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Détail de l'auteur
Auteur Gilles J. GUILLEMIN |
Documents disponibles écrits par cet auteur (1)
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Altered kynurenine pathway metabolism in autism: Implication for immune-induced glutamatergic activity / Chai K. LIM in Autism Research, 9-6 (June 2016)
[article]
Titre : Altered kynurenine pathway metabolism in autism: Implication for immune-induced glutamatergic activity Type de document : Texte imprimé et/ou numérique Auteurs : Chai K. LIM, Auteur ; Musthafa M. ESSA, Auteur ; Roberta DE PAULA MARTINS, Auteur ; David B. LOVEJOY, Auteur ; Ayse A. BILGIN, Auteur ; Mostafa I. WALY, Auteur ; Yahya M. AL-FARSI, Auteur ; Marwan M. AL-SHARBATI, Auteur ; Mohammed A. AL-SHAFFAE, Auteur ; Gilles J. GUILLEMIN, Auteur Article en page(s) : p.621-631 Langues : Anglais (eng) Mots-clés : kynurenine pathway quinolinic acid excitotoxicity autism neuroinflammation glutamatergic activity Index. décimale : PER Périodiques Résumé : Dysfunction of the serotoninergic and glutamatergic systems is implicated in the pathogenesis of autism spectrum disorder (ASD) together with various neuroinflammatory mediators. As the kynurenine pathway (KP) of tryptophan degradation is activated in neuroinflammatory states, we hypothesized that there may be a link between inflammation in ASD and enhanced KP activation resulting in reduced serotonin synthesis from tryptophan and production of KP metabolites capable of modulating glutamatergic activity. A cross-sectional study of 15 different Omani families with newly diagnosed children with ASD (n?=?15) and their age-matched healthy siblings (n?=?12) was designed. Immunological profile and the KP metabolic signature were characterized in the study participants. Our data indicated that there were alterations to the KP in ASD. Specifically, increased production of the downstream metabolite, quinolinic acid, which is capable of enhancing glutamatergic neurotransmission was noted. Correlation studies also demonstrated that the presence of inflammation induced KP activation in ASD. Until now, previous studies have failed to establish a link between inflammation, glutamatergic activity, and the KP. Our findings also suggest that increased quinolinic acid may be linked to 16p11.2 mutations leading to abnormal glutamatergic activity associated with ASD pathogenesis and may help rationalize the efficacy of sulforaphane treatment in ASD. Autism Res 2016, 9: 621–631. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1565 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=290
in Autism Research > 9-6 (June 2016) . - p.621-631[article] Altered kynurenine pathway metabolism in autism: Implication for immune-induced glutamatergic activity [Texte imprimé et/ou numérique] / Chai K. LIM, Auteur ; Musthafa M. ESSA, Auteur ; Roberta DE PAULA MARTINS, Auteur ; David B. LOVEJOY, Auteur ; Ayse A. BILGIN, Auteur ; Mostafa I. WALY, Auteur ; Yahya M. AL-FARSI, Auteur ; Marwan M. AL-SHARBATI, Auteur ; Mohammed A. AL-SHAFFAE, Auteur ; Gilles J. GUILLEMIN, Auteur . - p.621-631.
Langues : Anglais (eng)
in Autism Research > 9-6 (June 2016) . - p.621-631
Mots-clés : kynurenine pathway quinolinic acid excitotoxicity autism neuroinflammation glutamatergic activity Index. décimale : PER Périodiques Résumé : Dysfunction of the serotoninergic and glutamatergic systems is implicated in the pathogenesis of autism spectrum disorder (ASD) together with various neuroinflammatory mediators. As the kynurenine pathway (KP) of tryptophan degradation is activated in neuroinflammatory states, we hypothesized that there may be a link between inflammation in ASD and enhanced KP activation resulting in reduced serotonin synthesis from tryptophan and production of KP metabolites capable of modulating glutamatergic activity. A cross-sectional study of 15 different Omani families with newly diagnosed children with ASD (n?=?15) and their age-matched healthy siblings (n?=?12) was designed. Immunological profile and the KP metabolic signature were characterized in the study participants. Our data indicated that there were alterations to the KP in ASD. Specifically, increased production of the downstream metabolite, quinolinic acid, which is capable of enhancing glutamatergic neurotransmission was noted. Correlation studies also demonstrated that the presence of inflammation induced KP activation in ASD. Until now, previous studies have failed to establish a link between inflammation, glutamatergic activity, and the KP. Our findings also suggest that increased quinolinic acid may be linked to 16p11.2 mutations leading to abnormal glutamatergic activity associated with ASD pathogenesis and may help rationalize the efficacy of sulforaphane treatment in ASD. Autism Res 2016, 9: 621–631. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1565 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=290