54 recherche sur le mot-clé 'Neurodevelopment'

Expression Changes in Epigenetic Gene Pathways Associated With One-Carbon Nutritional Metabolites in Maternal Blood From Pregnancies Resulting in Autism and Non-Typical Neurodevelopment / Yihui ZHU in Autism Research, 14-1 (January 2021)  

Public ISBD [article]  inAutism Research > 14-1 (January 2021) . - p.11-28 Titre : Expression Changes in Epigenetic Gene Pathways Associated With One-Carbon Nutritional Metabolites in Maternal Blood From Pregnancies Resulting in Autism and Non-Typical Neurodevelopment Type de document : Texte imprimé et/ou numérique Auteurs : Yihui ZHU, Auteur ; Charles E. MORDAUNT, Auteur ; Blythe DURBIN-JOHNSON, Auteur ; Marie A. CAUDILL, Auteur ; Olga V. MALYSHEVA, Auteur ; Joshua W. MILLER, Auteur ; Ralph GREEN, Auteur ; S. Jill JAMES, Auteur ; Stepan B. MELNYK, Auteur ; M. Daniele FALLIN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Janine M. LASALLE, Auteur Article en page(s) : p.11-28 Langues : Anglais (eng) Mots-clés : autism spectrum disorder  maternal blood  neurodevelopment  nutrition  one-carbon metabolites  prenatal  transcriptome Index. décimale : PER Périodiques Résumé : The prenatal period is a critical window for the development of autism spectrum disorder (ASD). The relationship between prenatal nutrients and gestational gene expression in mothers of children later diagnosed with ASD or non-typical development (Non-TD) is poorly understood. Maternal blood collected prospectively during pregnancy provides insights into the effects of nutrition, particularly one-carbon metabolites, on gene pathways and neurodevelopment. Genome-wide transcriptomes were measured with microarrays in 300 maternal blood samples in Markers of Autism Risk in Babies-Learning Early Signs. Sixteen different one-carbon metabolites, including folic acid, betaine, 5'-methyltretrahydrofolate (5-MeTHF), and dimethylglycine (DMG) were measured. Differential expression analysis and weighted gene correlation network analysis (WGCNA) were used to compare gene expression between children later diagnosed as typical development (TD), Non-TD and ASD, and to one-carbon metabolites. Using differential gene expression analysis, six transcripts (TGR-AS1, SQSTM1, HLA-C, and RFESD) were associated with child outcomes (ASD, Non-TD, and TD) with genome-wide significance. Genes nominally differentially expressed between ASD and TD significantly overlapped with seven high confidence ASD genes. WGCNA identified co-expressed gene modules significantly correlated with 5-MeTHF, folic acid, DMG, and betaine. A module enriched in DNA methylation functions showed a suggestive protective association with folic acid/5-MeTHF concentrations and ASD risk. Maternal plasma betaine and DMG concentrations were associated with a block of co-expressed genes enriched for adaptive immune, histone modification, and RNA processing functions. These results suggest that the prenatal maternal blood transcriptome is a sensitive indicator of gestational one-carbon metabolite status and changes relevant to children's later neurodevelopmental outcomes. LAY SUMMARY: Pregnancy is a time when maternal nutrition could interact with genetic risk for autism spectrum disorder. Blood samples collected during pregnancy from mothers who had a prior child with autism were examined for gene expression and nutrient metabolites, then compared to the diagnosis of the child at age three. Expression differences in gene pathways related to the immune system and gene regulation were observed for pregnancies of children with autism and non-typical