Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Résultat de la recherche
6 recherche sur le mot-clé 'competing interests.Springer Nature remains neutral with regard to jurisdictional'
Affiner la recherche Générer le flux rss de la recherche
Partager le résultat de cette recherche Faire une suggestion
Functional MRI connectivity of children with autism and low verbal and cognitive performance / T. P. GABRIELSEN in Molecular Autism, 9 (2018)
[article]
Titre : Functional MRI connectivity of children with autism and low verbal and cognitive performance Type de document : Texte imprimé et/ou numérique Auteurs : T. P. GABRIELSEN, Auteur ; Jeffrey S. ANDERSON, Auteur ; K. G. STEPHENSON, Auteur ; J. BECK, Auteur ; J. B. KING, Auteur ; R. KELLEMS, Auteur ; D. N. TOP, Auteur ; N. C. C. RUSSELL, Auteur ; Emily I. ANDERBERG, Auteur ; R. A. LUNDWALL, Auteur ; B. HANSEN, Auteur ; M. SOUTH, Auteur Article en page(s) : 67 p. Langues : Anglais (eng) Mots-clés : Adolescent Autistic Disorder/*diagnostic imaging/physiopathology Case-Control Studies Child *Cognition Female Humans Intelligence *Language Development Magnetic Resonance Imaging Male *Autism spectrum disorder *Functional connectivity *Imaging methodology *Intelligence *Language Institutional Review Board, protocol #F25403. Written informed consent was obtained from parents, with assent obtained from participants following video review of procedures.The boy who modeled the MRI procedures in the video modeling procedure was filmed, and the final video was shared, with written permission of both of his parents and with his own assent.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Functional neuroimaging research in autism spectrum disorder has reported patterns of decreased long-range, within-network, and interhemispheric connectivity. Research has also reported increased corticostriatal connectivity and between-network connectivity for default and attentional networks. Past studies have excluded individuals with autism and low verbal and cognitive performance (LVCP), so connectivity in individuals more significantly affected with autism has not yet been studied. This represents a critical gap in our understanding of brain function across the autism spectrum. Methods: Using behavioral support procedures adapted from Nordahl, et al. (J Neurodev Disord 8:20-20, 2016), we completed non-sedated structural and functional MRI scans of 56 children ages 7-17, including LVCP children (n = 17, mean IQ = 54), children with autism and higher performance (HVCP, n = 20, mean IQ = 106), and neurotypical children (NT, n = 19, mean IQ = 111). Preparation included detailed intake questionnaires, video modeling, behavioral and anxiety reduction techniques, active noise-canceling headphones, and in-scan presentation of the Inscapes movie paradigm from Vanderwal et al. (Neuroimage 122:222-32, 2015). A high temporal resolution multiband echoplanar fMRI protocol analyzed motion-free time series data, extracted from concatenated volumes to mitigate the influence of motion artifact. All participants had > 200 volumes of motion-free fMRI scanning. Analyses were corrected for multiple comparisons. Results: LVCP showed decreased within-network connectivity in default, salience, auditory, and frontoparietal networks (LVCP < HVCP) and decreased interhemispheric connectivity (LVCP < HVCP=NT). Between-network connectivity was higher for LVCP than NT between default and dorsal attention and frontoparietal networks. Lower IQ was associated with decreased connectivity within the default network and increased connectivity between default and dorsal attention networks. Conclusions: This study demonstrates that with moderate levels of support, including readily available techniques, information about brain similarities and differences in LVCP individuals can be further studied. This initial study suggested decreased network segmentation and integration in LVCP individuals. Further imaging studies of LVCP individuals with larger samples will add to understanding of origins and effects of autism on brain function and behavior. En ligne : https://dx.doi.org/10.1186/s13229-018-0248-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389
in Molecular Autism > 9 (2018) . - 67 p.[article] Functional MRI connectivity of children with autism and low verbal and cognitive performance [Texte imprimé et/ou numérique] / T. P. GABRIELSEN, Auteur ; Jeffrey S. ANDERSON, Auteur ; K. G. STEPHENSON, Auteur ; J. BECK, Auteur ; J. B. KING, Auteur ; R. KELLEMS, Auteur ; D. N. TOP, Auteur ; N. C. C. RUSSELL, Auteur ; Emily I. ANDERBERG, Auteur ; R. A. LUNDWALL, Auteur ; B. HANSEN, Auteur ; M. SOUTH, Auteur . - 67 p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 67 p.
