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Auteur Radhika KINI |
Documents disponibles écrits par cet auteur (1)
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Prenatal and Postnatal Epigenetic Programming: Implications for GI, Immune, and Neuronal Function in Autism / Mostafa WALY in Autism Research and Treatment, (May 2012)
[article]
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
in Autism Research and Treatment > (May 2012) . - 13 p.[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