neurodevelopment and were associated with maternal nutrients. En ligne : http://dx.doi.org/10.1002/aur.2428 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=441 [article] Expression Changes in Epigenetic Gene Pathways Associated With One-Carbon Nutritional Metabolites in Maternal Blood From Pregnancies Resulting in Autism and Non-Typical Neurodevelopment [Texte imprimé et/ou numérique] / Yihui ZHU, Auteur ; Charles E. MORDAUNT, Auteur ; Blythe DURBIN-JOHNSON, Auteur ; Marie A. CAUDILL, Auteur ; Olga V. MALYSHEVA, Auteur ; Joshua W. MILLER, Auteur ; Ralph GREEN, Auteur ; S. Jill JAMES, Auteur ; Stepan B. MELNYK, Auteur ; M. Daniele FALLIN, Auteur ; Irva HERTZ-PICCIOTTO, Auteur ; Rebecca J. SCHMIDT, Auteur ; Janine M. LASALLE, Auteur . - p.11-28. Langues : Anglais (eng) in Autism Research > 14-1 (January 2021) . - p.11-28 Mots-clés : autism spectrum disorder  maternal blood  neurodevelopment  nutrition  one-carbon metabolites  prenatal  transcriptome Index. décimale : PER Périodiques Résumé : The prenatal period is a critical window for the development of autism spectrum disorder (ASD). The relationship between prenatal nutrients and gestational gene expression in mothers of children later diagnosed with ASD or non-typical development (Non-TD) is poorly understood. Maternal blood collected prospectively during pregnancy provides insights into the effects of nutrition, particularly one-carbon metabolites, on gene pathways and neurodevelopment. Genome-wide transcriptomes were measured with microarrays in 300 maternal blood samples in Markers of Autism Risk in Babies-Learning Early Signs. Sixteen different one-carbon metabolites, including folic acid, betaine, 5'-methyltretrahydrofolate (5-MeTHF), and dimethylglycine (DMG) were measured. Differential expression analysis and weighted gene correlation network analysis (WGCNA) were used to compare gene expression between children later diagnosed as typical development (TD), Non-TD and ASD, and to one-carbon metabolites. Using differential gene expression analysis, six transcripts (TGR-AS1, SQSTM1, HLA-C, and RFESD) were associated with child outcomes (ASD, Non-TD, and TD) with genome-wide significance. Genes nominally differentially expressed between ASD and TD significantly overlapped with seven high confidence ASD genes. WGCNA identified co-expressed gene modules significantly correlated with 5-MeTHF, folic acid, DMG, and betaine. A module enriched in DNA methylation functions showed a suggestive protective association with folic acid/5-MeTHF concentrations and ASD risk. Maternal plasma betaine and DMG concentrations were associated with a block of co-expressed genes enriched for adaptive immune, histone modification, and RNA processing functions. These results suggest that the prenatal maternal blood transcriptome is a sensitive indicator of gestational one-carbon metabolite status and changes relevant to children's later neurodevelopmental outcomes. LAY SUMMARY: Pregnancy is a time when maternal nutrition could interact with genetic risk for autism spectrum disorder. Blood samples collected during pregnancy from mothers who had a prior child with autism were examined for gene expression and nutrient metabolites, then compared to the diagnosis of the child at age three. Expression differences in gene pathways related to the immune system and gene regulation were observed for pregnancies of children with autism and non-typical neurodevelopment and were associated with maternal nutrients. En ligne : http://dx.doi.org/10.1002/aur.2428 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=441

