Copy number variation in Han Chinese individuals with autism spectrum disorder / M. J. GAZZELLONE in Journal of Neurodevelopmental Disorders, 6-1 (December 2014)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 6-1 (December 2014) . - p.34 Titre : Copy number variation in Han Chinese individuals with autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : M. J. GAZZELLONE, Auteur ; X. ZHOU, Auteur ; A. C. LIONEL, Auteur ; M. UDDIN, Auteur ; B. THIRUVAHINDRAPURAM, Auteur ; S. LIANG, Auteur ; C. SUN, Auteur ; J. WANG, Auteur ; M. ZOU, Auteur ; K. TAMMIMIES, Auteur ; S. WALKER, Auteur ; T. SELVANAYAGAM, Auteur ; J. WEI, Auteur ; Z. WANG, Auteur ; L. WU, Auteur ; Stephen SCHERER, Auteur Article en page(s) : p.34 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder (ASD)  Copy number variations (CNVs)  Han Chinese  Microarray diagnostic testing Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASDs) are a group of neurodevelopmental conditions with a demonstrated genetic etiology. Rare (<1% frequency) copy number variations (CNVs) account for a proportion of the genetic events involved, but the contribution of these events in non-European ASD populations has not been well studied. Here, we report on rare CNVs detected in a cohort of individuals with ASD of Han Chinese background. METHODS: DNA samples were obtained from 104 ASD probands and their parents who were recruited from Harbin, China. Samples were genotyped on the Affymetrix CytoScan HD platform. Rare CNVs were identified by comparing data with 873 technology-matched controls from Ontario and 1,235 additional population controls of Han Chinese ethnicity. RESULTS: Of the probands, 8.6% had at least 1 de novo CNV (overlapping the GIGYF2, SPRY1, 16p13.3, 16p11.2, 17p13.3-17p13.2, DMD, and NAP1L6 genes/loci). Rare inherited CNVs affected other plausible neurodevelopmental candidate genes including GRID2, LINGO2, and SLC39A12. A 24-kb duplication was also identified at YWHAE, a gene previously implicated in ASD and other developmental disorders. This duplication is observed at a similar frequency in cases and in population controls and is likely a benign Asian-specific copy number polymorphism. CONCLUSIONS: Our findings help define genomic features relevant to ASD in the Han Chinese and emphasize the importance of using ancestry-matched controls in medical genetic interpretations. En ligne : http://dx.doi.org/10.1186/1866-1955-6-34 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=346 [article] Copy number variation in Han Chinese individuals with autism spectrum disorder [Texte imprimé et/ou numérique] / M. J. GAZZELLONE, Auteur ; X. ZHOU, Auteur ; A. C. LIONEL, Auteur ; M. UDDIN, Auteur ; B. THIRUVAHINDRAPURAM, Auteur ; S. LIANG, Auteur ; C. SUN, Auteur ; J. WANG, Auteur ; M. ZOU, Auteur ; K. TAMMIMIES, Auteur ; S. WALKER, Auteur ; T. SELVANAYAGAM, Auteur ; J. WEI, Auteur ; Z. WANG, Auteur ; L. WU, Auteur ; Stephen SCHERER, Auteur . - p.34. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 6-1 (December 2014) . - p.34 Mots-clés : Autism spectrum disorder (ASD)  Copy number variations (CNVs)  Han Chinese  Microarray diagnostic testing Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASDs) are a group of neurodevelopmental conditions with a demonstrated genetic etiology. Rare (<1% frequency) copy number variations (CNVs) account for a proportion of the genetic events involved, but the contribution of these events in non-European ASD populations has not been well studied. Here, we report on rare CNVs detected in a cohort of individuals with ASD of Han Chinese background. METHODS: DNA samples were obtained from 104 ASD probands and their parents who were recruited from Harbin, China. Samples were genotyped on the Affymetrix CytoScan HD platform. Rare CNVs were identified by comparing data with 873 technology-matched controls from Ontario and 1,235 additional population controls of Han Chinese ethnicity. RESULTS: Of the probands, 8.6% had at least 1 de novo CNV (overlapping the GIGYF2, SPRY1, 16p13.3, 16p11.2, 17p13.3-17p13.2, DMD, and NAP1L6 genes/loci). Rare inherited CNVs affected other plausible neurodevelopmental candidate genes including GRID2, LINGO2, and SLC39A12. A 24-kb duplication was also identified at YWHAE, a gene previously implicated in ASD and other developmental disorders. This duplication is observed at a similar frequency in cases and in population controls and is likely a benign Asian-specific copy number polymorphism. CONCLUSIONS: Our findings help define genomic features relevant to ASD in the Han Chinese and emphasize the importance of using ancestry-matched controls in medical genetic interpretations. En ligne : http://dx.doi.org/10.1186/1866-1955-6-34 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=346

