Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model / Jane C. NAVIAUX in Molecular Autism, (January 2015)  

Public ISBD [article]  inMolecular Autism > (January 2015) . - p.1-20 Titre : Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model Type de document : texte imprimé 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 [article] Antipurinergic therapy corrects the autism-like features in the Fragile X (Fmr1 knockout) mouse model [texte imprimé] / 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

Public ISBD in The Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM Titre : Mitochondria and Autism Spectrum Disorders Type de document : texte imprimé 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 in The Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM Mitochondria and Autism Spectrum Disorders [texte imprimé] / 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

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The 3-Hit Metabolic Signaling Model for Autism Spectrum Disorder: A Summary / Robert K. NAVIAUX in Autism Research, 19-5 (May 2026)  

Public ISBD [article]  inAutism Research > 19-5 (May 2026) . - p.e70228 Titre : The 3-Hit Metabolic Signaling Model for Autism Spectrum Disorder: A Summary Type de document : texte imprimé Auteurs : Robert K. NAVIAUX, Auteur Article en page(s) : p.e70228 Langues : Anglais (eng) Mots-clés : autism spectrum disorder  CDR stacking  cell danger response  exposomics  metabolic signaling  metabolomics  mitochondria  network analysis  salugenesis Index. décimale : PER Périodiques Résumé : ABSTRACT Autism spectrum disorder (ASD) is a highly heritable yet environmentally sensitive neurodevelopmental condition whose biological heterogeneity has resisted a unifying causal explanation for over 100?years. The 3-hit metabolic signaling model proposes that ASD arises from abnormal persistence of an evolutionarily conserved stress-response program?the cell danger response (CDR)?during critical windows of neurodevelopment. In this framework, ASD emerges from the sequential interaction of: (1) inherited genetic or epigenetic variants that sensitize mitochondrial metabolism, intracellular calcium handling, and purinergic signaling to environmental change; (2) early prenatal or postnatal activation of the CDR by infection, immune dysregulation, metabolic disturbance, or environmental toxicant exposure; and (3) prolonged or recurrent exposure to CDR-activating triggers for 3?6?months from the late 1st trimester to 18?36?months of age. The CDR is initiated by extracellular ATP (eATP)-associated purinergic signaling and mitochondrial changes that are resource- and energy-intensive. Persistent or recurrent activation of the CDR during the critical neurodevelopmental window is proposed to sensitize developing cells to eATP-related signaling, leading to false alarms and a mixture of chemical, immune, and neurosensory under- and over-responsivity. More frequent cycles of CDR activation and recovery are proposed to cause cellular competition for key bioenergetic, mitochondrial, and metabolic resources needed to support the normal trajectory of child development. Phenylketonuria (PKU) provides a proof-of-principle example. Untreated PKU historically caused intellectual disability and autistic features, while universal newborn screening and early treatment interrupt this sequence and prevent or decrease these outcomes despite strong genetic predisposition. En ligne : https://doi.org/10.1002/aur.70228 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=587 [article] The 3-Hit Metabolic Signaling Model for Autism Spectrum Disorder: A Summary [texte imprimé] / Robert K. NAVIAUX, Auteur . - p.e70228. Langues : Anglais (eng) in Autism Research > 19-5 (May 2026) . - p.e70228 Mots-clés : autism spectrum disorder  CDR stacking  cell danger response  exposomics  metabolic signaling  metabolomics  mitochondria  network analysis  salugenesis Index. décimale : PER Périodiques Résumé : ABSTRACT Autism spectrum disorder (ASD) is a highly heritable yet environmentally sensitive neurodevelopmental condition whose biological heterogeneity has resisted a unifying causal explanation for over 100?years. The 3-hit metabolic signaling model proposes that ASD arises from abnormal persistence of an evolutionarily conserved stress-response program?the cell danger response (CDR)?during critical windows of neurodevelopment. In this framework, ASD emerges from the sequential interaction of: (1) inherited genetic or epigenetic variants that sensitize mitochondrial metabolism, intracellular calcium handling, and purinergic signaling to environmental change; (2) early prenatal or postnatal activation of the CDR by infection, immune dysregulation, metabolic disturbance, or environmental toxicant exposure; and (3) prolonged or recurrent exposure to CDR-activating triggers for 3?6?months from the late 1st trimester to 18?36?months of age. The CDR is initiated by extracellular ATP (eATP)-associated purinergic signaling and mitochondrial changes that are resource- and energy-intensive. Persistent or recurrent activation of the CDR during the critical neurodevelopmental window is proposed to sensitize developing cells to eATP-related signaling, leading to false alarms and a mixture of chemical, immune, and neurosensory under- and over-responsivity. More frequent cycles of CDR activation and recovery are proposed to cause cellular competition for key bioenergetic, mitochondrial, and metabolic resources needed to support the normal trajectory of child development. Phenylketonuria (PKU) provides a proof-of-principle example. Untreated PKU historically caused intellectual disability and autistic features, while universal newborn screening and early treatment interrupt this sequence and prevent or decrease these outcomes despite strong genetic predisposition. En ligne : https://doi.org/10.1002/aur.70228 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=587

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