Ethical dimensions of translational developmental neuroscience research in autism / A. MANZINI in Journal of Child Psychology and Psychiatry, 62-11 (November 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-11 (November 2021) . - p.1363-1373 Titre : Ethical dimensions of translational developmental neuroscience research in autism Type de document : Texte imprimé et/ou numérique Auteurs : A. MANZINI, Auteur ; E. J. H. JONES, Auteur ; Tony CHARMAN, Auteur ; M. ELSABBAGH, Auteur ; M. H. JOHNSON, Auteur ; I. SINGH, Auteur Article en page(s) : p.1363-1373 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/diagnosis/genetics  Autistic Disorder  Brain  Child  Early Intervention, Educational  Humans  Neurosciences  Parents  Autism  biomarkers  ethics  genetics  infant siblings  neurodevelopment  Ltd. and Servier  and has received royalties from Sage Publications and Guilford  Publications. Index. décimale : PER Périodiques Résumé : BACKGROUND: Since the 1990s, increasing research has been devoted to the identification of biomarkers for autism to help attain more objective diagnosis; enable early prediction of prognosis; and guide individualized intervention options. Early studies focused on the identification of genetic variants associated with autism, but more recently, research has expanded to investigate neurodevelopmental markers. While ethicists have extensively discussed issues around advances in autism genomics, much less ethical scrutiny has focused on research on early neurodevelopment and on the interventions being developed as a result. OBJECTIVES: We summarize the current state of the science on the identification of early markers for autism and its potential clinical applications, before providing an overview of the ethical issues arising from increasing understanding of children's neurodevelopment in very early life. RESULTS: Advances in the understanding of brain and behavioral trajectories preceding later autism diagnosis raise ethical concerns around three themes: (a) New models for understanding autism; (b) Risks and benefits of early identification and intervention; and (c) Communication of early concerns to families. These ethical issues should be further investigated in research conducted in partnership with autistic people and their families. CONCLUSIONS: This paper highlights the need for ethical scrutiny of early neurodevelopmental research in autism. Scrutiny requires expertise and methods from the basic sciences and bioethics, as well as constructive collaborations among autistic people, their parents, and autism researchers to anticipate early interventions that serve the community's interests and accommodate the varied experiences and preferences of people on the spectrum and their families. En ligne : http://dx.doi.org/10.1111/jcpp.13494 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Ethical dimensions of translational developmental neuroscience research in autism [Texte imprimé et/ou numérique] / A. MANZINI, Auteur ; E. J. H. JONES, Auteur ; Tony CHARMAN, Auteur ; M. ELSABBAGH, Auteur ; M. H. JOHNSON, Auteur ; I. SINGH, Auteur . - p.1363-1373. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-11 (November 2021) . - p.1363-1373 Mots-clés : Autism Spectrum Disorder/diagnosis/genetics  Autistic Disorder  Brain  Child  Early Intervention, Educational  Humans  Neurosciences  Parents  Autism  biomarkers  ethics  genetics  infant siblings  neurodevelopment  Ltd. and Servier  and has received royalties from Sage Publications and Guilford  Publications. Index. décimale : PER Périodiques Résumé : BACKGROUND: Since the 1990s, increasing research has been devoted to the identification of biomarkers for autism to help attain more objective diagnosis; enable early prediction of prognosis; and guide individualized intervention options. Early studies focused on the identification of genetic variants associated with autism, but more recently, research has expanded to investigate neurodevelopmental markers. While ethicists have extensively discussed issues around advances in autism genomics, much less ethical scrutiny has focused on research on early neurodevelopment and on the interventions being developed as a result. OBJECTIVES: We summarize the current state of the science on the identification of early markers for autism and its potential clinical applications, before providing an overview of the ethical issues arising from increasing understanding of children's neurodevelopment in very early life. RESULTS: Advances in the understanding of brain and behavioral trajectories preceding later autism diagnosis raise ethical concerns around three themes: (a) New models for understanding autism; (b) Risks and benefits of early identification and intervention; and (c) Communication of early concerns to families. These ethical issues should be further investigated in research conducted in partnership with autistic people and their families. CONCLUSIONS: This paper highlights the need for ethical scrutiny of early neurodevelopmental research in autism. Scrutiny requires expertise and methods from the basic sciences and bioethics, as well as constructive collaborations among autistic people, their parents, and autism researchers to anticipate early interventions that serve the community's interests and accommodate the varied experiences and preferences of people on the spectrum and their families. En ligne : http://dx.doi.org/10.1111/jcpp.13494 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

