
- <Centre d'Information et de documentation du CRA Rhône-Alpes
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Centre d'information et de documentation
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du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexLundi au Vendredi
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9h00-12h00 13h30-16h00Tél: +33(0)4 37 91 54 65
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Fax: +33(0)4 37 91 54 37
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Mention de date : October 2013
Paru le : 01/10/2013 |
[n° ou bulletin]
[n° ou bulletin]
- October 2013 [Texte imprimé et/ou numérique] . - 2013. Langues : Anglais (eng)
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[article]
Titre : Epigenetics and Autism Type de document : Texte imprimé et/ou numérique Auteurs : Tafari MBADIWE, Auteur ; Richard M. MILLIS, Auteur Année de publication : 2013 Article en page(s) : 9 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This review identifies mechanisms for altering DNA-histone interactions of cell chromatin to upregulate or downregulate gene expression that could serve as epigenetic targets for therapeutic interventions in autism. DNA methyltransferases (DNMTs) can phosphorylate histone H3 at T6. Aided by protein kinase C?1, the DNMT lysine-specific demethylase-1 prevents demethylation of H3 at K4. During androgen-receptor-(AR-) dependent gene activation, this sequence may produce AR-dependent gene overactivation which may partly explain the male predominance of autism. AR-dependent gene overactivation in conjunction with a DNMT mechanism for methylating oxytocin receptors could produce high arousal inputs to the amygdala resulting in aberrant socialization, a prime characteristic of autism. Dysregulation of histone methyltransferases and histone deacetylases (HDACs) associated with low activity of methyl CpG binding protein-2 at cytosine-guanine sites in genes may reduce the capacity for condensing chromatin and silencing genes in frontal cortex, a site characterized by decreased cortical interconnectivity in autistic subjects. HDAC1 inhibition can overactivate mRNA transcription, a putative mechanism for the increased number of cerebral cortical columns and local frontal cortex hyperactivity in autistic individuals. These epigenetic mechanisms underlying male predominance, aberrant social interaction, and low functioning frontal cortex may be novel targets for autism prevention and treatment strategies. En ligne : http://dx.doi.org/10.1155/2013/826156 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=228
in Autism Research and Treatment > (October 2013) . - 9 p.[article] Epigenetics and Autism [Texte imprimé et/ou numérique] / Tafari MBADIWE, Auteur ; Richard M. MILLIS, Auteur . - 2013 . - 9 p.
Langues : Anglais (eng)
in Autism Research and Treatment > (October 2013) . - 9 p.
Index. décimale : PER Périodiques Résumé : This review identifies mechanisms for altering DNA-histone interactions of cell chromatin to upregulate or downregulate gene expression that could serve as epigenetic targets for therapeutic interventions in autism. DNA methyltransferases (DNMTs) can phosphorylate histone H3 at T6. Aided by protein kinase C?1, the DNMT lysine-specific demethylase-1 prevents demethylation of H3 at K4. During androgen-receptor-(AR-) dependent gene activation, this sequence may produce AR-dependent gene overactivation which may partly explain the male predominance of autism. AR-dependent gene overactivation in conjunction with a DNMT mechanism for methylating oxytocin receptors could produce high arousal inputs to the amygdala resulting in aberrant socialization, a prime characteristic of autism. Dysregulation of histone methyltransferases and histone deacetylases (HDACs) associated with low activity of methyl CpG binding protein-2 at cytosine-guanine sites in genes may reduce the capacity for condensing chromatin and silencing genes in frontal cortex, a site characterized by decreased cortical interconnectivity in autistic subjects. HDAC1 inhibition can overactivate mRNA transcription, a putative mechanism for the increased number of cerebral cortical columns and local frontal cortex hyperactivity in autistic individuals. These epigenetic mechanisms underlying male predominance, aberrant social interaction, and low functioning frontal cortex may be novel targets for autism prevention and treatment strategies. En ligne : http://dx.doi.org/10.1155/2013/826156 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=228 Neuropathology and Animal Models of Autism: Genetic and Environmental Factors / Bharathi S. GADAD in Autism Research and Treatment, (October 2013)
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[article]
Titre : Neuropathology and Animal Models of Autism: Genetic and Environmental Factors Type de document : Texte imprimé et/ou numérique Auteurs : Bharathi S. GADAD, Auteur ; Laura HEWITSON, Auteur ; Keith A. YOUNG, Auteur ; Dwight C. GERMAN, Auteur Année de publication : 2013 Article en page(s) : 12 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism is a heterogeneous behaviorally defined neurodevelopmental disorder. It is defined by the presence of marked social deficits, specific language abnormalities, and stereotyped repetitive patterns of behavior. Because of the variability in the behavioral phenotype of the disorder among patients, the term autism spectrum disorder has been established. In the first part of this review, we provide an overview of neuropathological findings from studies of autism postmortem brains and identify the cerebellum as one of the key brain regions that can play a role in the autism phenotype. We review research findings that indicate possible links between the environment and autism including the role of mercury and immune-related factors. Because both genes and environment can alter the structure of the developing brain in different ways, it is not surprising that there is heterogeneity in the behavioral and neuropathological phenotypes of autism spectrum disorders. Finally, we describe animal models of autism that occur following insertion of different autism-related genes and exposure to environmental factors, highlighting those models which exhibit both autism-like behavior and neuropathology. En ligne : http://dx.doi.org/10.1155/2013/731935 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=228
in Autism Research and Treatment > (October 2013) . - 12 p.[article] Neuropathology and Animal Models of Autism: Genetic and Environmental Factors [Texte imprimé et/ou numérique] / Bharathi S. GADAD, Auteur ; Laura HEWITSON, Auteur ; Keith A. YOUNG, Auteur ; Dwight C. GERMAN, Auteur . - 2013 . - 12 p.
Langues : Anglais (eng)
in Autism Research and Treatment > (October 2013) . - 12 p.
Index. décimale : PER Périodiques Résumé : Autism is a heterogeneous behaviorally defined neurodevelopmental disorder. It is defined by the presence of marked social deficits, specific language abnormalities, and stereotyped repetitive patterns of behavior. Because of the variability in the behavioral phenotype of the disorder among patients, the term autism spectrum disorder has been established. In the first part of this review, we provide an overview of neuropathological findings from studies of autism postmortem brains and identify the cerebellum as one of the key brain regions that can play a role in the autism phenotype. We review research findings that indicate possible links between the environment and autism including the role of mercury and immune-related factors. Because both genes and environment can alter the structure of the developing brain in different ways, it is not surprising that there is heterogeneity in the behavioral and neuropathological phenotypes of autism spectrum disorders. Finally, we describe animal models of autism that occur following insertion of different autism-related genes and exposure to environmental factors, highlighting those models which exhibit both autism-like behavior and neuropathology. En ligne : http://dx.doi.org/10.1155/2013/731935 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=228