Dépouillements

Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism / Mostafa WALY in Autism Research and Treatment, (May 2012)  

Public ISBD [article]  inAutism Research and Treatment > (May 2012) . - 13 p. Titre : Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism Type de document : Texte imprimé et/ou numérique Auteurs : Mostafa WALY, Auteur ; Mady HORNIG, Auteur ; Malav TRIVEDI, Auteur ; Nathaniel HODGSON, Auteur ; Radhika KINI, Auteur ; Akio OHTA, Auteur ; Richard DETH, Auteur Année de publication : 2012 Article en page(s) : 13 p. Langues : Anglais (eng) Mots-clés : Maladie gastro-intestinale Index. décimale : PER Périodiques Résumé : Although autism is first and foremost a disorder of the central nervous system, comorbid dysfunction of the gastrointestinal (GI) and immune systems is common, suggesting that all three systems may be affected by common molecular mechanisms. Substantial systemic deficits in the antioxidant glutathione and its precursor, cysteine, have been documented in autism in association with oxidative stress and impaired methylation. DNA and histone methylation provide epigenetic regulation of gene expression during prenatal and postnatal development. Prenatal epigenetic programming (PrEP) can be affected by the maternal metabolic and nutritional environment, whereas postnatal epigenetic programming (PEP) importantly depends upon nutritional support provided through the GI tract. Cysteine absorption from the GI tract is a crucial determinant of antioxidant capacity, and systemic deficits of glutathione and cysteine in autism are likely to reflect impaired cysteine absorption. Excitatory amino acid transporter 3 (EAAT3) provides cysteine uptake for GI epithelial, neuronal, and immune cells, and its activity is decreased during oxidative stress. Based upon these observations, we propose that neurodevelopmental, GI, and immune aspects of autism each reflect manifestations of inadequate antioxidant capacity, secondary to impaired cysteine uptake by the GI tract. Genetic and environmental factors that adversely affect antioxidant capacity can disrupt PrEP and/or PEP, increasing vulnerability to autism. En ligne : http://dx.doi.org/10.1155/2012/190930 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=179 [article] Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism [Texte imprimé et/ou numérique] / Mostafa WALY, Auteur ; Mady HORNIG, Auteur ; Malav TRIVEDI, Auteur ; Nathaniel HODGSON, Auteur ; Radhika KINI, Auteur ; Akio OHTA, Auteur ; Richard DETH, Auteur . - 2012 . - 13 p. Langues : Anglais (eng) in Autism Research and Treatment > (May 2012) . - 13 p. Mots-clés : Maladie gastro-intestinale Index. décimale : PER Périodiques Résumé : Although autism is first and foremost a disorder of the central nervous system, comorbid dysfunction of the gastrointestinal (GI) and immune systems is common, suggesting that all three systems may be affected by common molecular mechanisms. Substantial systemic deficits in the antioxidant glutathione and its precursor, cysteine, have been documented in autism in association with oxidative stress and impaired methylation. DNA and histone methylation provide epigenetic regulation of gene expression during prenatal and postnatal development. Prenatal epigenetic programming (PrEP) can be affected by the maternal metabolic and nutritional environment, whereas postnatal epigenetic programming (PEP) importantly depends upon nutritional support provided through the GI tract. Cysteine absorption from the GI tract is a crucial determinant of antioxidant capacity, and systemic deficits of glutathione and cysteine in autism are likely to reflect impaired cysteine absorption. Excitatory amino acid transporter 3 (EAAT3) provides cysteine uptake for GI epithelial, neuronal, and immune cells, and its activity is decreased during oxidative stress. Based upon these observations, we propose that neurodevelopmental, GI, and immune aspects of autism each reflect manifestations of inadequate antioxidant capacity, secondary to impaired cysteine uptake by the GI tract. Genetic and environmental factors that adversely affect antioxidant capacity can disrupt PrEP and/or PEP, increasing vulnerability to autism. En ligne : http://dx.doi.org/10.1155/2012/190930 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=179

The Development of Executive Function in Autism / Elizabeth PELLICANO in Autism Research and Treatment, (May 2012)  

