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Mitochondria, Microbiome and Their Potential Psychiatric Modulation / Christopher SNYDER in Autism - Open Access, 5-2 ([01/03/2015])
[article]
Titre : Mitochondria, Microbiome and Their Potential Psychiatric Modulation Type de document : Texte imprimé et/ou numérique Auteurs : Christopher SNYDER, Auteur ; Richard M. KREAM, Auteur ; Radek PTACEK, Auteur ; George B. STEFAN, Auteur Article en page(s) : 4 p. Langues : Anglais (eng) Mots-clés : Gut Microbiome Mitochondria Metabolic Syndrome Autism Index. décimale : PER Périodiques Résumé : Pervasive developmental disorders, or autism spectrum disorders, are multifaceted and have a high rate of occurrence. Additionally, the origin of Autism appears to be multidimensional and largely unknown. Thus, it would appear novel approaches and concepts are needed in this area of scientific endeavor. In this regard, microbial cells harbored within the human gut and elsewhere are being studied to understand their multi-functional properties and their ability to affect physiological activities in their “host” organism. The communities of approximately 10 trillion microbial cells that live within the gut are involved in functions such as metabolism, nutrition and immune regulation. We and others surmise this microbiota can contribute to disruption of normal activities, causing harmful pathologies such as gastrointestinal complications, obesity, and diabetes and autism. They have the ability to trigger inappropriate immune activation, especially macrophages, which can travel from the gut and penetrate the blood brain barrier and communicate inappropriately with neural cells, altering behavior. Normally these immune cells can enter the brain and become microglia. However, being abnormally stimulated, many more can enter the brain, awakening the sentinel microglia and establishing a pro inflammatory state, inducing hypoxia (altering mitochondrial performance). Thus, the microbiome has the potential to extend its influence into the brain, suggesting this may also take place within the parameters of normal activity. In part, the behavioral outcome of such an inappropriate invasion would depend on the region(s) penetrated, manifesting itself with a multidimensional behavioral profile such as occurs in autism. En ligne : https://dx.doi.org/10.4172/2165-7890.1000144 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409
in Autism - Open Access > 5-2 [01/03/2015] . - 4 p.[article] Mitochondria, Microbiome and Their Potential Psychiatric Modulation [Texte imprimé et/ou numérique] / Christopher SNYDER, Auteur ; Richard M. KREAM, Auteur ; Radek PTACEK, Auteur ; George B. STEFAN, Auteur . - 4 p.
Langues : Anglais (eng)
in Autism - Open Access > 5-2 [01/03/2015] . - 4 p.
Mots-clés : Gut Microbiome Mitochondria Metabolic Syndrome Autism Index. décimale : PER Périodiques Résumé : Pervasive developmental disorders, or autism spectrum disorders, are multifaceted and have a high rate of occurrence. Additionally, the origin of Autism appears to be multidimensional and largely unknown. Thus, it would appear novel approaches and concepts are needed in this area of scientific endeavor. In this regard, microbial cells harbored within the human gut and elsewhere are being studied to understand their multi-functional properties and their ability to affect physiological activities in their “host” organism. The communities of approximately 10 trillion microbial cells that live within the gut are involved in functions such as metabolism, nutrition and immune regulation. We and others surmise this microbiota can contribute to disruption of normal activities, causing harmful pathologies such as gastrointestinal complications, obesity, and diabetes and autism. They have the ability to trigger inappropriate immune activation, especially macrophages, which can travel from the gut and penetrate the blood brain barrier and communicate inappropriately with neural cells, altering behavior. Normally these immune cells can enter the brain and become microglia. However, being abnormally stimulated, many