Mots-clés : Adolescent Autistic Disorder/*diagnostic imaging/physiopathology Case-Control Studies Child *Cognition Female Humans Intelligence *Language Development Magnetic Resonance Imaging Male *Autism spectrum disorder *Functional connectivity *Imaging methodology *Intelligence *Language Institutional Review Board, protocol #F25403. Written informed consent was obtained from parents, with assent obtained from participants following video review of procedures.The boy who modeled the MRI procedures in the video modeling procedure was filmed, and the final video was shared, with written permission of both of his parents and with his own assent.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Functional neuroimaging research in autism spectrum disorder has reported patterns of decreased long-range, within-network, and interhemispheric connectivity. Research has also reported increased corticostriatal connectivity and between-network connectivity for default and attentional networks. Past studies have excluded individuals with autism and low verbal and cognitive performance (LVCP), so connectivity in individuals more significantly affected with autism has not yet been studied. This represents a critical gap in our understanding of brain function across the autism spectrum. Methods: Using behavioral support procedures adapted from Nordahl, et al. (J Neurodev Disord 8:20-20, 2016), we completed non-sedated structural and functional MRI scans of 56 children ages 7-17, including LVCP children (n = 17, mean IQ = 54), children with autism and higher performance (HVCP, n = 20, mean IQ = 106), and neurotypical children (NT, n = 19, mean IQ = 111). Preparation included detailed intake questionnaires, video modeling, behavioral and anxiety reduction techniques, active noise-canceling headphones, and in-scan presentation of the Inscapes movie paradigm from Vanderwal et al. (Neuroimage 122:222-32, 2015). A high temporal resolution multiband echoplanar fMRI protocol analyzed motion-free time series data, extracted from concatenated volumes to mitigate the influence of motion artifact. All participants had > 200 volumes of motion-free fMRI scanning. Analyses were corrected for multiple comparisons. Results: LVCP showed decreased within-network connectivity in default, salience, auditory, and frontoparietal networks (LVCP < HVCP) and decreased interhemispheric connectivity (LVCP < HVCP=NT). Between-network connectivity was higher for LVCP than NT between default and dorsal attention and frontoparietal networks. Lower IQ was associated with decreased connectivity within the default network and increased connectivity between default and dorsal attention networks. Conclusions: This study demonstrates that with moderate levels of support, including readily available techniques, information about brain similarities and differences in LVCP individuals can be further studied. This initial study suggested decreased network segmentation and integration in LVCP individuals. Further imaging studies of LVCP individuals with larger samples will add to understanding of origins and effects of autism on brain function and behavior. En ligne : https://dx.doi.org/10.1186/s13229-018-0248-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389 Loss of the Chr16p11.2 ASD candidate gene QPRT leads to aberrant neuronal differentiation in the SH-SY5Y neuronal cell model / D. HASLINGER in Molecular Autism, 9 (2018)
[article]