Public ISBD [article]  inAutism Research and Treatment > (May 2012) . - 8 p. Titre : The Development of Executive Function in Autism Type de document : Texte imprimé et/ou numérique Auteurs : Elizabeth PELLICANO, Auteur Année de publication : 2012 Article en page(s) : 8 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism is a common and often highly debilitating neurodevelopmental condition, whose core behavioral features are believed to be rooted in disrupted neurocognitive processes, including especially “executive function.” Researchers have predominantly focused upon understanding the putative causal relationship between difficulties in EF and autistic symptomatology. This paper suggests, however, that the effects of individual differences in EF should be more far-reaching, playing a significant part in the real-life outcomes of individuals with autism, including their social competence, everyday adaptive behavior, and academic achievement. It further considers the nature of the EF-outcome relationship, including the possible determinants of individual differences in EF, and makes several recommendations for future research. En ligne : http://dx.doi.org/10.1155/2012/146132 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=179 [article] The Development of Executive Function in Autism [Texte imprimé et/ou numérique] / Elizabeth PELLICANO, Auteur . - 2012 . - 8 p. Langues : Anglais (eng) in Autism Research and Treatment > (May 2012) . - 8 p. Index. décimale : PER Périodiques Résumé : Autism is a common and often highly debilitating neurodevelopmental condition, whose core behavioral features are believed to be rooted in disrupted neurocognitive processes, including especially “executive function.” Researchers have predominantly focused upon understanding the putative causal relationship between difficulties in EF and autistic symptomatology. This paper suggests, however, that the effects of individual differences in EF should be more far-reaching, playing a significant part in the real-life outcomes of individuals with autism, including their social competence, everyday adaptive behavior, and academic achievement. It further considers the nature of the EF-outcome relationship, including the possible determinants of individual differences in EF, and makes several recommendations for future research. En ligne : http://dx.doi.org/10.1155/2012/146132 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=179

Identification of Four Novel Synonymous Substitutions in the X-Linked Genes Neuroligin 3 and Neuroligin 4X in Japanese Patients with Autistic Spectrum Disorder / Kumiko YANAGI in Autism Research and Treatment, (May 2012)  

Public ISBD [article]  inAutism Research and Treatment > (May 2012) . - 5 p. Titre : Identification of Four Novel Synonymous Substitutions in the X-Linked Genes Neuroligin 3 and Neuroligin 4X in Japanese Patients with Autistic Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Kumiko YANAGI, Auteur ; Tadashi KANAME, Auteur ; Keiko WAKUI, Auteur ; Ohiko HASHIMOTO, Auteur ; Yoshimitsu FUKUSHIMA, Auteur ; Kenji NARITOMI, Auteur Année de publication : 2012 Article en page(s) : 5 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Mutations in the X-linked genes neuroligin 3 (NLGN3) and neuroligin 4X (NLGN4X) were first implicated in the pathogenesis of X-linked autism in Swedish families. However, reports of mutations in these genes in autism spectrum disorder (ASD) patients from various ethnic backgrounds present conflicting results regarding the etiology of ASD, possibly because of genetic heterogeneity and/or differences in their ethnic background. Additional mutation screening study on another ethnic background could help to clarify the relevance of the genes to ASD. We scanned the entire coding regions of NLGN3 and NLGN4X in 62 Japanese patients with ASD by polymerase chain reaction-high-resolution melting curve and direct sequencing analyses. Four synonymous substitutions, one in NLGN3 and three in NLGN4X, were identified in four of the 62 patients. These substitutions were not present in 278 control X-chromosomes from unrelated Japanese individuals and were not registered in the database of Single Nucleotide Polymorphisms build 132 or in the Japanese Single Nucleotide Polymorphisms database, indicating that they were novel and specific to ASD. Though further analysis is necessary to determine the physiological and clinical importance of such substitutions, the possibility of the relevance of both synonymous and nonsynonymous substitutions with the etiology of ASD should be considered. En ligne : http://dx.doi.org/10.1155/2012/724072 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=179 [article] Identification of Four Novel Synonymous Substitutions in the X-Linked Genes Neuroligin 3 and Neuroligin 4X in Japanese Patients with Autistic Spectrum Disorder [Texte imprimé et/ou numérique] / Kumiko YANAGI, Auteur ; Tadashi KANAME, Auteur ; Keiko WAKUI, Auteur ; Ohiko HASHIMOTO, Auteur ; Yoshimitsu FUKUSHIMA, Auteur ; Kenji NARITOMI, Auteur . - 2012 . - 5 p. Langues : Anglais (eng) in Autism Research and Treatment > (May 2012) . - 5 p. Index. décimale : PER Périodiques Résumé : Mutations in the X-linked genes neuroligin 3 (NLGN3) and neuroligin 4X (NLGN4X) were first implicated in the pathogenesis of X-linked autism in Swedish families. However, reports of mutations in these genes in autism spectrum disorder (ASD) patients from various ethnic backgrounds present conflicting results regarding the etiology of ASD, possibly because of genetic heterogeneity and/or differences in their ethnic background. Additional mutation screening study on another ethnic background could help to clarify the relevance of the genes to ASD. We scanned the entire coding regions of NLGN3 and NLGN4X in 62 Japanese patients with ASD by polymerase chain reaction-high-resolution melting curve and direct sequencing analyses. Four synonymous substitutions, one in NLGN3 and three in NLGN4X, were identified in four of the 62 patients. These substitutions were not present in 278 control X-chromosomes from unrelated Japanese individuals and were not registered in the database of Single Nucleotide Polymorphisms build 132 or in the Japanese Single Nucleotide Polymorphisms database, indicating that they were novel and specific to ASD. Though further analysis is necessary to determine the physiological and clinical importance of such substitutions, the possibility of the relevance of both synonymous and nonsynonymous substitutions with the etiology of ASD should be considered. En ligne : http://dx.doi.org/10.1155/2012/724072 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=179