more can enter the brain, awakening the sentinel microglia and establishing a pro inflammatory state, inducing hypoxia (altering mitochondrial performance). Thus, the microbiome has the potential to extend its influence into the brain, suggesting this may also take place within the parameters of normal activity. In part, the behavioral outcome of such an inappropriate invasion would depend on the region(s) penetrated, manifesting itself with a multidimensional behavioral profile such as occurs in autism. En ligne : https://dx.doi.org/10.4172/2165-7890.1000144 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes / Lucia JANICKOVA in Molecular Autism, 11 (2020)
[article]
Titre : Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes Type de document : Texte imprimé et/ou numérique Auteurs : Lucia JANICKOVA, Auteur ; Karin Farah RECHBERGER, Auteur ; Lucas WEY, Auteur ; Beat SCHWALLER, Auteur Article en page(s) : 47 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Calcium homeostasis Calcium-binding protein Mitochondria Parvalbumin Pvalb neurons Index. décimale : PER Périodiques Résumé : BACKGROUND: In fast firing, parvalbumin (PV)-expressing (Pvalb) interneurons, PV acts as an intracellular Ca(2+) signal modulator with slow-onset kinetics. In Purkinje cells of PV(-/-) mice, adaptive/homeostatic mechanisms lead to an increase in mitochondria, organelles equally capable of delayed Ca(2+) sequestering/buffering. An inverse regulation of PV and mitochondria likewise operates in cell model systems in vitro including myotubes, epithelial cells, and oligodendrocyte-like cells overexpressing PV. Whether such opposite regulation pertains to all Pvalb neurons is currently unknown. In oligodendrocyte-like cells, PV additionally decreases growth and branching of processes in a cell-autonomous manner. METHODS: The in vivo effects of absence of PV were investigated in inhibitory Pvalb neurons expressing EGFP, present in the somatosensory and medial prefrontal cortex, striatum, thalamic reticular nucleus, hippocampal regions DG, CA3, and CA1 and cerebellum of mice either wild-type or knockout (PV(-/-)) for the Pvalb gene. Changes in Pvalb neuron morphology and PV concentrations were determined using immunofluorescence, followed by 3D-reconstruction and quantitative image analyses. RESULTS: PV deficiency led to an increase in mitochondria volume and density in the soma; the magnitude of the effect was positively correlated with the estimated PV concentrations in the various Pvalb neuron subpopulations in wild-type neurons. The increase in dendrite length and branching, as well as thickness of proximal dendrites of selected PV(-/-) Pvalb neurons is likely the result of the observed increased density and length of mitochondria in these PV(-/-) Pvalb neuron dendrites. The increased branching and soma size directly linked to the absence of PV is assumed to contribute to the increased volume of the neocortex present in juvenile PV(-/-) mice. The extended dendritic branching is in line with the hypothesis of local hyperconnectivity in autism spectrum disorder (ASD) and ASD mouse models including PV(-/-) mice, which display all ASD core symptoms and several comorbidities including cortical macrocephaly at juvenile age. CONCLUSION: PV is involved in most proposed mechanisms implicated in ASD etiology: alterations in Ca(2+) signaling affecting E/I balance, changes in mitochondria structure/function, and increased dendritic length and branching, possibly resulting in local hyperconnectivity, all in a likely cell autonomous way. En ligne : http://dx.doi.org/10.1186/s13229-020-00323-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Molecular Autism > 11 (2020) . - 47 p.[article] Absence of parvalbumin increases mitochondria volume and branching of dendrites in inhibitory Pvalb neurons in vivo: a point of convergence of autism spectrum disorder (ASD) risk gene phenotypes [Texte imprimé et/ou numérique] / Lucia JANICKOVA, Auteur ; Karin Farah RECHBERGER, Auteur ; Lucas WEY, Auteur ; Beat SCHWALLER, Auteur . - 47 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 47 p.