Titre : Loss of the Chr16p11.2 ASD candidate gene QPRT leads to aberrant neuronal differentiation in the SH-SY5Y neuronal cell model Type de document : Texte imprimé et/ou numérique Auteurs : D. HASLINGER, Auteur ; R. WALTES, Auteur ; A. YOUSAF, Auteur ; S. LINDLAR, Auteur ; I. SCHNEIDER, Auteur ; C. K. LIM, Auteur ; M. M. TSAI, Auteur ; B. K. GARVALOV, Auteur ; A. ACKER-PALMER, Auteur ; N. KREZDORN, Auteur ; B. ROTTER, Auteur ; T. ACKER, Auteur ; G. J. GUILLEMIN, Auteur ; S. FULDA, Auteur ; C. M. FREITAG, Auteur ; Andreas G. CHIOCCHETTI, Auteur Article en page(s) : 56p. Langues : Anglais (eng) Mots-clés : 16p11.2 Autism CRISPR/Cas9 Kynurenine Quinolinate phosphoribosyltransferase Quinolinic acid Sholl analysis has been positively reviewed by the ethic's committee Frankfurt (No 267/09).All authors agree to publish the presented work.All authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Altered neuronal development is discussed as the underlying pathogenic mechanism of autism spectrum disorders (ASD). Copy number variations of 16p11.2 have recurrently been identified in individuals with ASD. Of the 29 genes within this region, quinolinate phosphoribosyltransferase (QPRT) showed the strongest regulation during neuronal differentiation of SH-SY5Y neuroblastoma cells. We hypothesized a causal relation between this tryptophan metabolism-related enzyme and neuronal differentiation. We thus analyzed the effect of QPRT on the differentiation of SH-SY5Y and specifically focused on neuronal morphology, metabolites of the tryptophan pathway, and the neurodevelopmental transcriptome. Methods: The gene dosage-dependent change of QPRT expression following Chr16p11.2 deletion was investigated in a lymphoblastoid cell line (LCL) of a deletion carrier and compared to his non-carrier parents. Expression of QPRT was tested for correlation with neuromorphology in SH-SY5Y cells. QPRT function was inhibited in SH-SY5Y neuroblastoma cells using (i) siRNA knockdown (KD), (ii) chemical mimicking of loss of QPRT, and (iii) complete CRISPR/Cas9-mediated knock out (KO). QPRT-KD cells underwent morphological analysis. Chemically inhibited and QPRT-KO cells were characterized using viability assays. Additionally, QPRT-KO cells underwent metabolite and whole transcriptome analyses. Genes differentially expressed upon KO of QPRT were tested for enrichment in biological processes and co-regulated gene-networks of the human brain. Results: QPRT expression was reduced in the LCL of the deletion carrier and significantly correlated with the neuritic complexity of SH-SY5Y. The reduction of QPRT altered neuronal morphology of differentiated SH-SY5Y cells. Chemical inhibition as well as complete KO of the gene were lethal upon induction of neuronal differentiation, but not proliferation. The QPRT-associated tryptophan pathway was not affected by KO. At the transcriptome level, genes linked to neurodevelopmental processes and synaptic structures were affected. Differentially regulated genes were enriched for ASD candidates, and co-regulated gene networks were implicated in the development of the dorsolateral prefrontal cortex, the hippocampus, and the amygdala. Conclusions: In this study, QPRT was causally related to in vitro neuronal differentiation of SH-SY5Y cells and affected the regulation of genes and gene networks previously implicated in ASD. Thus, our data suggest that QPRT may play an important role in the pathogenesis of ASD in Chr16p11.2 deletion carriers. En ligne : https://dx.doi.org/10.1186/s13229-018-0239-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 56p.[article] Loss of the Chr16p11.2 ASD candidate gene QPRT leads to aberrant neuronal differentiation in the SH-SY5Y neuronal cell model [Texte imprimé et/ou numérique] / D. HASLINGER, Auteur ; R. WALTES, Auteur ; A. YOUSAF, Auteur ; S. LINDLAR, Auteur ; I. SCHNEIDER, Auteur ; C. K. LIM, Auteur ; M. M. TSAI, Auteur ; B. K. GARVALOV, Auteur ; A. ACKER-PALMER, Auteur ; N. KREZDORN, Auteur ; B. ROTTER, Auteur ; T. ACKER, Auteur ; G. J. GUILLEMIN, Auteur ; S. FULDA, Auteur ; C. M. FREITAG, Auteur ; Andreas G. CHIOCCHETTI, Auteur . - 56p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 56p.
