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Détail de l'auteur
Auteur Robert K. NAVIAUX |
Documents disponibles écrits par cet auteur (2)
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Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model / Jane C. NAVIAUX in Molecular Autism, (January 2015)
[article]
Titre : Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model Type de document : Texte imprimé et/ou numérique Auteurs : Jane C. NAVIAUX, Auteur ; Lin WANG, Auteur ; Kefeng LI, Auteur ; A. Taylor BRIGHT, Auteur ; William A. ALAYNICK, Auteur ; Kenneth R. WILLIAMS, Auteur ; Susan B. POWELL, Auteur ; Robert K. NAVIAUX, Auteur Article en page(s) : p.1-20 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This study was designed to test a new approach to drug treatment of autism spectrum disorders (ASDs) in the Fragile X (Fmr1) knockout mouse model. En ligne : http://dx.doi.org/10.1186/2040-2392-6-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277
in Molecular Autism > (January 2015) . - p.1-20[article] Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model [Texte imprimé et/ou numérique] / Jane C. NAVIAUX, Auteur ; Lin WANG, Auteur ; Kefeng LI, Auteur ; A. Taylor BRIGHT, Auteur ; William A. ALAYNICK, Auteur ; Kenneth R. WILLIAMS, Auteur ; Susan B. POWELL, Auteur ; Robert K. NAVIAUX, Auteur . - p.1-20.
Langues : Anglais (eng)
in Molecular Autism > (January 2015) . - p.1-20
Index. décimale : PER Périodiques Résumé : This study was designed to test a new approach to drug treatment of autism spectrum disorders (ASDs) in the Fragile X (Fmr1) knockout mouse model. En ligne : http://dx.doi.org/10.1186/2040-2392-6-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277 Mitochondria and Autism Spectrum Disorders / Robert K. NAVIAUX
Titre : Mitochondria and Autism Spectrum Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Robert K. NAVIAUX, Auteur Année de publication : 2013 Importance : p.179-193 Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Recently, the connections between mitochondria and autism spectrum disorders (ASD) have become increasingly clear. The nature of this connection is more complex than previously thought. A simple reduction in mitochondrial function does not cause ASD. A small but informative fraction of autism is caused by single-gene defects or DNA copy number variations, with the large majority of ASD being the result of variation in hundreds of genes and loci, interacting with environmental and other factors. The crossroads of genes and environment is metabolism. Mitocellular hormesis is the adaptation of cellular and mitochondrial metabolism to environmental change. Changes in nutrition, infectious agents, environmental toxicants, intellectual attention, and physical activity each play a role in mitocellular hormesis during children’s development. Definite mitochondrial disease is responsible for less than 5% of ASD, however, pathological disturbances in mitochondrial metabolism leading to excitotoxicity may lie at the heart of a larger proportion of ASD. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 Mitochondria and Autism Spectrum Disorders [Texte imprimé et/ou numérique] / Robert K. NAVIAUX, Auteur . - 2013 . - p.179-193.
Langues : Anglais (eng)
Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Recently, the connections between mitochondria and autism spectrum disorders (ASD) have become increasingly clear. The nature of this connection is more complex than previously thought. A simple reduction in mitochondrial function does not cause ASD. A small but informative fraction of autism is caused by single-gene defects or DNA copy number variations, with the large majority of ASD being the result of variation in hundreds of genes and loci, interacting with environmental and other factors. The crossroads of genes and environment is metabolism. Mitocellular hormesis is the adaptation of cellular and mitochondrial metabolism to environmental change. Changes in nutrition, infectious agents, environmental toxicants, intellectual attention, and physical activity each play a role in mitocellular hormesis during children’s development. Definite mitochondrial disease is responsible for less than 5% of ASD, however, pathological disturbances in mitochondrial metabolism leading to excitotoxicity may lie at the heart of a larger proportion of ASD. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 Exemplaires
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