A Familial Heterozygous Null Mutation of MET in Autism Spectrum Disorder / Nelle LAMBERT in Autism Research, 7-5 (October 2014)  

Public ISBD [article]  inAutism Research > 7-5 (October 2014) . - p.617-622 Titre : A Familial Heterozygous Null Mutation of MET in Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Nelle LAMBERT, Auteur ; Vanessa WERMENBOL, Auteur ; Bruno PICHON, Auteur ; Sandra T. ACOSTA, Auteur ; Jelle VAN DEN AMEELE, Auteur ; Camille PERAZZOLO, Auteur ; Diana MESSINA, Auteur ; Maria-Franca MUSUMECI, Auteur ; Barbara DESSARS, Auteur ; Anne DE LEENER, Auteur ; Marc ABRAMOWICZ, Auteur ; Catheline VILAIN, Auteur Article en page(s) : p.617-622 Langues : Anglais (eng) Mots-clés : autism spectrum disorder  c-MET  social brain  neurodevelopment Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) results from interactions of genetic and environmental factors. The MET proto-oncogene has been identified as a candidate gene for autism susceptibility, and is implicated in neurodevelopment and social brain circuitry. Here, we describe the first case of a familial mutation of MET, consisting of an interstitial genomic deletion removing exons 12 through 15, causing a frameshift and premature stop codon, with evidence of nonsense-mediated mRNA decay. On the other allele, patients carried the C allele of the MET promoter rs1858830 polymorphism, known to decrease MET expression and previously associated with autism susceptibility. The heterozygous mutation was associated with autism in one patient, and language and social impairment in a sibling. Our observations delineate the phenotypic spectrum associated with a clearly defined, very likely complete loss of function mutation of MET. Incomplete penetrance in this family was consistent with MET as a partial susceptibility gene for ASD. Implication of MET in normal and pathological brain development opens new perspectives for understanding the pathophysiology of autism and for eventual therapeutical clues. Autism Res 2014, 7: 617–622. © 2014 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=241 [article] A Familial Heterozygous Null Mutation of MET in Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Nelle LAMBERT, Auteur ; Vanessa WERMENBOL, Auteur ; Bruno PICHON, Auteur ; Sandra T. ACOSTA, Auteur ; Jelle VAN DEN AMEELE, Auteur ; Camille PERAZZOLO, Auteur ; Diana MESSINA, Auteur ; Maria-Franca MUSUMECI, Auteur ; Barbara DESSARS, Auteur ; Anne DE LEENER, Auteur ; Marc ABRAMOWICZ, Auteur ; Catheline VILAIN, Auteur . - p.617-622. Langues : Anglais (eng) in Autism Research > 7-5 (October 2014) . - p.617-622 Mots-clés : autism spectrum disorder  c-MET  social brain  neurodevelopment Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) results from interactions of genetic and environmental factors. The MET proto-oncogene has been identified as a candidate gene for autism susceptibility, and is implicated in neurodevelopment and social brain circuitry. Here, we describe the first case of a familial mutation of MET, consisting of an interstitial genomic deletion removing exons 12 through 15, causing a frameshift and premature stop codon, with evidence of nonsense-mediated mRNA decay. On the other allele, patients carried the C allele of the MET promoter rs1858830 polymorphism, known to decrease MET expression and previously associated with autism susceptibility. The heterozygous mutation was associated with autism in one patient, and language and social impairment in a sibling. Our observations delineate the phenotypic spectrum associated with a clearly defined, very likely complete loss of function mutation of MET. Incomplete penetrance in this family was consistent with MET as a partial susceptibility gene for ASD. Implication of MET in normal and pathological brain development opens new perspectives for understanding the pathophysiology of autism and for eventual therapeutical clues. Autism Res 2014, 7: 617–622. © 2014 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1396 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=241

The role of prenatal immune activation in the pathogenesis of autism and schizophrenia: A literature review / Amanda EASSON in Research in Autism Spectrum Disorders, 8-3 (March 2014)  

