric patients, identified 13 variants in the coding region of ADNP gene, and evaluated their clinical phenotypes. Additionally, we constructed the corresponding ADNP variants and performed western blotting and immunofluorescence analysis to examine their protein expression and subcellular localization in human HEK293T and SH-SY5Y cells. RESULTS: Our study conducted a thorough characterization of the clinical manifestations in 15 children with ADNP variants, and revealed a broad spectrum of symptoms including global developmental delay, intellectual disability, ASD, facial abnormalities, and other features. In vitro studies were carried out to check the expression of ADNP with identified variants. Two cases presented missense variants, while the remainder exhibited nonsense or frameshift variants, leading to truncated mutants in in vitro overexpression systems. Both overexpressed wildtype ADNP and all the different mutants were found to be confined to the nuclei in HEK293T cells; however, the distinctive pattern of nuclear bodies formed by the wildtype ADNP was either partially or entirely disrupted by the mutant proteins. Moreover, two variants of p.Y719* on the nuclear localization signal (NLS) of ADNP disrupted the nuclear expression pattern, predominantly manifesting in the cytoplasm in SH-SY5Y cells. LIMITATIONS: Our study was limited by a relatively small sample size and the absence of a longitudinal framework to monitor the progression of patient conditions over time. Additionally, we lacked in vivo evidence to further indicate the causal implications of the identified ADNP variants. CONCLUSIONS: Our study reported the first cohort of HVDAS patients in the Chinese population and provided systematic clinical presentations and laboratory examinations. Furthermore, we identified multiple genetic variants and validated them in vitro. Our findings offered valuable insights into the diverse genetic variants associated with HVDAS. En ligne : https://dx.doi.org/10.1186/s13229-024-00584-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538

CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors / Chun-Xue LIU in Molecular Autism, 9 (2018)  

Public ISBD [article]  inMolecular Autism > 9 (2018) . - 23p. Titre : CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors Type de document : texte imprimé Auteurs : Chun-Xue LIU, Auteur ; Chun-Yang LI, Auteur ; Chun-Chun HU, Auteur ; Yao WANG, Auteur ; Jia LIN, Auteur ; Yong-hui JIANG, Auteur ; Qiang LI, Auteur ; Xiu XU, Auteur Article en page(s) : 23p. Langues : Anglais (eng) Mots-clés : Asd  Animal model  CRISPR/Cas9  Social behavior  Zebrafish  shank3 Index. décimale : PER Périodiques Résumé : Background: Human genetic and genomic studies have supported a strong causal role of SHANK3 deficiency in autism spectrum disorder (ASD). However, the molecular mechanism underlying SHANK3 deficiency resulting in ASD is not fully understood. Recently, the zebrafish has become an attractive organism to model ASD because of its high efficiency of genetic manipulation and robust behavioral phenotypes. The orthologous gene to human SHANK3 is duplicated in the zebrafish genome and has two homologs, shank3a and shank3b. Previous studies have reported shank3 morphants in zebrafish using the morpholino method. Here, we report the generation and characterization of shank3b mutant zebrafish in larval and adult stages using the CRISPR/Cas9 genome editing technique. Methods: CRISPR/Cas9 was applied to generate a shank3b loss-of-function mutation (shank3b(-/-) ) in zebrafish. A series of morphological measurements, behavioral tests, and molecular analyses were performed to systematically characterize the behavioral and molecular changes in shank3b mutant zebrafish. Results: shank3b(-/-) zebrafish exhibited abnormal morphology in early development. They showed reduced locomotor activity both as larvae and adults, reduced social interaction and time spent near conspecifics, and significant repetitive swimming behaviors. Additionally, the levels of both postsynaptic homer1 and presynaptic synaptophysin were significantly reduced in the adult brain of shank3b-deficient zebrafish. Conclusions: We generated the first inheritable shank3b mutant zebrafish model using CRISPR/Cas9 gene editing approach. shank3b(-/-) zebrafish displayed robust autism-like behaviors and altered levels of the synaptic proteins homer1 and synaptophysin. The versatility of zebrafish as a model for studying neurodevelopment and conducting drug screening will likely have a significant contribution to future studies of human SHANK3 function and ASD. En ligne : http://dx.doi.org/10.1186/s13229-018-0204-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=354 [article] CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors [texte imprimé] / Chun-Xue LIU, Auteur ; Chun-Yang LI, Auteur ; Chun-Chun HU, Auteur ; Yao WANG, Auteur ; Jia LIN, Auteur ; Yong-hui JIANG, Auteur ; Qiang LI, Auteur ; Xiu XU, Auteur . - 23p. Langues : Anglais (eng) in Molecular Autism > 9 (2018) . - 23p. Mots-clés : Asd  Animal model  CRISPR/Cas9  Social behavior  Zebrafish  shank3 Index. décimale : PER Périodiques Résumé : Background: Human genetic and genomic studies have supported a strong causal role of SHANK3 deficiency in autism spectrum disorder (ASD). However, the molecular mechanism underlying SHANK3 deficiency resulting in ASD is not fully understood. Recently, the zebrafish has become an attractive organism to model ASD because of its high efficiency of genetic manipulation and robust behavioral phenotypes. The orthologous gene to human SHANK3 is duplicated in the zebrafish genome and has two homologs, shank3a and shank3b. Previous studies have reported shank3 morphants in zebrafish using the morpholino method. Here, we report the generation and characterization of shank3b mutant zebrafish in larval and adult stages using the CRISPR/Cas9 genome editing technique. Methods: CRISPR/Cas9 was applied to generate a shank3b loss-of-function mutation (shank3b(-/-) ) in zebrafish. A series of morphological measurements, behavioral tests, and molecular analyses were performed to systematically characterize the behavioral and molecular changes in shank3b mutant zebrafish. Results: shank3b(-/-) zebrafish exhibited abnormal morphology in early development. They showed reduced locomotor activity both as larvae and adults, reduced social interaction and time spent near conspecifics, and significant repetitive swimming behaviors. Additionally, the levels of both postsynaptic homer1 and presynaptic synaptophysin were significantly reduced in the adult brain of shank3b-deficient zebrafish. Conclusions: We generated the first inheritable shank3b mutant zebrafish model using CRISPR/Cas9 gene editing approach. shank3b(-/-) zebrafish displayed robust autism-like behaviors and altered levels of the synaptic proteins homer1 and synaptophysin. The versatility of zebrafish as a model for studying neurodevelopment and conducting drug screening will likely have a significant contribution to future studies of human SHANK3 function and ASD. En ligne : http://dx.doi.org/10.1186/s13229-018-0204-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=354