Mots-clés : Autism spectrum disorder Calcium homeostasis Calcium-binding protein Mitochondria Parvalbumin Pvalb neurons Index. décimale : PER Périodiques Résumé : BACKGROUND: In fast firing, parvalbumin (PV)-expressing (Pvalb) interneurons, PV acts as an intracellular Ca(2+) signal modulator with slow-onset kinetics. In Purkinje cells of PV(-/-) mice, adaptive/homeostatic mechanisms lead to an increase in mitochondria, organelles equally capable of delayed Ca(2+) sequestering/buffering. An inverse regulation of PV and mitochondria likewise operates in cell model systems in vitro including myotubes, epithelial cells, and oligodendrocyte-like cells overexpressing PV. Whether such opposite regulation pertains to all Pvalb neurons is currently unknown. In oligodendrocyte-like cells, PV additionally decreases growth and branching of processes in a cell-autonomous manner. METHODS: The in vivo effects of absence of PV were investigated in inhibitory Pvalb neurons expressing EGFP, present in the somatosensory and medial prefrontal cortex, striatum, thalamic reticular nucleus, hippocampal regions DG, CA3, and CA1 and cerebellum of mice either wild-type or knockout (PV(-/-)) for the Pvalb gene. Changes in Pvalb neuron morphology and PV concentrations were determined using immunofluorescence, followed by 3D-reconstruction and quantitative image analyses. RESULTS: PV deficiency led to an increase in mitochondria volume and density in the soma; the magnitude of the effect was positively correlated with the estimated PV concentrations in the various Pvalb neuron subpopulations in wild-type neurons. The increase in dendrite length and branching, as well as thickness of proximal dendrites of selected PV(-/-) Pvalb neurons is likely the result of the observed increased density and length of mitochondria in these PV(-/-) Pvalb neuron dendrites. The increased branching and soma size directly linked to the absence of PV is assumed to contribute to the increased volume of the neocortex present in juvenile PV(-/-) mice. The extended dendritic branching is in line with the hypothesis of local hyperconnectivity in autism spectrum disorder (ASD) and ASD mouse models including PV(-/-) mice, which display all ASD core symptoms and several comorbidities including cortical macrocephaly at juvenile age. CONCLUSION: PV is involved in most proposed mechanisms implicated in ASD etiology: alterations in Ca(2+) signaling affecting E/I balance, changes in mitochondria structure/function, and increased dendritic length and branching, possibly resulting in local hyperconnectivity, all in a likely cell autonomous way. En ligne : http://dx.doi.org/10.1186/s13229-020-00323-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 Brain region-specific altered expression and association of mitochondria-related genes in autism / Ayyappan ANITHA in Molecular Autism, (November 2012)
[article]
Titre : Brain region-specific altered expression and association of mitochondria-related genes in autism Type de document : Texte imprimé et/ou numérique Auteurs : Ayyappan ANITHA, Auteur ; Kazuhiko NAKAMURA, Auteur ; Ismail THANSEEM, Auteur ; Kazuo YAMADA, Auteur ; Yoshimi IWAYAMA, Auteur ; Tomoko TOYOTA, Auteur ; Hideo MATSUZAKI, Auteur ; Taishi MIYACHI, Auteur ; Satoru YAMADA, Auteur ; Masatsugu TSUJII, Auteur ; Kenji J. TSUCHIYA, Auteur ; Kaori MATSUMOTO, Auteur ; Yasuhide IWATA, Auteur ; Katsuaki SUZUKI, Auteur ; Hironobu ICHIKAWA, Auteur ; Toshiro