Mots-clés : 16p11.2 Autism CRISPR/Cas9 Kynurenine Quinolinate phosphoribosyltransferase Quinolinic acid Sholl analysis has been positively reviewed by the ethic's committee Frankfurt (No 267/09).All authors agree to publish the presented work.All authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Altered neuronal development is discussed as the underlying pathogenic mechanism of autism spectrum disorders (ASD). Copy number variations of 16p11.2 have recurrently been identified in individuals with ASD. Of the 29 genes within this region, quinolinate phosphoribosyltransferase (QPRT) showed the strongest regulation during neuronal differentiation of SH-SY5Y neuroblastoma cells. We hypothesized a causal relation between this tryptophan metabolism-related enzyme and neuronal differentiation. We thus analyzed the effect of QPRT on the differentiation of SH-SY5Y and specifically focused on neuronal morphology, metabolites of the tryptophan pathway, and the neurodevelopmental transcriptome. Methods: The gene dosage-dependent change of QPRT expression following Chr16p11.2 deletion was investigated in a lymphoblastoid cell line (LCL) of a deletion carrier and compared to his non-carrier parents. Expression of QPRT was tested for correlation with neuromorphology in SH-SY5Y cells. QPRT function was inhibited in SH-SY5Y neuroblastoma cells using (i) siRNA knockdown (KD), (ii) chemical mimicking of loss of QPRT, and (iii) complete CRISPR/Cas9-mediated knock out (KO). QPRT-KD cells underwent morphological analysis. Chemically inhibited and QPRT-KO cells were characterized using viability assays. Additionally, QPRT-KO cells underwent metabolite and whole transcriptome analyses. Genes differentially expressed upon KO of QPRT were tested for enrichment in biological processes and co-regulated gene-networks of the human brain. Results: QPRT expression was reduced in the LCL of the deletion carrier and significantly correlated with the neuritic complexity of SH-SY5Y. The reduction of QPRT altered neuronal morphology of differentiated SH-SY5Y cells. Chemical inhibition as well as complete KO of the gene were lethal upon induction of neuronal differentiation, but not proliferation. The QPRT-associated tryptophan pathway was not affected by KO. At the transcriptome level, genes linked to neurodevelopmental processes and synaptic structures were affected. Differentially regulated genes were enriched for ASD candidates, and co-regulated gene networks were implicated in the development of the dorsolateral prefrontal cortex, the hippocampus, and the amygdala. Conclusions: In this study, QPRT was causally related to in vitro neuronal differentiation of SH-SY5Y cells and affected the regulation of genes and gene networks previously implicated in ASD. Thus, our data suggest that QPRT may play an important role in the pathogenesis of ASD in Chr16p11.2 deletion carriers. En ligne : https://dx.doi.org/10.1186/s13229-018-0239-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 The effect of age on vertex-based measures of the grey-white matter tissue contrast in autism spectrum disorder / C. MANN in Molecular Autism, 9 (2018)
The within-subject application of diffusion tensor MRI and CLARITY reveals brain structural changes in Nrxn2 deletion mice / E. PERVOLARAKI in Molecular Autism, 10 (2019)
[article]
Titre : The within-subject application of diffusion tensor MRI and CLARITY reveals brain structural changes in Nrxn2 deletion mice Type de document : Texte imprimé et/ou numérique Auteurs : E. PERVOLARAKI, Auteur ; A. L. TYSON, Auteur ; F. PIBIRI, Auteur ; S. L. POULTER, Auteur ; A. C. REICHELT, Auteur ; R. J. RODGERS, Auteur ; S. J. CLAPCOTE, Auteur ; C. LEVER, Auteur ; L. C. ANDREAE, Auteur ; J. DACHTLER, Auteur Article en page(s) : 8 p. Langues : Anglais (eng) Mots-clés : *Autism *Axons *clarity *Diffusion *Imaging *mri *Social *Structure in accordance with the Animals (Scientific Procedures) Act 1986, and with the approval of the University of Leeds and Durham University Animal Ethical and Welfare Review Boards.Not applicableThe authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Of the many genetic mutations known to increase the risk of autism spectrum disorder, a large proportion cluster upon synaptic proteins. One such family of presynaptic proteins are the neurexins (NRXN), and recent genetic and mouse evidence has suggested a causative role for NRXN2 in generating altered social behaviours. Autism has been conceptualised as a disorder of atypical connectivity, yet how single-gene mutations affect such connectivity remains under-explored. To attempt to address this, we have developed a quantitative analysis of microstructure and structural connectivity leveraging diffusion tensor MRI (DTI) with high-resolution 3D imaging in optically cleared (CLARITY) brain tissue in the same mouse, applied here to the Nrxn2alpha knockout (KO) model. Methods: Fixed brains of Nrxn2alpha KO mice underwent DTI using 9.4 T MRI, and diffusion properties of socially relevant brain regions were quantified. The same tissue was then subjected to CLARITY to immunolabel axons and cell bodies, which were also quantified. Results: DTI revealed increases in fractional anisotropy in the amygdala (including the basolateral nuclei), the anterior cingulate cortex, the orbitofrontal cortex and the hippocampus. Axial diffusivity of the anterior cingulate cortex and orbitofrontal cortex was significantly increased in Nrxn2alpha KO mice, as were tracts between the amygdala and the orbitofrontal cortex. Using CLARITY, we find significantly altered axonal orientation in the amygdala, orbitofrontal cortex and the anterior cingulate cortex, which was unrelated to cell density. Conclusions: Our findings demonstrate that deleting a single neurexin gene (Nrxn2alpha) induces atypical structural connectivity within socially relevant brain regions. More generally, our combined within-subject DTI and CLARITY approach presents a new, more sensitive method of revealing hitherto undetectable differences in the autistic brain. En ligne : https://dx.doi.org/10.1186/s13229-019-0261-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389
in Molecular Autism > 10 (2019) . - 8 p.[article] The within-subject application of diffusion tensor MRI and CLARITY reveals brain structural changes in Nrxn2 deletion mice [Texte imprimé et/ou numérique] / E. PERVOLARAKI, Auteur ; A. L. TYSON, Auteur ; F. PIBIRI, Auteur ; S. L. POULTER, Auteur ; A. C. REICHELT, Auteur ; R. J. RODGERS, Auteur ; S. J. CLAPCOTE, Auteur ; C. LEVER, Auteur ; L. C. ANDREAE, Auteur ; J. DACHTLER, Auteur . - 8 p.