Depicting the composition of gut microbiota in children with tic disorders: an exploratory study / W. XI in Journal of Child Psychology and Psychiatry, 62-10 (October 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1246-1254 Titre : Depicting the composition of gut microbiota in children with tic disorders: an exploratory study Type de document : Texte imprimé et/ou numérique Auteurs : W. XI, Auteur ; X. GAO, Auteur ; H. ZHAO, Auteur ; X. LUO, Auteur ; J. LI, Auteur ; X. TAN, Auteur ; L. WANG, Auteur ; J. B. ZHAO, Auteur ; J. WANG, Auteur ; G. YANG, Auteur ; L. Y. LIU, Auteur ; Y. Y. WANG, Auteur ; L. PENG, Auteur ; L. P. ZOU, Auteur ; Y. YANG, Auteur Article en page(s) : p.1246-1254 Langues : Anglais (eng) Mots-clés : Bacteroides  Child  Gastrointestinal Microbiome  Humans  Prevotella  Ruminococcus  Streptococcus  Tic Disorders  dopamine receptor antagonists  gut microbiota  metabolic pathways  metagenomics Index. décimale : PER Périodiques Résumé : BACKGROUND: Symptom improvement in children with tic disorder (TD) following fecal microbiota transplantation led us to investigate the gut microbiota in TD. This exploratory study aims to depict the gut microbial profile in patients with TD and explore the impact of dopamine receptor antagonist (DRA) drugs on the composition and metabolic function of the gut microbiota. METHODS: The gut microbiota were profiled in fecal samples of 49 children with TD and 50 matched healthy controls (HC) using shotgun metagenomic sequencing. A random forest (RF) model was constructed using the gut bacterial species to distinguish TD from HC. Associations between clinical metadata and microbial abundance or function were analyzed using MaAsLin2 and Spearman correlation. RESULTS: The gut microbiota in children with TD was featured by higher abundances of Bacteroides plebeius and Ruminococcus lactaris (a potential pro-inflammatory taxon) and lower abundances of Prevotella stercorea and Streptococcus lutetiensis compared to HC. The constructed RF model accurately distinguished TD from HC based on the gut microbiota profile, resulting in an AUC of 0.884. Significant correlations were observed between tic symptom severity and the abundances of multiple bacterial species and gut microbiota metabolic functions. Multivariate analysis identified an upregulation of 4-aminobutanoate (GABA) degradation in the gut microbiota associated with TD status. The gut microbiota of DRA-treated TD children showed a distinct gut microbiota compared to the treatment-naïve group, represented by an increase in some potential enteric pathogens such as Escherichia coli, a decline in several species including Akkermansia muciniphila, and alterations in various metabolic functions. CONCLUSIONS: Bacterial species promoting inflammatory responses and those modulating neurotransmitters such as GABA may be involved in the pathogenesis of TD. The use of DRA drugs is likely to induce overgrowth of some enteric pathogens and alter the gut microbiota metabolism. En ligne : http://dx.doi.org/10.1111/jcpp.13409 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Depicting the composition of gut microbiota in children with tic disorders: an exploratory study [Texte imprimé et/ou numérique] / W. XI, Auteur ; X. GAO, Auteur ; H. ZHAO, Auteur ; X. LUO, Auteur ; J. LI, Auteur ; X. TAN, Auteur ; L. WANG, Auteur ; J. B. ZHAO, Auteur ; J. WANG, Auteur ; G. YANG, Auteur ; L. Y. LIU, Auteur ; Y. Y. WANG, Auteur ; L. PENG, Auteur ; L. P. ZOU, Auteur ; Y. YANG, Auteur . - p.1246-1254. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-10 (October 2021) . - p.1246-1254 Mots-clés : Bacteroides  Child  Gastrointestinal Microbiome  Humans  Prevotella  Ruminococcus  Streptococcus  Tic Disorders  dopamine receptor antagonists  gut microbiota  metabolic pathways  metagenomics Index. décimale : PER Périodiques Résumé : BACKGROUND: Symptom improvement in children with tic disorder (TD) following fecal microbiota transplantation led us to investigate the gut microbiota in TD. This exploratory study aims to depict the gut microbial profile in patients with TD and explore the impact of dopamine receptor antagonist (DRA) drugs on the composition and metabolic function of the gut microbiota. METHODS: The gut microbiota were profiled in fecal samples of 49 children with TD and 50 matched healthy controls (HC) using shotgun metagenomic sequencing. A random forest (RF) model was constructed using the gut bacterial species to distinguish TD from HC. Associations between clinical metadata and microbial abundance or function were analyzed using MaAsLin2 and Spearman correlation. RESULTS: The gut microbiota in children with TD was featured by higher abundances of Bacteroides plebeius and Ruminococcus lactaris (a potential pro-inflammatory taxon) and lower abundances of Prevotella stercorea and Streptococcus lutetiensis compared to HC. The constructed RF model accurately distinguished TD from HC based on the gut microbiota profile, resulting in an AUC of 0.884. Significant correlations were observed between tic symptom severity and the abundances of multiple bacterial species and gut microbiota metabolic functions. Multivariate analysis identified an upregulation of 4-aminobutanoate (GABA) degradation in the gut microbiota associated with TD status. The gut microbiota of DRA-treated TD children showed a distinct gut microbiota compared to the treatment-naïve group, represented by an increase in some potential enteric pathogens such as Escherichia coli, a decline in several species including Akkermansia muciniphila, and alterations in various metabolic functions. CONCLUSIONS: Bacterial species promoting inflammatory responses and those modulating neurotransmitters such as GABA may be involved in the pathogenesis of TD. The use of DRA drugs is likely to induce overgrowth of some enteric pathogens and alter the gut microbiota metabolism. En ligne : http://dx.doi.org/10.1111/jcpp.13409 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

