Dépouillements

Task-related functional connectivity in autism spectrum conditions: an EEG study using wavelet transform coherence / Ana CATARINO in Molecular Autism, (January 2013)  

Public ISBD [article]  inMolecular Autism > (January 2013) . - 14 p. Titre : Task-related functional connectivity in autism spectrum conditions: an EEG study using wavelet transform coherence Type de document : Texte imprimé et/ou numérique Auteurs : Ana CATARINO, Auteur ; Alexandre ANDRADE, Auteur ; Owen CHURCHES, Auteur ; Adam WAGNER, Auteur ; Simon BARON-COHEN, Auteur ; Howard RING, Auteur Année de publication : 2013 Article en page(s) : 14 p. Mots-clés : Autism spectrum conditions  Interhemispheric coherence  Atypical connectivity  Wavelet transform coherence Index. décimale : PER Périodiques Résumé : BACKGROUND:Autism Spectrum Conditions (ASC) are a set of pervasive neurodevelopmental conditions characterized by a wide range of lifelong signs and symptoms. Recent explanatory models of autism propose abnormal neural connectivity and are supported by studies showing decreased interhemispheric coherence in individuals with ASC. The first aim of this study was to test the hypothesis of reduced interhemispheric coherence in ASC, and secondly to investigate specific effects of task performance on interhemispheric coherence in ASC.METHODS:We analyzed electroencephalography (EEG) data from 15 participants with ASC and 15 typical controls, using Wavelet Transform Coherence (WTC) to calculate interhemispheric coherence during face and chair matching tasks, for EEG frequencies from 5 to 40 Hz and during the first 400 ms post-stimulus onset.RESULTS:Results demonstrate a reduction of interhemispheric coherence in the ASC group, relative to the control group, in both tasks and for all electrode pairs studied. For both tasks, group differences were generally observed after around 150 ms and at frequencies lower than 13 Hz. Regarding within-group task comparisons, while the control group presented differences in interhemispheric coherence between faces and chairs tasks at various electrode pairs (FT7-FT8, TP7-TP8, P7-P8), such differences were only seen for one electrode pair in the ASC group (T7-T8). No significant differences in EEG power spectra were observed between groups.CONCLUSIONS:Interhemispheric coherence is reduced in people with ASC, in a time and frequency specific manner, during visual perception and categorization of both social and inanimate stimuli and this reduction in coherence is widely dispersed across the brain.Results of within-group task comparisons may reflect an impairment in task differentiation in people with ASC relative to typically developing individuals.Overall, the results of this research support the value of WTC in examining the time-frequency microstructure of task-related interhemispheric EEG coherence in people with ASC. En ligne : http://dx.doi.org/10.1186/2040-2392-4-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 [article] Task-related functional connectivity in autism spectrum conditions: an EEG study using wavelet transform coherence [Texte imprimé et/ou numérique] / Ana CATARINO, Auteur ; Alexandre ANDRADE, Auteur ; Owen CHURCHES, Auteur ; Adam WAGNER, Auteur ; Simon BARON-COHEN, Auteur ; Howard RING, Auteur . - 2013 . - 14 p. in Molecular Autism > (January 2013) . - 14 p. Mots-clés : Autism spectrum conditions  Interhemispheric coherence  Atypical connectivity  Wavelet transform coherence Index. décimale : PER Périodiques Résumé : BACKGROUND:Autism Spectrum Conditions (ASC) are a set of pervasive neurodevelopmental conditions characterized by a wide range of lifelong signs and symptoms. Recent explanatory models of autism propose abnormal neural connectivity and are supported by studies showing decreased interhemispheric coherence in individuals with ASC. The first aim of this study was to test the hypothesis of reduced interhemispheric coherence in ASC, and secondly to investigate specific effects of task performance on interhemispheric coherence in ASC.METHODS:We analyzed electroencephalography (EEG) data from 15 participants with ASC and 15 typical controls, using Wavelet Transform Coherence (WTC) to calculate interhemispheric coherence during face and chair matching tasks, for EEG frequencies from 5 to 40 Hz and during the first 400 ms post-stimulus onset.RESULTS:Results demonstrate a reduction of interhemispheric coherence in the ASC group, relative to the control group, in both tasks and for all electrode pairs studied. For both tasks, group differences were generally observed after around 150 ms and at frequencies lower than 13 Hz. Regarding within-group task comparisons, while the control group presented differences in interhemispheric coherence between faces and chairs tasks at various electrode pairs (FT7-FT8, TP7-TP8, P7-P8), such differences were only seen for one electrode pair in the ASC group (T7-T8). No significant differences in EEG power spectra were observed between groups.CONCLUSIONS:Interhemispheric coherence is reduced in people with ASC, in a time and frequency specific manner, during visual perception and categorization of both social and inanimate stimuli and this reduction in coherence is widely dispersed across the brain.Results of within-group task comparisons may reflect an impairment in task differentiation in people with ASC relative to typically developing individuals.Overall, the results of this research support the value of WTC in examining the time-frequency microstructure of task-related interhemispheric EEG coherence in people with ASC. En ligne : http://dx.doi.org/10.1186/2040-2392-4-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202

Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism / Eleonora NAPOLI in Molecular Autism, (January 2013)  

Public ISBD [article]  inMolecular Autism > (January 2013) . - 8 p. Titre : Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism Type de document : Texte imprimé et/ou numérique Auteurs : Eleonora NAPOLI, Auteur ; Sarah WONG, Auteur ; Cecilia GIULIVI, Auteur Année de publication : 2013 Article en page(s) : 8 p. Mots-clés : Autism  Mitochondria  Mitochondrial DNA  Oxidative damage  Bioenergetics Index. décimale : PER Périodiques Résumé : BACKGROUND:The mitochondrial genome (mtDNA) is particularly susceptible to damage mediated by reactive oxygen species (ROS). Although elevated ROS production and elevated biomarkers of oxidative stress have been found in tissues from children with autism spectrum disorders, evidence for damage to mtDNA is lacking.FINDINGS:mtDNA deletions were evaluated in peripheral blood monocytic cells (PBMC) isolated from 2-5 year old children with full autism (AU; n = 67), and typically developing children (TD; n = 46) and their parents enrolled in the CHildhood Autism Risk from Genes and Environment study (CHARGE) at University of California Davis. Sequence variants were evaluated in mtDNA segments from AU and TD children (n = 10; each) and their mothers representing 31.2% coverage of the entire human mitochondrial genome. Increased mtDNA damage in AU children was evidenced by (i) higher frequency of mtDNA deletions (2-fold), (ii) higher number of GC-AT transitions (2.4-fold), being GC preferred sites for oxidative damage, and (iii) higher frequency of G,C,T-A transitions (1.6-fold) suggesting a higher incidence of polymerase gamma incorporating mainly A at bypassed apurinic/apyrimidinic sites, probably originated from oxidative stress. The last two outcomes were identical to their mothers suggesting the inheritance of a template consistent with increased oxidative damage, whereas the frequency of mtDNA deletions in AU children was similar to that of their fathers.CONCLUSIONS:These results suggest that a combination of genetic and epigenetic factors, taking place during perinatal periods, results in a mtDNA template in children with autism similar to that expected for older individuals. En ligne : http://dx.doi.org/10.1186/2040-2392-4-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 [article] Evidence of reactive oxygen species-mediated damage to mitochondrial DNA in children with typical autism [Texte imprimé et/ou numérique] / Eleonora NAPOLI, Auteur ; Sarah WONG, Auteur ; Cecilia GIULIVI, Auteur . - 2013 . - 8 p. in Molecular Autism > (January 2013) . - 8 p. Mots-clés : Autism  Mitochondria  Mitochondrial DNA  Oxidative damage  Bioenergetics Index. décimale : PER Périodiques Résumé : BACKGROUND:The mitochondrial genome (mtDNA) is particularly susceptible to damage mediated by reactive oxygen species (ROS). Although elevated ROS production and elevated biomarkers of oxidative stress have been found in tissues from children with autism spectrum disorders, evidence for damage to mtDNA is lacking.FINDINGS:mtDNA deletions were evaluated in peripheral blood monocytic cells (PBMC) isolated from 2-5 year old children with full autism (AU; n = 67), and typically developing children (TD; n = 46) and their parents enrolled in the CHildhood Autism Risk from Genes and Environment study (CHARGE) at University of California Davis. Sequence variants were evaluated in mtDNA segments from AU and TD children (n = 10; each) and their mothers representing 31.2% coverage of the entire human mitochondrial genome. Increased mtDNA damage in AU children was evidenced by (i) higher frequency of mtDNA deletions (2-fold), (ii) higher number of GC-AT transitions (2.4-fold), being GC preferred sites for oxidative damage, and (iii) higher frequency of G,C,T-A transitions (1.6-fold) suggesting a higher incidence of polymerase gamma incorporating mainly A at bypassed apurinic/apyrimidinic sites, probably originated from oxidative stress. The last two outcomes were identical to their mothers suggesting the inheritance of a template consistent with increased oxidative damage, whereas the frequency of mtDNA deletions in AU children was similar to that of their fathers.CONCLUSIONS:These results suggest that a combination of genetic and epigenetic factors, taking place during perinatal periods, results in a mtDNA template in children with autism similar to that expected for older individuals. En ligne : http://dx.doi.org/10.1186/2040-2392-4-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202

MeCP2 modulates gene expression pathways in astrocytes / Dag H. YASUI in Molecular Autism, (January 2013)  