Public ISBD [article]  inResearch in Autism Spectrum Disorders > 8-3 (March 2014) . - p.312-316 Titre : The role of prenatal immune activation in the pathogenesis of autism and schizophrenia: A literature review Type de document : Texte imprimé et/ou numérique Auteurs : Amanda EASSON, Auteur ; Marc WOODBURY-SMITH, Auteur Article en page(s) : p.312-316 Langues : Anglais (eng) Mots-clés : Autism  Schizophrenia  Prenatal  Immune activation  Neurodevelopment Index. décimale : PER Périodiques Résumé : Abstract Autism spectrum disorder (ASD) and schizophrenia (SZ) are two neurodevelopmental disorders that, despite having distinct diagnostic criteria, share certain clinical and etiological features. The genetic origin of the two disorders is beyond doubt, with evidence for unique and overlapping genetic risk factors. However, lower estimates of heritability have recently been reported for both disorders, lending support to a significant contribution from non-genetic factors. Notably, there is increasing evidence that immune activation during prenatal life may act as a risk factor for ASD and SZ. In this review, evidence supporting the hypothesis that prenatal immune activation (PIA) influences the onset and progression of ASD and SZ is analyzed. Results show that the detrimental effects of PIA on neurodevelopment include morphological changes in various brain regions, with perhaps the most notable being the hippocampus and prefrontal cortex, as well as altered activity of neurotransmitter systems such as the serotonergic system and impairments in working memory and prepulse inhibition. An examination of the risk factor of PIA offers new insight into the pathophysiology of ASD and SZ, and in this way opens up new possibilities for the treatment of these two disorders. En ligne : http://dx.doi.org/10.1016/j.rasd.2013.12.007 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=224 [article] The role of prenatal immune activation in the pathogenesis of autism and schizophrenia: A literature review [Texte imprimé et/ou numérique] / Amanda EASSON, Auteur ; Marc WOODBURY-SMITH, Auteur . - p.312-316. Langues : Anglais (eng) in Research in Autism Spectrum Disorders > 8-3 (March 2014) . - p.312-316 Mots-clés : Autism  Schizophrenia  Prenatal  Immune activation  Neurodevelopment Index. décimale : PER Périodiques Résumé : Abstract Autism spectrum disorder (ASD) and schizophrenia (SZ) are two neurodevelopmental disorders that, despite having distinct diagnostic criteria, share certain clinical and etiological features. The genetic origin of the two disorders is beyond doubt, with evidence for unique and overlapping genetic risk factors. However, lower estimates of heritability have recently been reported for both disorders, lending support to a significant contribution from non-genetic factors. Notably, there is increasing evidence that immune activation during prenatal life may act as a risk factor for ASD and SZ. In this review, evidence supporting the hypothesis that prenatal immune activation (PIA) influences the onset and progression of ASD and SZ is analyzed. Results show that the detrimental effects of PIA on neurodevelopment include morphological changes in various brain regions, with perhaps the most notable being the hippocampus and prefrontal cortex, as well as altered activity of neurotransmitter systems such as the serotonergic system and impairments in working memory and prepulse inhibition. An examination of the risk factor of PIA offers new insight into the pathophysiology of ASD and SZ, and in this way opens up new possibilities for the treatment of these two disorders. En ligne : http://dx.doi.org/10.1016/j.rasd.2013.12.007 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=224