Effects of a social stimulus on gene expression in a mouse model of fragile X syndrome / T. D. ROGERS in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 30p. Titre : Effects of a social stimulus on gene expression in a mouse model of fragile X syndrome Type de document : Texte imprimé et/ou numérique Auteurs : T. D. ROGERS, Auteur ; A. M. J. ANACKER, Auteur ; T. M. KERR, Auteur ; C. G. FORSBERG, Auteur ; J. WANG, Auteur ; B. ZHANG, Auteur ; J. VEENSTRA-VANDERWEELE, Auteur Article en page(s) : 30p. Langues : Anglais (eng) Mots-clés : Amygdala  Autism spectrum disorder  Fragile X syndrome  Prefrontal cortex  RNA sequencing  Social behavior Index. décimale : PER Périodiques Résumé : BACKGROUND: People with fragile X syndrome (FXS) often have deficits in social behavior, and a substantial portion meet criteria for autism spectrum disorder. Though the genetic cause of FXS is known to be due to the silencing of FMR1, and the Fmr1 null mouse model representing this lesion has been extensively studied, the contributions of this gene and its protein product, FMRP, to social behavior are not well understood. METHODS: Fmr1 null mice and wildtype littermates were exposed to a social or non-social stimulus. In one experiment, subjects were assessed for expression of the inducible transcription factor c-Fos in response to the stimulus, to detect brain regions with social-specific activity. In a separate experiment, tissue was taken from those brain regions showing differential activity, and RNA sequencing was performed. RESULTS: Immunohistochemistry revealed a significantly greater number of c-Fos-positive cells in the lateral amygdala and medial amygdala in the brains of mice exposed to a social stimulus, compared to a non-social stimulus. In the prelimbic cortex, there was no significant effect of social stimulus; although the number of c-Fos-positive cells was lower in the social condition compared to the non-social condition, and negatively correlated with c-Fos in the amygdala. RNA sequencing revealed differentially expressed genes enriched for molecules known to interact with FMRP and also for autism-related genes identified in the Simons Foundation Autism Research Initiative gene database. Ingenuity Pathway Analysis detected enrichment of differentially expressed genes in networks and pathways related to neuronal development, intracellular signaling, and inflammatory response. CONCLUSIONS: Using the Fmr1 null mouse model of fragile X syndrome, we have identified brain regions, gene networks, and molecular pathways responsive to a social stimulus. These findings, and future experiments following up on the role of specific gene networks, may shed light on the neural mechanisms underlying dysregulated social behaviors in fragile X syndrome and more broadly. En ligne : http://dx.doi.org/10.1186/s13229-017-0148-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330 [article] Effects of a social stimulus on gene expression in a mouse model of fragile X syndrome [Texte imprimé et/ou numérique] / T. D. ROGERS, Auteur ; A. M. J. ANACKER, Auteur ; T. M. KERR, Auteur ; C. G. FORSBERG, Auteur ; J. WANG, Auteur ; B. ZHANG, Auteur ; J. VEENSTRA-VANDERWEELE, Auteur . - 30p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 30p. Mots-clés : Amygdala  Autism spectrum disorder  Fragile X syndrome  Prefrontal cortex  RNA sequencing  Social behavior Index. décimale : PER Périodiques Résumé : BACKGROUND: People with fragile X syndrome (FXS) often have deficits in social behavior, and a substantial portion meet criteria for autism spectrum disorder. Though the genetic cause of FXS is known to be due to the silencing of FMR1, and the Fmr1 null mouse model representing this lesion has been extensively studied, the contributions of this gene and its protein product, FMRP, to social behavior are not well understood. METHODS: Fmr1 null mice and wildtype littermates were exposed to a social or non-social stimulus. In one experiment, subjects were assessed for expression of the inducible transcription factor c-Fos in response to the stimulus, to detect brain regions with social-specific activity. In a separate experiment, tissue was taken from those brain regions showing differential activity, and RNA sequencing was performed. RESULTS: Immunohistochemistry revealed a significantly greater number of c-Fos-positive cells in the lateral amygdala and medial amygdala in the brains of mice exposed to a social stimulus, compared to a non-social stimulus. In the prelimbic cortex, there was no significant effect of social stimulus; although the number of c-Fos-positive cells was lower in the social condition compared to the non-social condition, and negatively correlated with c-Fos in the amygdala. RNA sequencing revealed differentially expressed genes enriched for molecules known to interact with FMRP and also for autism-related genes identified in the Simons Foundation Autism Research Initiative gene database. Ingenuity Pathway Analysis detected enrichment of differentially expressed genes in networks and pathways related to neuronal development, intracellular signaling, and inflammatory response. CONCLUSIONS: Using the Fmr1 null mouse model of fragile X syndrome, we have identified brain regions, gene networks, and molecular pathways responsive to a social stimulus. These findings, and future experiments following up on the role of specific gene networks, may shed light on the neural mechanisms underlying dysregulated social behaviors in fragile X syndrome and more broadly. En ligne : http://dx.doi.org/10.1186/s13229-017-0148-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330

Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome / L. E. ETHRIDGE in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 38p. Titre : Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome Type de document : Texte imprimé et/ou numérique Auteurs : L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur Article en page(s) : 38p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : [This corrects the article DOI: 10.1186/s13229-017-0140-1.]. En ligne : http://dx.doi.org/10.1186/s13229-017-0150-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330 [article] Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome [Texte imprimé et/ou numérique] / L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur . - 38p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 38p. Index. décimale : PER Périodiques Résumé : [This corrects the article DOI: 10.1186/s13229-017-0140-1.]. En ligne : http://dx.doi.org/10.1186/s13229-017-0150-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330

Few individuals with Lennox-Gastaut syndrome have autism spectrum disorder: a comparison with Dravet syndrome / N. HE in Journal of Neurodevelopmental Disorders, 10-1 (December 2018)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 10-1 (December 2018) . - p.10 Titre : Few individuals with Lennox-Gastaut syndrome have autism spectrum disorder: a comparison with Dravet syndrome Type de document : Texte imprimé et/ou numérique Auteurs : N. HE, Auteur ; B. M. LI, Auteur ; Z. X. LI, Auteur ; J. WANG, Auteur ; X. R. LIU, Auteur ; H. MENG, Auteur ; B. TANG, Auteur ; W. J. BIAN, Auteur ; Y. W. SHI, Auteur ; W. P. LIAO, Auteur Article en page(s) : p.10 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder  Dravet syndrome  Epileptic encephalopathy  Intellectual disability  Lennox-Gastaut syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) in epilepsy has been a topic of increasing interest, which in general occurs in 15-35% of the patients with epilepsy, more frequently in those with intellectual disability (ID). Lennox-Gastaut syndrome (LGS) and Dravet syndrome (DS) are two typical forms of intractable epileptic encephalopathy associated with ID. We previously reported that ASD was diagnosed in 24.3% of patients with DS, higher in those with profound ID. Given the severe epilepsy and high frequency of ID in LGS, it is necessary to know whether ASD is a common psychomotor co-morbidity of LGS. This study evaluated the autistic behaviors and intelligence in patients with LGS and further compared that between LGS and DS, aiming to understand the complex pathogenesis of epilepsy-ASD-ID triad. METHODS: A total of 50 patients with LGS and 45 patients with DS were enrolled and followed up for at least 3 years. The clinical characteristics were analyzed, and evaluations of ASD and ID were performed. RESULTS: No patients with LGS fully met the diagnostic criteria for ASD, but three of them exhibited more or less autistic behaviors. Majority (86%) of LGS patients presented ID, among which moderate to severe ID was the most common. Early onset age and symptomatic etiology were risk predictors for ID. The prevalence of ASD in LGS was significantly lower than that in DS (0/50 vs. 10/45, p < 0.001), while the prevalence and severity of ID showed no significant difference between the two forms of epileptic encephalopathy. CONCLUSIONS: This study demonstrated a significant difference in the co-morbidity of ASD between LGS and DS, although they had a similar prevalence and severity of ID, refuting the proposal that the prevalence of ASD in epilepsy is accounted for by ID. These findings suggest that the co-morbidity of ASD, ID, and epilepsy may result from multifaceted pathogenic mechanisms. En ligne : http://dx.doi.org/10.1186/s11689-018-9229-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=351 [article] Few individuals with Lennox-Gastaut syndrome have autism spectrum disorder: a comparison with Dravet syndrome [Texte imprimé et/ou numérique] / N. HE, Auteur ; B. M. LI, Auteur ; Z. X. LI, Auteur ; J. WANG, Auteur ; X. R. LIU, Auteur ; H. MENG, Auteur ; B. TANG, Auteur ; W. J. BIAN, Auteur ; Y. W. SHI, Auteur ; W. P. LIAO, Auteur . - p.10. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 10-1 (December 2018) . - p.10 Mots-clés : Autism spectrum disorder  Dravet syndrome  Epileptic encephalopathy  Intellectual disability  Lennox-Gastaut syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) in epilepsy has been a topic of increasing interest, which in general occurs in 15-35% of the patients with epilepsy, more frequently in those with intellectual disability (ID). Lennox-Gastaut syndrome (LGS) and Dravet syndrome (DS) are two typical forms of intractable epileptic encephalopathy associated with ID. We previously reported that ASD was diagnosed in 24.3% of patients with DS, higher in those with profound ID. Given the severe epilepsy and high frequency of ID in LGS, it is necessary to know whether ASD is a common psychomotor co-morbidity of LGS. This study evaluated the autistic behaviors and intelligence in patients with LGS and further compared that between LGS and DS, aiming to understand the complex pathogenesis of epilepsy-ASD-ID triad. METHODS: A total of 50 patients with LGS and 45 patients with DS were enrolled and followed up for at least 3 years. The clinical characteristics were analyzed, and evaluations of ASD and ID were performed. RESULTS: No patients with LGS fully met the diagnostic criteria for ASD, but three of them exhibited more or less autistic behaviors. Majority (86%) of LGS patients presented ID, among which moderate to severe ID was the most common. Early onset age and symptomatic etiology were risk predictors for ID. The prevalence of ASD in LGS was significantly lower than that in DS (0/50 vs. 10/45, p < 0.001), while the prevalence and severity of ID showed no significant difference between the two forms of epileptic encephalopathy. CONCLUSIONS: This study demonstrated a significant difference in the co-morbidity of ASD between LGS and DS, although they had a similar prevalence and severity of ID, refuting the proposal that the prevalence of ASD in epilepsy is accounted for by ID. These findings suggest that the co-morbidity of ASD, ID, and epilepsy may result from multifaceted pathogenic mechanisms. En ligne : http://dx.doi.org/10.1186/s11689-018-9229-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=351

Genomic sequencing of a dyslexia susceptibility haplotype encompassing ROBO1 / S. MASSINEN in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

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A granular perspective on inclusion: Objectively measured interactions of preschoolers with and without autism / R. M. FASANO in Autism Research, 14-8 (August 2021)  

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Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome / L. E. ETHRIDGE in Molecular Autism, 8 (2017)  

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Refractive Status and Amblyopia Risk Factors in Chinese Children with Autism Spectrum Disorder / J. WANG in Journal of Autism and Developmental Disorders, 48-5 (May 2018)  

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A resting EEG study of neocortical hyperexcitability and altered functional connectivity in fragile X syndrome / J. WANG in Journal of Neurodevelopmental Disorders, 9-1 (December 2017)  

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Resting state EEG abnormalities in autism spectrum disorders / J. WANG in Journal of Neurodevelopmental Disorders, 5-1 (December 2013)  

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