Public ISBD [article]  inMolecular Autism > (January 2013) . - 11 p. Titre : MeCP2 modulates gene expression pathways in astrocytes Type de document : Texte imprimé et/ou numérique Auteurs : Dag H. YASUI, Auteur ; Huichun XU, Auteur ; Keith DUNAWAY, Auteur ; Janine M. LASALLE, Auteur ; Lee-Way JIN, Auteur ; Izumi MAEZAWA, Auteur Année de publication : 2013 Article en page(s) : 11 p. Mots-clés : MeCP2  Epigenetics  Astrocytes  Rett syndrome  ChIP-seq  Transcription Factors/chemistry/genetics Index. décimale : PER Périodiques Résumé : BACKGROUND:Mutations in MECP2 encoding methyl-CpG-binding protein 2 (MeCP2) cause the X-linked neurodevelopmental disorder Rett syndrome. Rett syndrome patients exhibit neurological symptoms that include irregular breathing, impaired mobility, stereotypic hand movements, and loss of speech. MeCP2 protein epigenetically modulates gene expression through genome-wide binding to methylated CpG dinucleotides. While neurons have the highest level of MeCP2 expression, astrocytes and other cell types also express detectable levels of MeCP2. Recent studies suggest that astrocytes likely control the progression of Rett syndrome. Thus, the object of these studies was to identify gene targets that are affected by loss of MeCP2 binding in astrocytes.METHODS:To identify gene targets of MeCP2 in astrocytes, combined approaches of expression microarray and chromatin immunoprecipitation of MeCP2 followed by sequencing (ChIP-seq) were compared between wild-type and MeCP2-deficient astrocytes. MeCP2 gene targets were compared with genes in the top 10% of MeCP2 binding levels in gene windows either within 2 kb upstream of the transcription start site, or the 'gene body' that extended from transcription start to end site, or 2 kb downstream of the transcription end site.RESULTS:A total of 118 gene transcripts surpassed the highly significant threshold (P 0.005, fold change 1.2) in expression microarray analysis from triplicate cultures. The top 10% of genes with the highest levels of MeCP2 binding were identified in two independent ChIP-seq experiments. Together this integrated, genome-wide screen for MeCP2 target genes provided an overlapping list of 19 high-confidence MeCP2-responsive gene transcripts in astrocytes. Validation of candidate target gene transcripts by RT-PCR revealed that expression of Apoc2, Cdon, Csrp and Nrep were consistently responsive to MeCP2 deficiency in astrocytes.CONCLUSIONS:The first MeCP2 ChIP-seq and gene expression microarray analysis in astrocytes reveals a set of potential MeCP2 target genes that may contribute to normal astrocyte signaling, cell division and neuronal support functions, the loss of which may contribute to the Rett syndrome phenotype. En ligne : http://dx.doi.org/10.1186/2040-2392-4-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 [article] MeCP2 modulates gene expression pathways in astrocytes [Texte imprimé et/ou numérique] / Dag H. YASUI, Auteur ; Huichun XU, Auteur ; Keith DUNAWAY, Auteur ; Janine M. LASALLE, Auteur ; Lee-Way JIN, Auteur ; Izumi MAEZAWA, Auteur . - 2013 . - 11 p. in Molecular Autism > (January 2013) . - 11 p. Mots-clés : MeCP2  Epigenetics  Astrocytes  Rett syndrome  ChIP-seq  Transcription Factors/chemistry/genetics Index. décimale : PER Périodiques Résumé : BACKGROUND:Mutations in MECP2 encoding methyl-CpG-binding protein 2 (MeCP2) cause the X-linked neurodevelopmental disorder Rett syndrome. Rett syndrome patients exhibit neurological symptoms that include irregular breathing, impaired mobility, stereotypic hand movements, and loss of speech. MeCP2 protein epigenetically modulates gene expression through genome-wide binding to methylated CpG dinucleotides. While neurons have the highest level of MeCP2 expression, astrocytes and other cell types also express detectable levels of MeCP2. Recent studies suggest that astrocytes likely control the progression of Rett syndrome. Thus, the object of these studies was to identify gene targets that are affected by loss of MeCP2 binding in astrocytes.METHODS:To identify gene targets of MeCP2 in astrocytes, combined approaches of expression microarray and chromatin immunoprecipitation of MeCP2 followed by sequencing (ChIP-seq) were compared between wild-type and MeCP2-deficient astrocytes. MeCP2 gene targets were compared with genes in the top 10% of MeCP2 binding levels in gene windows either within 2 kb upstream of the transcription start site, or the 'gene body' that extended from transcription start to end site, or 2 kb downstream of the transcription end site.RESULTS:A total of 118 gene transcripts surpassed the highly significant threshold (P 0.005, fold change 1.2) in expression microarray analysis from triplicate cultures. The top 10% of genes with the highest levels of MeCP2 binding were identified in two independent ChIP-seq experiments. Together this integrated, genome-wide screen for MeCP2 target genes provided an overlapping list of 19 high-confidence MeCP2-responsive gene transcripts in astrocytes. Validation of candidate target gene transcripts by RT-PCR revealed that expression of Apoc2, Cdon, Csrp and Nrep were consistently responsive to MeCP2 deficiency in astrocytes.CONCLUSIONS:The first MeCP2 ChIP-seq and gene expression microarray analysis in astrocytes reveals a set of potential MeCP2 target genes that may contribute to normal astrocyte signaling, cell division and neuronal support functions, the loss of which may contribute to the Rett syndrome phenotype. En ligne : http://dx.doi.org/10.1186/2040-2392-4-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202