SUGIYAMA, Auteur ; Takeo YOSHIKAWA, Auteur ; Norio MORI, Auteur Année de publication : 2012 Article en page(s) : 12 p. Langues : Anglais (eng) Mots-clés : Autism Mitochondria Postmortem brain NEFL Uncoupling protein Metaxin Index. décimale : PER Périodiques Résumé : BACKGROUND:Mitochondrial dysfunction (MtD) has been observed in approximately five percent of children with autism spectrum disorders (ASD). MtD could impair highly energy-dependent processes such as neurodevelopment, thereby contributing to autism. Most of the previous studies of MtD in autism have been restricted to the biomarkers of energy metabolism, while most of the genetic studies have been based on mutations in the mitochondrial DNA (mtDNA). Despite the mtDNA, most of the proteins essential for mitochondrial replication and function are encoded by the genomic DNA; so far, there have been very few studies of those genes. Therefore, we carried out a detailed study involving gene expression and genetic association studies of genes related to diverse mitochondrial functions.METHODS:For gene expression analysis, postmortem brain tissues (anterior cingulate gyrus (ACG), motor cortex (MC) and thalamus (THL)) from autism patients (n=8) and controls (n=10) were obtained from the Autism Tissue Program (Princeton, NJ, USA). Quantitative real-time PCR arrays were used to quantify the expression of 84 genes related to diverse functions of mitochondria, including biogenesis, transport, translocation and apoptosis. We used the delta delta Ct ([increment][increment]Ct) method for quantification of gene expression. DNA samples from 841 Caucasian and 188 Japanese families were used in the association study of genes selected from the gene expression analysis. FBAT was used to examine genetic association with autism.RESULTS:Several genes showed brain region-specific expression alterations in autism patients compared to controls. Metaxin 2 (MTX2), neurofilament, light polypeptide (NEFL) and solute carrier family 25, member 27 (SLC25A27) showed consistently reduced expression in the ACG, MC and THL of autism patients. NEFL (P = 0.038; Z-score 2.066) and SLC25A27 (P = 0.046; Z-score 1.990) showed genetic association with autism in Caucasian and Japanese samples, respectively. The expression of DNAJC19, DNM1L, LRPPRC, SLC25A12, SLC25A14, SLC25A24 and TOMM20 were reduced in at least two of the brain regions of autism patients.CONCLUSIONS:Our study, though preliminary, brings to light some new genes associated with MtD in autism. If MtD is detected in early stages, treatment strategies aimed at reducing its impact may be adopted. En ligne : http://dx.doi.org/10.1186/2040-2392-3-12 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202
in Molecular Autism > (November 2012) . - 12 p.[article] Brain region-specific altered expression and association of mitochondria-related genes in autism [Texte imprimé et/ou numérique] / Ayyappan ANITHA, Auteur ; Kazuhiko NAKAMURA, Auteur ; Ismail THANSEEM, Auteur ; Kazuo YAMADA, Auteur ; Yoshimi IWAYAMA, Auteur ; Tomoko TOYOTA, Auteur ; Hideo MATSUZAKI, Auteur ; Taishi MIYACHI, Auteur ; Satoru YAMADA, Auteur ; Masatsugu TSUJII, Auteur ; Kenji J. TSUCHIYA, Auteur ; Kaori MATSUMOTO, Auteur ; Yasuhide IWATA, Auteur ; Katsuaki SUZUKI, Auteur ; Hironobu ICHIKAWA, Auteur ; Toshiro SUGIYAMA, Auteur ; Takeo YOSHIKAWA, Auteur ; Norio MORI, Auteur . - 2012 . - 12 p.
Langues : Anglais (eng)
in Molecular Autism > (November 2012) . - 12 p.
