Oxidative brain damage in Mecp2-mutant murine models of Rett syndrome
Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patien...
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| Published in | Neurobiology of disease Vol. 68; no. 100; pp. 66 - 77 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.08.2014
Elsevier Academic Press |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both −/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress.
•Oxidative damage is demonstrated in the brain, and more specifically in the neurons, of Mecp2 mutant mouse models.•A direct evidence between enhanced oxidative stress and Mecp2 deficiency is provided.•Oxidative damage precedes the behavioral abnormalities in Mecp2 mutant mice.•Mecp2 is likely involved in the protection of the brain from oxidative stress. |
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| AbstractList | Abstract Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 ( MECP2 ). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2 -null (pre-symptomatic, symptomatic, and rescued) and Mecp2 -308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2 -isoprostanes, F4 -neuroprostanes, F2 -dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2 -null (both −/y and stop/y) and Mecp2 -308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2 -null and Mecp2 -308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2 -reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both -/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress.Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both -/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelmingmajority of the cases by loss-of-functionmutations in the gene encodingmethyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both −/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both -/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 ( MECP2 ). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2 -null (pre-symptomatic, symptomatic, and rescued) and Mecp2 -308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F 2 -isoprostanes, F 4 -neuroprostanes, F 2 -dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2 -null (both −/y and stop/y) and Mecp2 -308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2 -null and Mecp2 -308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2 -reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. • Oxidative damage is demonstrated in the brain, and more specifically in the neurons, of Mecp2 mutant mouse models. • A direct evidence between enhanced oxidative stress and Mecp2 deficiency is provided. • Oxidative damage precedes the behavioral abnormalities in Mecp2 mutant mice. • Mecp2 is likely involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F sub(2)-isoprostanes, F sub(4)-neuroprostanes, F sub(2)-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both -/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both −/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. •Oxidative damage is demonstrated in the brain, and more specifically in the neurons, of Mecp2 mutant mouse models.•A direct evidence between enhanced oxidative stress and Mecp2 deficiency is provided.•Oxidative damage precedes the behavioral abnormalities in Mecp2 mutant mice.•Mecp2 is likely involved in the protection of the brain from oxidative stress. Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by loss-of-function mutations in the gene encoding methyl-CpG binding protein 2 (MECP2). High circulating levels of oxidative stress (OS) markers in patients suggest the involvement of OS in the RTT pathogenesis. To investigate the occurrence of oxidative brain damage in Mecp2 mutant mouse models, several OS markers were evaluated in whole brains of Mecp2-null (pre-symptomatic, symptomatic, and rescued) and Mecp2-308 mutated (pre-symptomatic and symptomatic) mice, and compared to those of wild type littermates. Selected OS markers included non-protein-bound iron, isoprostanes (F2-isoprostanes, F4-neuroprostanes, F2-dihomo-isoprostanes) and 4-hydroxy-2-nonenal protein adducts. Our findings indicate that oxidative brain damage 1) occurs in both Mecp2-null (both −/y and stop/y) and Mecp2-308 (both 308/y males and 308/+ females) mouse models of RTT; 2) precedes the onset of symptoms in both Mecp2-null and Mecp2-308 models; and 3) is rescued by Mecp2 brain specific gene reactivation. Our data provide direct evidence of the link between Mecp2 deficiency, oxidative stress and RTT pathology, as demonstrated by the rescue of the brain oxidative homeostasis following brain-specifically Mecp2-reactivated mice. The present study indicates that oxidative brain damage is a previously unrecognized hallmark feature of murine RTT, and suggests that Mecp2 is involved in the protection of the brain from oxidative stress. |
| Author | Hayek, Joussef Marracino, Federico Belmonte, Giuseppe Della Ragione, Floriana Ciccoli, Lucia Leoncini, Silvia Oger, Camille Bultel-Poncé, Valérie D'Esposito, Maurizio De Felice, Claudio Galano, Jean-Marie Guy, Alexandre Ricceri, Laura Filosa, Stefania Durand, Thierry Valacchi, Giuseppe Madonna, Michele Guy, Jacky Signorini, Cinzia Laviola, Giovanni Scalabrì, Francesco Pecorelli, Alessandra De Filippis, Bianca |
| AuthorAffiliation | b Institute of Genetics and Biophysics “A. Buzzati-Traverso”, Naples, Italy e Child Neuropsychiatry Unit, University Hospital AOUS, Siena, Italy g Department of Life Sciences and Biotechnologies, University of Ferrara, Ferrara, Italy f Department of Cell Biology and Neuroscience, ISS, Rome, Italy i Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh, United Kingdom c IRCCS Neuromed, Pozzilli, Italy d Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy h Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France a Neonatal Intensive Care Unit, University Hospital AOUS, Siena, Italy |