Decreased homotopic interhemispheric functional connectivity in children with autism spectrum disorder / Shuxia YAO in Autism Research, 14-8 (August 2021)  

Public ISBD [article]  inAutism Research > 14-8 (August 2021) . - p.1609-1620 Titre : Decreased homotopic interhemispheric functional connectivity in children with autism spectrum disorder Type de document : texte imprimé Auteurs : Shuxia YAO, Auteur ; Menghan ZHOU, Auteur ; Yuan ZHANG, Auteur ; Feng ZHOU, Auteur ; Qianqian ZHANG, Auteur ; Zhongbo ZHAO, Auteur ; Xi JIANG, Auteur ; Xiu XU, Auteur ; Benjamin BECKER, Auteur ; Keith M. KENDRICK, Auteur Année de publication : 2021 Article en page(s) : p.1609-1620 Langues : Anglais (eng) Mots-clés : Adolescent  Adult  Autism Spectrum Disorder/diagnostic imaging  Brain/diagnostic imaging  Brain Mapping  Child  Child, Preschool  Corpus Callosum/diagnostic imaging  Humans  Magnetic Resonance Imaging  Neural Pathways/diagnostic imaging  autism spectrum disorder  children  corpus callosum  homotopic interhemispheric functional connectivity  resting-state Index. décimale : PER Périodiques Résumé : While several functional and structural changes occur in large-scale brain networks in autism spectrum disorder (ASD), reduced interhemispheric resting-state functional connectivity (rsFC) between homotopic regions may be of particular importance as a biomarker. ASD is an early-onset developmental disorder and neural alterations are often age-dependent. Although there is some evidence for homotopic interhemispheric rsFC alterations in language processing regions in ASD children, wider analyses using large data sets have not been performed. The present study, therefore, conducted a voxel-based homotopic interhemispheric rsFC analysis in 146 ASD and 175 typically developing children under-age 10 and examined associations with symptom severity in the autism brain imaging data exchange data sets. Given the role of corpus callosum (CC) in interhemispheric connectivity and reported CC volume changes in ASD we additionally examined whether there were parallel volumetric changes. Results demonstrated decreased homotopic rsFC in ASD children in the posterior cingulate cortex (PCC) and precuneus of the default mode network, the precentral gyrus of the mirror neuron system, and the caudate of the reward system. Homotopic rsFC of the PCC was associated with symptom severity. Furthermore, although no significant CC volume changes were found in ASD children, there was a significant negative correlation between the anterior CC volumes and homotopic rsFC strengths in the caudate. The present study shows that a reduced pattern of homotopic interhemispheric rsFC in ASD adults/adolescents is already present in children of 5-10 years old and further supports their potential use as a general ASD biomarker. LAY SUMMARY: Homotopic interhemispheric functional connectivity plays an important role in synchronizing activity between the two hemispheres and is altered in adults and adolescents with autism spectrum disorder (ASD). In the present study focused on children with ASD, we have observed a similar pattern of decreased homotopic connectivity, suggesting that alterations in homotopic interhemispheric connectivity may occur early in ASD and be a useful general biomarker across ages. En ligne : http://dx.doi.org/10.1002/aur.2523 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=449 [article] Decreased homotopic interhemispheric functional connectivity in children with autism spectrum disorder [texte imprimé] / Shuxia YAO, Auteur ; Menghan ZHOU, Auteur ; Yuan ZHANG, Auteur ; Feng ZHOU, Auteur ; Qianqian ZHANG, Auteur ; Zhongbo ZHAO, Auteur ; Xi JIANG, Auteur ; Xiu XU, Auteur ; Benjamin BECKER, Auteur ; Keith M. KENDRICK, Auteur . - 2021 . - p.1609-1620. Langues : Anglais (eng) in Autism Research > 14-8 (August 2021) . - p.1609-1620 Mots-clés : Adolescent  Adult  Autism Spectrum Disorder/diagnostic imaging  Brain/diagnostic imaging  Brain Mapping  Child  