Mots-clés : Autism Mitochondria Postmortem brain NEFL Uncoupling protein Metaxin Index. décimale : PER Périodiques Résumé : BACKGROUND:Mitochondrial dysfunction (MtD) has been observed in approximately five percent of children with autism spectrum disorders (ASD). MtD could impair highly energy-dependent processes such as neurodevelopment, thereby contributing to autism. Most of the previous studies of MtD in autism have been restricted to the biomarkers of energy metabolism, while most of the genetic studies have been based on mutations in the mitochondrial DNA (mtDNA). Despite the mtDNA, most of the proteins essential for mitochondrial replication and function are encoded by the genomic DNA; so far, there have been very few studies of those genes. Therefore, we carried out a detailed study involving gene expression and genetic association studies of genes related to diverse mitochondrial functions.METHODS:For gene expression analysis, postmortem brain tissues (anterior cingulate gyrus (ACG), motor cortex (MC) and thalamus (THL)) from autism patients (n=8) and controls (n=10) were obtained from the Autism Tissue Program (Princeton, NJ, USA). Quantitative real-time PCR arrays were used to quantify the expression of 84 genes related to diverse functions of mitochondria, including biogenesis, transport, translocation and apoptosis. We used the delta delta Ct ([increment][increment]Ct) method for quantification of gene expression. DNA samples from 841 Caucasian and 188 Japanese families were used in the association study of genes selected from the gene expression analysis. FBAT was used to examine genetic association with autism.RESULTS:Several genes showed brain region-specific expression alterations in autism patients compared to controls. Metaxin 2 (MTX2), neurofilament, light polypeptide (NEFL) and solute carrier family 25, member 27 (SLC25A27) showed consistently reduced expression in the ACG, MC and THL of autism patients. NEFL (P = 0.038; Z-score 2.066) and SLC25A27 (P = 0.046; Z-score 1.990) showed genetic association with autism in Caucasian and Japanese samples, respectively. The expression of DNAJC19, DNM1L, LRPPRC, SLC25A12, SLC25A14, SLC25A24 and TOMM20 were reduced in at least two of the brain regions of autism patients.CONCLUSIONS:Our study, though preliminary, brings to light some new genes associated with MtD in autism. If MtD is detected in early stages, treatment strategies aimed at reducing its impact may be adopted. En ligne : http://dx.doi.org/10.1186/2040-2392-3-12 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 Next Generation Sequencing Mitochondrial DNA Analysis in Autism Spectrum Disorder / Ashok PATOWARY in Autism Research, 10-8 (August 2017)
[article]
Titre : Next Generation Sequencing Mitochondrial DNA Analysis in Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Ashok PATOWARY, Auteur ; Ryan NESBITT, Auteur ; Marilyn ARCHER, Auteur ; Raphael BERNIER, Auteur ; Zoran BRKANAC, Auteur Article en page(s) : p.1338-1343 Langues : Anglais (eng) Mots-clés : mitochondria autism spectrum disorder whole exome sequencing single nucleotide variation next generation sequencing Index. décimale : PER Périodiques Résumé : Autism is a complex genetic disorder where both de-novo and inherited genetics factors play a role. Next generation sequencing approaches have been extensively used to identify rare variants associated with autism. To date, all such studies were focused on nuclear genome; thereby leaving the role of mitochondrial DNA (mtDNA) variation in autism unexplored. Recently, analytical tools have been developed to evaluate mtDNA in whole-exome data. We have analyzed the mtDNA sequence derived from whole-exome sequencing in 10 multiplex families. In one of the families we have identified two variants of interest in MT-ND5 gene that were previously determined to impair mitochondrial function. In addition in a second family we have identified two VOIs; mtDNA variant in MT-ATP6 and nuclear DNA variant in NDUFS4, where both VOIs are within mitochondrial Respiratory Chain Complex. Our findings provide further support for the role of mitochondria in ASD and confirm that whole-exome sequencing allows for analysis of mtDNA, which sets a stage for further comprehensive genetic investigations of the role of mitochondria in autism. En ligne : http://dx.doi.org/10.1002/aur.1792 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=310
in Autism Research > 10-8 (August 2017) . - p.1338-1343[article] Next Generation Sequencing Mitochondrial DNA Analysis in Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Ashok PATOWARY, Auteur ; Ryan NESBITT, Auteur ; Marilyn ARCHER, Auteur ; Raphael BERNIER, Auteur ; Zoran BRKANAC, Auteur . - p.1338-1343.