| AuthorAffiliation_xml | – name: a Neonatal Intensive Care Unit, University Hospital AOUS, Siena, Italy – name: e Child Neuropsychiatry Unit, University Hospital AOUS, Siena, Italy – name: g Department of Life Sciences and Biotechnologies, University of Ferrara, Ferrara, Italy – name: h Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France – name: i Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh, United Kingdom – name: f Department of Cell Biology and Neuroscience, ISS, Rome, Italy – name: c IRCCS Neuromed, Pozzilli, Italy – name: b Institute of Genetics and Biophysics “A. Buzzati-Traverso”, Naples, Italy – name: d Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy |
| Author_xml | – sequence: 1 givenname: Claudio surname: De Felice fullname: De Felice, Claudio email: geniente@gmail.com organization: Neonatal Intensive Care Unit, University Hospital AOUS, Siena, Italy – sequence: 2 givenname: Floriana surname: Della Ragione fullname: Della Ragione, Floriana organization: Institute of Genetics and Biophysics “A. Buzzati-Traverso”, Naples, Italy – sequence: 3 givenname: Cinzia surname: Signorini fullname: Signorini, Cinzia organization: Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy – sequence: 4 givenname: Silvia surname: Leoncini fullname: Leoncini, Silvia organization: Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy – sequence: 5 givenname: Alessandra surname: Pecorelli fullname: Pecorelli, Alessandra organization: Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy – sequence: 6 givenname: Lucia surname: Ciccoli fullname: Ciccoli, Lucia organization: Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy – sequence: 7 givenname: Francesco surname: Scalabrì fullname: Scalabrì, Francesco organization: IRCCS Neuromed, Pozzilli, Italy – sequence: 8 givenname: Federico surname: Marracino fullname: Marracino, Federico organization: IRCCS Neuromed, Pozzilli, Italy – sequence: 9 givenname: Michele surname: Madonna fullname: Madonna, Michele organization: IRCCS Neuromed, Pozzilli, Italy – sequence: 10 givenname: Giuseppe surname: Belmonte fullname: Belmonte, Giuseppe organization: Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy – sequence: 11 givenname: Laura surname: Ricceri fullname: Ricceri, Laura organization: Department of Cell Biology and Neuroscience, ISS, Rome, Italy – sequence: 12 givenname: Bianca surname: De Filippis fullname: De Filippis, Bianca organization: Department of Cell Biology and Neuroscience, ISS, Rome, Italy – sequence: 13 givenname: Giovanni surname: Laviola fullname: Laviola, Giovanni organization: Department of Cell Biology and Neuroscience, ISS, Rome, Italy – sequence: 14 givenname: Giuseppe surname: Valacchi fullname: Valacchi, Giuseppe organization: Department of Life Sciences and Biotechnologies, University of Ferrara, Ferrara, Italy – sequence: 15 givenname: Thierry surname: Durand fullname: Durand, Thierry organization: Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France – sequence: 16 givenname: Jean-Marie surname: Galano fullname: Galano, Jean-Marie organization: Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France – sequence: 17 givenname: Camille surname: Oger fullname: Oger, Camille organization: Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France – sequence: 18 givenname: Alexandre surname: Guy fullname: Guy, Alexandre organization: Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France – sequence: 19 givenname: Valérie surname: Bultel-Poncé fullname: Bultel-Poncé, Valérie organization: Institut des Biomolécules Max Mousseron (IBMM), UMR 5247-CNRS-UM I-UM II-ENSCM, Montpellier, France – sequence: 20 givenname: Jacky surname: Guy fullname: Guy, Jacky organization: Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh, United Kingdom – sequence: 21 givenname: Stefania surname: Filosa fullname: Filosa, Stefania organization: Institute of Genetics and Biophysics “A. Buzzati-Traverso”, Naples, Italy – sequence: 22 givenname: Joussef surname: Hayek fullname: Hayek, Joussef organization: Child Neuropsychiatry Unit, University Hospital AOUS, Siena, Italy – sequence: 23 givenname: Maurizio surname: D'Esposito fullname: D'Esposito, Maurizio email: maurizio.desposito@igb.cnr.it organization: Institute of Genetics and Biophysics “A. Buzzati-Traverso”, Naples, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24769161$$D View this record in MEDLINE/PubMed https://hal.science/hal-00997408$$DView record in HAL |
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| Copyright | 2014 The Authors The Authors Copyright © 2014. Published by Elsevier Inc. Attribution - NonCommercial - NoDerivatives 2014 The Authors 2014 |
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| Snippet | Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by... Abstract Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelming majority of the cases by... Rett syndrome (RTT) is a rare neurodevelopmental disorder affecting almost exclusively females, caused in the overwhelmingmajority of the cases by... |
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| SubjectTerms | Aldehydes - metabolism Analysis of Variance Animals Arachidonic Acid - metabolism Biochemistry, Molecular Biology Brain damage Brain Injuries - blood Brain Injuries - etiology Brain Injuries - pathology Disease Models, Animal Docosahexaenoic Acids - metabolism Female Gas Chromatography-Mass Spectrometry Genomics Isoprostanes - metabolism Life Sciences Lipid peroxidation Male Methyl-CpG-Binding Protein 2 - genetics Mice Mice, Inbred C57BL Mice, Transgenic Murine models Mutation - genetics Nestin - genetics Neurobiology Neurodevelopmental disorder Neurology Neurons and Cognition Neuroprostanes - metabolism Oxidative stress Oxidative Stress - physiology Rett syndrome Rett Syndrome - blood Rett Syndrome - complications Rett Syndrome - genetics |
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| Title | Oxidative brain damage in Mecp2-mutant murine models of Rett syndrome |
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