Loss of the neurodevelopmental disease-associated gene miR-146a impairs neural progenitor differentiation and causes learning and memory deficits / Julien FREGEAC in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) . - 22 p. Titre : Loss of the neurodevelopmental disease-associated gene miR-146a impairs neural progenitor differentiation and causes learning and memory deficits Type de document : Texte imprimé et/ou numérique Auteurs : Julien FREGEAC, Auteur ; Stéphanie MORICEAU, Auteur ; Antoine POLI, Auteur ; Lam Son NGUYEN, Auteur ; Franck OURY, Auteur ; Laurence COLLEAUX, Auteur Article en page(s) : 22 p. Langues : Anglais (eng) Mots-clés : Hippocampus-dependent cognitive functions  MicroRNA  Neural stem cells differentiation  Neurodevelopment  Neurodevelopmental disorders  miR-146a Index. décimale : PER Périodiques Résumé : BACKGROUND: Formation and maintenance of appropriate neural networks require tight regulation of neural stem cell proliferation, differentiation, and neurogenesis. microRNAs (miRNAs) play an important role in brain development and plasticity, and dysregulated miRNA profiles have been linked to neurodevelopmental disorders including autism, schizophrenia, or intellectual disability. Yet, the functional role of miRNAs in neural development and postnatal brain functions remains unclear. METHODS: Using a combination of cell biology techniques as well as behavioral studies and brain imaging, we characterize mouse models with either constitutive inactivation or selectively hippocampal knockdown of the neurodevelopmental disease-associated gene Mir146a, the most commonly deregulated miRNA in developmental brain disorders (DBD). RESULTS: We first show that during development, loss of miR-146a impairs the differentiation of radial glial cells, neurogenesis process, and neurite extension. In the mouse adult brain, loss of miR-146a correlates with an increased hippocampal asymmetry coupled with defects in spatial learning and memory performances. Moreover, selective hippocampal downregulation of miR-146a in adult mice causes severe hippocampal-dependent memory impairments indicating for the first time a role for this miRNA in postnatal brain functions. CONCLUSION: Our results show that miR-146a expression is critical for correct differentiation of neural stem cell during brain development and provide for the first time a strong argument for a postnatal role of miR-146a in regulating hippocampal-dependent memory. Furthermore, the demonstration that the Mir146a(-/-) mouse recapitulates several aspects reported in DBD patients, including impaired neurogenesis, abnormal brain anatomy, and working and spatial memories deficits, provides convincing evidence that the dysregulation of miR146a contributes to the pathogenesis of DBDs. En ligne : http://dx.doi.org/10.1186/s13229-020-00328-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 [article] Loss of the neurodevelopmental disease-associated gene miR-146a impairs neural progenitor differentiation and causes learning and memory deficits [Texte imprimé et/ou numérique] / Julien FREGEAC, Auteur ; Stéphanie MORICEAU, Auteur ; Antoine POLI, Auteur ; Lam Son NGUYEN, Auteur ; Franck OURY, Auteur ; Laurence COLLEAUX, Auteur . - 22 p. Langues : Anglais (eng) in Molecular Autism > 11 (2020) . - 22 p. Mots-clés : Hippocampus-dependent cognitive functions  MicroRNA  Neural stem cells differentiation  Neurodevelopment  Neurodevelopmental disorders  miR-146a Index. décimale : PER Périodiques Résumé : BACKGROUND: Formation and maintenance of appropriate neural networks require tight regulation of neural stem cell proliferation, differentiation, and neurogenesis. microRNAs (miRNAs) play an important role in brain development and plasticity, and dysregulated miRNA profiles have been linked to neurodevelopmental disorders including autism, schizophrenia, or intellectual disability. Yet, the functional role of miRNAs in neural development and postnatal brain functions remains unclear. METHODS: Using a combination of cell biology techniques as well as behavioral studies and brain imaging, we characterize mouse models with either constitutive inactivation or selectively hippocampal knockdown of the neurodevelopmental disease-associated gene Mir146a, the most commonly deregulated miRNA in developmental brain disorders (DBD). RESULTS: We first show that during development, loss of miR-146a impairs the differentiation of radial glial cells, neurogenesis process, and neurite extension. In the mouse adult brain, loss of miR-146a correlates with an increased hippocampal asymmetry coupled with defects in spatial learning and memory performances. Moreover, selective hippocampal downregulation of miR-146a in adult mice causes severe hippocampal-dependent memory impairments indicating for the first time a role for this miRNA in postnatal brain functions. CONCLUSION: Our results show that miR-146a expression is critical for correct differentiation of neural stem cell during brain development and provide for the first time a strong argument for a postnatal role of miR-146a in regulating hippocampal-dependent memory. Furthermore, the demonstration that the Mir146a(-/-) mouse recapitulates several aspects reported in DBD patients, including impaired neurogenesis, abnormal brain anatomy, and working and spatial memories deficits, provides convincing evidence that the dysregulation of miR146a contributes to the pathogenesis of DBDs. En ligne : http://dx.doi.org/10.1186/s13229-020-00328-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427

An investigation of NFXL1, a gene implicated in a study of specific language impairment / R. NUDEL in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

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Analysis of neuroanatomical differences in mice with genetically modified serotonin transporters assessed by structural magnetic resonance imaging / J. ELLEGOOD in Molecular Autism, 9 (2018)  

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Analysis of the expression pattern of the schizophrenia-risk and intellectual disability gene TCF4 in the developing and adult brain suggests a role in development and plasticity of cortical and hippocampal neurons / M. JUNG in Molecular Autism, 9 (2018)  

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Brief Report: Facial Asymmetry and Autistic-Like Traits in the General Population / Maryam BOUTRUS in Journal of Autism and Developmental Disorders, 51-6 (June 2021)  

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Brinp1(-/-) mice exhibit autism-like behaviour, altered memory, hyperactivity and increased parvalbumin-positive cortical interneuron density / S. R. BERKOWICZ in Molecular Autism, 7 (2016)  

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