Langues : Anglais (eng)
in Autism Research > 10-8 (August 2017) . - p.1338-1343
Mots-clés : mitochondria autism spectrum disorder whole exome sequencing single nucleotide variation next generation sequencing Index. décimale : PER Périodiques Résumé : Autism is a complex genetic disorder where both de-novo and inherited genetics factors play a role. Next generation sequencing approaches have been extensively used to identify rare variants associated with autism. To date, all such studies were focused on nuclear genome; thereby leaving the role of mitochondrial DNA (mtDNA) variation in autism unexplored. Recently, analytical tools have been developed to evaluate mtDNA in whole-exome data. We have analyzed the mtDNA sequence derived from whole-exome sequencing in 10 multiplex families. In one of the families we have identified two variants of interest in MT-ND5 gene that were previously determined to impair mitochondrial function. In addition in a second family we have identified two VOIs; mtDNA variant in MT-ATP6 and nuclear DNA variant in NDUFS4, where both VOIs are within mitochondrial Respiratory Chain Complex. Our findings provide further support for the role of mitochondria in ASD and confirm that whole-exome sequencing allows for analysis of mtDNA, which sets a stage for further comprehensive genetic investigations of the role of mitochondria in autism. En ligne : http://dx.doi.org/10.1002/aur.1792 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=310 Resveratrol ameliorates prenatal progestin exposure-induced autism-like behavior through ERbeta activation / W. XIE in Molecular Autism, 9 (2018)
[article]
Titre : Resveratrol ameliorates prenatal progestin exposure-induced autism-like behavior through ERbeta activation Type de document : Texte imprimé et/ou numérique Auteurs : W. XIE, Auteur ; X. GE, Auteur ; L. LI, Auteur ; A. YAO, Auteur ; X. WANG, Auteur ; M. LI, Auteur ; X. GONG, Auteur ; Z. CHU, Auteur ; Z. LU, Auteur ; X. HUANG, Auteur ; Y. JIAO, Auteur ; Y. WANG, Auteur ; M. XIAO, Auteur ; H. CHEN, Auteur ; W. XIANG, Auteur ; P. YAO, Auteur Article en page(s) : 43p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Estrogen receptor beta Lipid metabolism Mitochondria Oxidative stress Progestin Resveratrol Index. décimale : PER Périodiques Résumé : Background: Recent literatures indicate that maternal hormone exposure is a risk factor for autism spectrum disorder (ASD). We hypothesize that prenatal progestin exposure may counteract the neuroprotective effect of estrogen and contribute to ASD development, and we aim to develop a method to ameliorate prenatal progestin exposure-induced autism-like behavior. Methods: Experiment 1: Prenatal progestin exposure-induced offspring are treated with resveratrol (RSV) through either prenatal or postnatal exposure and then used for autism-like behavior testing and other biomedical analyses. Experiment 2: Prenatal norethindrone (NET) exposure-induced offspring are treated with ERbeta knockdown lentivirus together with RSV for further testing. Experiment 3: Pregnant dams are treated with prenatal NET exposure together with RSV, and the offspring are used for further testing. Results: Eight kinds of clinically relevant progestins were used for prenatal exposure in pregnant dams, and the offspring showed decreased ERbeta expression in the amygdala with autism-like behavior. Oral administration of either postnatal or prenatal RSV treatment significantly reversed this effect with ERbeta activation and ameliorated autism-like behavior. Further investigation showed that RSV activates ERbeta and its target genes by demethylation of DNA and histone on the ERbeta promoter, and then minimizes progestin-induced oxidative stress as well as the dysfunction of mitochondria and lipid metabolism in the brain, subsequently ameliorating autism-like behavior. Conclusions: We conclude that resveratrol ameliorates prenatal progestin exposure-induced autism-like behavior through ERbeta activation. Our data suggest that prenatal progestin exposure is a strong risk factor for autism-like behavior. Many potential clinical progestin applications, including oral contraceptive pills, preterm birth drugs, and progestin-contaminated drinking water or seafood, may be risk factors for ASD. In addition, RSV may be a good candidate for clinically rescuing or preventing ASD symptoms in humans, while high doses of resveratrol used in the animals may be a potential limitation for human application. En ligne : https://dx.doi.org/10.1186/s13229-018-0225-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 43p.[article] Resveratrol ameliorates prenatal progestin exposure-induced autism-like behavior through ERbeta activation [Texte imprimé et/ou numérique] / W. XIE, Auteur ; X. GE, Auteur ; L. LI, Auteur ; A. YAO, Auteur ; X. WANG, Auteur ; M. LI, Auteur ; X. GONG, Auteur ; Z. CHU, Auteur ; Z. LU, Auteur ; X. HUANG, Auteur ; Y. JIAO, Auteur ; Y. WANG, Auteur ; M. XIAO, Auteur ; H. CHEN, Auteur ; W. XIANG, Auteur ; P. YAO, Auteur . - 43p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 43p.