Langues : Anglais (eng)
in Molecular Autism > 10 (2019) . - 8 p.
Mots-clés : *Autism *Axons *clarity *Diffusion *Imaging *mri *Social *Structure in accordance with the Animals (Scientific Procedures) Act 1986, and with the approval of the University of Leeds and Durham University Animal Ethical and Welfare Review Boards.Not applicableThe authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Of the many genetic mutations known to increase the risk of autism spectrum disorder, a large proportion cluster upon synaptic proteins. One such family of presynaptic proteins are the neurexins (NRXN), and recent genetic and mouse evidence has suggested a causative role for NRXN2 in generating altered social behaviours. Autism has been conceptualised as a disorder of atypical connectivity, yet how single-gene mutations affect such connectivity remains under-explored. To attempt to address this, we have developed a quantitative analysis of microstructure and structural connectivity leveraging diffusion tensor MRI (DTI) with high-resolution 3D imaging in optically cleared (CLARITY) brain tissue in the same mouse, applied here to the Nrxn2alpha knockout (KO) model. Methods: Fixed brains of Nrxn2alpha KO mice underwent DTI using 9.4 T MRI, and diffusion properties of socially relevant brain regions were quantified. The same tissue was then subjected to CLARITY to immunolabel axons and cell bodies, which were also quantified. Results: DTI revealed increases in fractional anisotropy in the amygdala (including the basolateral nuclei), the anterior cingulate cortex, the orbitofrontal cortex and the hippocampus. Axial diffusivity of the anterior cingulate cortex and orbitofrontal cortex was significantly increased in Nrxn2alpha KO mice, as were tracts between the amygdala and the orbitofrontal cortex. Using CLARITY, we find significantly altered axonal orientation in the amygdala, orbitofrontal cortex and the anterior cingulate cortex, which was unrelated to cell density. Conclusions: Our findings demonstrate that deleting a single neurexin gene (Nrxn2alpha) induces atypical structural connectivity within socially relevant brain regions. More generally, our combined within-subject DTI and CLARITY approach presents a new, more sensitive method of revealing hitherto undetectable differences in the autistic brain. En ligne : https://dx.doi.org/10.1186/s13229-019-0261-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389 Neuroglia in the autistic brain: evidence from a preclinical model / M. R. BRONZUOLI in Molecular Autism, 9 (2018)
[article]
Titre : Neuroglia in the autistic brain: evidence from a preclinical model Type de document : Texte imprimé et/ou numérique Auteurs : M. R. BRONZUOLI, Auteur ; R. FACCHINETTI, Auteur ; D. INGRASSIA, Auteur ; M. SARVADIO, Auteur ; S. SCHIAVI, Auteur ; L. STEARDO, Auteur ; A. VERKHRATSKY, Auteur ; V. TREZZA, Auteur ; C. SCUDERI, Auteur Article en page(s) : 66 p. Langues : Anglais (eng) Mots-clés : Animals Autistic Disorder/etiology/*pathology/physiopathology Brain/drug effects/*pathology Female Male Neuroglia/drug effects/*pathology Rats Rats, Wistar Stereotyped Behavior Valproic Acid/pharmacology/toxicity Vocalization, Animal *Astrocyte *Autism spectrum disorder *Microglia *Oligodendrocyte *Valproic acid of the Italian Ministry of Health (D.L. 26/2014) and with the European Parliament directive 2010/63/EU.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Neuroglial cells that provide homeostatic support and form defence of the nervous system contribute to all neurological disorders. We analyzed three major types of neuroglia, astrocytes, oligodendrocytes, and microglia in the brains of an animal model of autism spectrum disorder, in which rats were exposed prenatally to antiepileptic and mood stabilizer drug valproic acid; this model being of acknowledged clinical relevance. Methods: We tested the autistic-like behaviors of valproic acid-prenatally exposed male rats by performing isolation-induced ultrasonic vocalizations, the three-chamber test, and the hole board test. To account for human infancy, adolescence, and adulthood, such tasks were performed at postnatal day 13, postnatal day 35, and postnatal day 