Child, Preschool  Corpus Callosum/diagnostic imaging  Humans  Magnetic Resonance Imaging  Neural Pathways/diagnostic imaging  autism spectrum disorder  children  corpus callosum  homotopic interhemispheric functional connectivity  resting-state Index. décimale : PER Périodiques Résumé : While several functional and structural changes occur in large-scale brain networks in autism spectrum disorder (ASD), reduced interhemispheric resting-state functional connectivity (rsFC) between homotopic regions may be of particular importance as a biomarker. ASD is an early-onset developmental disorder and neural alterations are often age-dependent. Although there is some evidence for homotopic interhemispheric rsFC alterations in language processing regions in ASD children, wider analyses using large data sets have not been performed. The present study, therefore, conducted a voxel-based homotopic interhemispheric rsFC analysis in 146 ASD and 175 typically developing children under-age 10 and examined associations with symptom severity in the autism brain imaging data exchange data sets. Given the role of corpus callosum (CC) in interhemispheric connectivity and reported CC volume changes in ASD we additionally examined whether there were parallel volumetric changes. Results demonstrated decreased homotopic rsFC in ASD children in the posterior cingulate cortex (PCC) and precuneus of the default mode network, the precentral gyrus of the mirror neuron system, and the caudate of the reward system. Homotopic rsFC of the PCC was associated with symptom severity. Furthermore, although no significant CC volume changes were found in ASD children, there was a significant negative correlation between the anterior CC volumes and homotopic rsFC strengths in the caudate. The present study shows that a reduced pattern of homotopic interhemispheric rsFC in ASD adults/adolescents is already present in children of 5-10 years old and further supports their potential use as a general ASD biomarker. LAY SUMMARY: Homotopic interhemispheric functional connectivity plays an important role in synchronizing activity between the two hemispheres and is altered in adults and adolescents with autism spectrum disorder (ASD). In the present study focused on children with ASD, we have observed a similar pattern of decreased homotopic connectivity, suggesting that alterations in homotopic interhemispheric connectivity may occur early in ASD and be a useful general biomarker across ages. En ligne : http://dx.doi.org/10.1002/aur.2523 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=449

Effects of Parent-Implemented Early Start Denver Model Intervention on Chinese Toddlers with Autism Spectrum Disorder: A Non-Randomized Controlled Trial / Bingrui ZHOU in Autism Research, 11-4 (April 2018)  

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How rare and common risk variation jointly affect liability for autism spectrum disorder / Lambertus KLEI in Molecular Autism, 12 (2021)  

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Improving the early screening procedure for autism spectrum disorder in young children: Experience from a community-based model in shanghai / Chunyang LI in Autism Research, 11-9 (September 2018)  

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A Novel Chd8 Mutant Mouse Displays Altered Ultrasonic Vocalizations and Enhanced Motor Coordination / Samuel W. HULBERT in Autism Research, 13-10 (October 2020)  

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Novel Variants of the SMARCA4 Gene Associated with Autistic Features Rather Than Typical Coffin-Siris Syndrome in Eight Chinese Pediatric Patients / Yanyan QIAN in Journal of Autism and Developmental Disorders, 52-11 (November 2022)  

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Prevalence and phenotypic impact of rare potentially damaging variants in autism spectrum disorder / Behrang MAHJANI in Molecular Autism, 12 (2021)  

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