Mots-clés : Autism spectrum disorder Estrogen receptor beta Lipid metabolism Mitochondria Oxidative stress Progestin Resveratrol Index. décimale : PER Périodiques Résumé : Background: Recent literatures indicate that maternal hormone exposure is a risk factor for autism spectrum disorder (ASD). We hypothesize that prenatal progestin exposure may counteract the neuroprotective effect of estrogen and contribute to ASD development, and we aim to develop a method to ameliorate prenatal progestin exposure-induced autism-like behavior. Methods: Experiment 1: Prenatal progestin exposure-induced offspring are treated with resveratrol (RSV) through either prenatal or postnatal exposure and then used for autism-like behavior testing and other biomedical analyses. Experiment 2: Prenatal norethindrone (NET) exposure-induced offspring are treated with ERbeta knockdown lentivirus together with RSV for further testing. Experiment 3: Pregnant dams are treated with prenatal NET exposure together with RSV, and the offspring are used for further testing. Results: Eight kinds of clinically relevant progestins were used for prenatal exposure in pregnant dams, and the offspring showed decreased ERbeta expression in the amygdala with autism-like behavior. Oral administration of either postnatal or prenatal RSV treatment significantly reversed this effect with ERbeta activation and ameliorated autism-like behavior. Further investigation showed that RSV activates ERbeta and its target genes by demethylation of DNA and histone on the ERbeta promoter, and then minimizes progestin-induced oxidative stress as well as the dysfunction of mitochondria and lipid metabolism in the brain, subsequently ameliorating autism-like behavior. Conclusions: We conclude that resveratrol ameliorates prenatal progestin exposure-induced autism-like behavior through ERbeta activation. Our data suggest that prenatal progestin exposure is a strong risk factor for autism-like behavior. Many potential clinical progestin applications, including oral contraceptive pills, preterm birth drugs, and progestin-contaminated drinking water or seafood, may be risk factors for ASD. In addition, RSV may be a good candidate for clinically rescuing or preventing ASD symptoms in humans, while high doses of resveratrol used in the animals may be a potential limitation for human application. En ligne : https://dx.doi.org/10.1186/s13229-018-0225-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism / Eleonora NAPOLI in Molecular Autism, (January 2013)
PermalinkIncreased cerebral lactate levels in adults with autism spectrum disorders compared to non-autistic controls: a magnetic resonance spectroscopy study / Kathrin NICKEL ; Thomas LANGE ; Georg OELTZSCHNER ; Michael DACKO ; Dominique ENDRES ; Kimon RUNGE ; Anke SCHUMANN ; Katharina DOMSCHKE ; Michalis ROUSOS ; Ludger TEBARTZ VAN ELST in Molecular Autism, 14 (2023)
PermalinkBiochemical Effects of Ribose and NADH Therapy in Children with Autism / Stuart H. FREEDENFELD in Autism Insights, 3 ([01/01/2011])
PermalinkGenetic modifications associated with ketogenic diet treatment in the BTBRT+Tf/J mouse model of autism spectrum disorder / Richelle MYCHASIUK in Autism Research, 10-3 (March 2017)
PermalinkA Metabolomics Approach to Screening for Autism Risk in the Children's Autism Metabolome Project / Alan M. SMITH in Autism Research, 13-8 (August 2020)
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