90, respectively. After sacrifice, we examined gene and protein expression of specific markers of neuroglia in hippocampus, prefrontal cortex, and cerebellum, these brain regions being associated with autism spectrum disorder pathogenesis. Results: Infant offspring of VPA-exposed dams emitted less ultrasonic vocalizations when isolated from their mothers and siblings and, in adolescence and adulthood, they showed altered sociability in the three chamber test and increased stereotypic behavior in the hole board test. Molecular analyses indicate that prenatal valproic acid exposure affects all types of neuroglia, mainly causing transcriptional modifications. The most prominent changes occur in prefrontal cortex and in the hippocampus of autistic-like animals; these changes are particularly evident during infancy and adolescence, while they appear to be mitigated in adulthood. Conclusions: Neuroglial pathological phenotype in autism spectrum disorder rat model appears to be rather mild with little signs of widespread and chronic neuroinflammation. En ligne : https://dx.doi.org/10.1186/s13229-018-0254-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389
in Molecular Autism > 9 (2018) . - 66 p.[article] Neuroglia in the autistic brain: evidence from a preclinical model [Texte imprimé et/ou numérique] / M. R. BRONZUOLI, Auteur ; R. FACCHINETTI, Auteur ; D. INGRASSIA, Auteur ; M. SARVADIO, Auteur ; S. SCHIAVI, Auteur ; L. STEARDO, Auteur ; A. VERKHRATSKY, Auteur ; V. TREZZA, Auteur ; C. SCUDERI, Auteur . - 66 p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 66 p.
Mots-clés : Animals Autistic Disorder/etiology/*pathology/physiopathology Brain/drug effects/*pathology Female Male Neuroglia/drug effects/*pathology Rats Rats, Wistar Stereotyped Behavior Valproic Acid/pharmacology/toxicity Vocalization, Animal *Astrocyte *Autism spectrum disorder *Microglia *Oligodendrocyte *Valproic acid of the Italian Ministry of Health (D.L. 26/2014) and with the European Parliament directive 2010/63/EU.Not applicable.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Index. décimale : PER Périodiques Résumé : Background: Neuroglial cells that provide homeostatic support and form defence of the nervous system contribute to all neurological disorders. We analyzed three major types of neuroglia, astrocytes, oligodendrocytes, and microglia in the brains of an animal model of autism spectrum disorder, in which rats were exposed prenatally to antiepileptic and mood stabilizer drug valproic acid; this model being of acknowledged clinical relevance. Methods: We tested the autistic-like behaviors of valproic acid-prenatally exposed male rats by performing isolation-induced ultrasonic vocalizations, the three-chamber test, and the hole board test. To account for human infancy, adolescence, and adulthood, such tasks were performed at postnatal day 13, postnatal day 35, and postnatal day 90, respectively. After sacrifice, we examined gene and protein expression of specific markers of neuroglia in hippocampus, prefrontal cortex, and cerebellum, these brain regions being associated with autism spectrum disorder pathogenesis. Results: Infant offspring of VPA-exposed dams emitted less ultrasonic vocalizations when isolated from their mothers and siblings and, in adolescence and adulthood, they showed altered sociability in the three chamber test and increased stereotypic behavior in the hole board test. Molecular analyses indicate that prenatal valproic acid exposure affects all types of neuroglia, mainly causing transcriptional modifications. The most prominent changes occur in prefrontal cortex and in the hippocampus of autistic-like animals; these changes are particularly evident during infancy and adolescence, while they appear to be mitigated in adulthood. Conclusions: Neuroglial pathological phenotype in autism spectrum disorder rat model appears to be rather mild with little signs of widespread and chronic neuroinflammation. En ligne : https://dx.doi.org/10.1186/s13229-018-0254-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=389 Savant syndrome has a distinct psychological profile in autism / J. E. A. HUGHES in Molecular Autism, 9 (2018)
Permalink