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
-
Détail de l'auteur
Auteur Christy C. ROSSI |
Documents disponibles écrits par cet auteur (2)
Faire une suggestion Affiner la recherche
Brief Report: Antibodies Reacting to Brain Tissue in Basque Spanish Children with Autism Spectrum Disorder and Their Mothers / Christy C. ROSSI in Journal of Autism and Developmental Disorders, 44-2 (February 2014)
[article]
Titre : Brief Report: Antibodies Reacting to Brain Tissue in Basque Spanish Children with Autism Spectrum Disorder and Their Mothers Type de document : Texte imprimé et/ou numérique Auteurs : Christy C. ROSSI, Auteur ; Joaquin FUENTES, Auteur ; Judy WATER, Auteur ; David G. AMARAL, Auteur Article en page(s) : p.459-465 Langues : Anglais (eng) Mots-clés : Autism spectrum disorders Autoantibody Brain International Index. décimale : PER Périodiques Résumé : Previous investigations found that a subset of children with autism spectrum disorder (ASD) in California possessed plasma autoantibodies that reacted intensely with brain interneurons or other neural profiles. Moreover, for several cohorts of American women, maternal autoantibody reactivity to specific fetal brain proteins was highly specific to mothers of children with ASD. We sought to determine whether children and their mothers from a regionally specific cohort from the Basque Country of Spain demonstrated similar reactivity. Some children’s plasma reacted to interneurons, beaded axons or other neural profiles with no difference in the occurrence of these antibodies in children with or without ASD. Findings on the maternal antibodies confirmed previous research; plasma reactivity to fetal brain a combination of proteins at 37 and 73 kDa or 39 and 73 kDa was found exclusively in mothers of children with ASD. En ligne : http://dx.doi.org/10.1007/s10803-013-1859-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=223
in Journal of Autism and Developmental Disorders > 44-2 (February 2014) . - p.459-465[article] Brief Report: Antibodies Reacting to Brain Tissue in Basque Spanish Children with Autism Spectrum Disorder and Their Mothers [Texte imprimé et/ou numérique] / Christy C. ROSSI, Auteur ; Joaquin FUENTES, Auteur ; Judy WATER, Auteur ; David G. AMARAL, Auteur . - p.459-465.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 44-2 (February 2014) . - p.459-465
Mots-clés : Autism spectrum disorders Autoantibody Brain International Index. décimale : PER Périodiques Résumé : Previous investigations found that a subset of children with autism spectrum disorder (ASD) in California possessed plasma autoantibodies that reacted intensely with brain interneurons or other neural profiles. Moreover, for several cohorts of American women, maternal autoantibody reactivity to specific fetal brain proteins was highly specific to mothers of children with ASD. We sought to determine whether children and their mothers from a regionally specific cohort from the Basque Country of Spain demonstrated similar reactivity. Some children’s plasma reacted to interneurons, beaded axons or other neural profiles with no difference in the occurrence of these antibodies in children with or without ASD. Findings on the maternal antibodies confirmed previous research; plasma reactivity to fetal brain a combination of proteins at 37 and 73 kDa or 39 and 73 kDa was found exclusively in mothers of children with ASD. En ligne : http://dx.doi.org/10.1007/s10803-013-1859-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=223 Further characterization of autoantibodies to GABAergic neurons in the central nervous system produced by a subset of children with autism / Sharifia WILLS in Molecular Autism, (April 2011)
[article]
Titre : Further characterization of autoantibodies to GABAergic neurons in the central nervous system produced by a subset of children with autism Type de document : Texte imprimé et/ou numérique Auteurs : Sharifia WILLS, Auteur ; Christy C. ROSSI, Auteur ; Jeffrey BENNETT, Auteur ; Veronica M. CERDENO, Auteur ; Paul ASHWOOD, Auteur ; David G. AMARAL, Auteur ; Judy VAN DE WATER, Auteur Année de publication : 2011 Article en page(s) : 15 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background
Autism is a neurodevelopmental disorder characterized by impairments in social interaction and deficits in verbal and nonverbal communication, together with the presence of repetitive behaviors or a limited repertoire of activities and interests. The causes of autism are currently unclear. In a previous study, we determined that 21% of children with autism have plasma autoantibodies that are immunoreactive with a population of neurons in the cerebellum that appear to be Golgi cells, which are GABAergic interneurons.
Methods
We have extended this analysis by examining plasma immunoreactivity in the remainder of the brain. To determine cell specificity, double-labeling studies that included one of the calcium-binding proteins that are commonly colocalized in GABAergic neurons (calbindin, parvalbumin or calretinin) were also carried out to determine which GABAergic neurons are immunoreactive. Coronal sections through the rostrocaudal extent of the macaque monkey brain were reacted with plasma from each of seven individuals with autism who had previously demonstrated positive Golgi cell staining, as well as six negative controls. In addition, brain sections from adult male mice were similarly examined.
Results
In each case, specific staining was observed for neurons that had the morphological appearance of interneurons. By double-labeling sections with plasma and with antibodies directed against γ-aminobutyric acid (GABA), we determined that all autoantibody-positive neurons were GABAergic. However, not all GABAergic neurons were autoantibody-positive. Calbindin was colabeled in several of the autoantibody-labeled cells, while parvalbumin colabeling was less frequently observed. Autoantibody-positive cells rarely expressed calretinin. Sections from the mouse brain processed similarly to the primate sections also demonstrated immunoreactivity to interneurons distributed throughout the neocortex and many subcortical regions. Some cell populations stained in the primate (such as the Golgi neurons in the cerebellum) were not as robustly immunoreactive in the mouse brain.
Conclusions
These results suggest that the earlier report of autoantibody immunoreactivity to specific cells in the cerebellum extend to other regions of the brain. Further, these findings confirm the autoantibody-targeted cells to be a subpopulation of GABAergic interneurons. The potential impact of these autoantibodies on GABAergic disruption with respect to the etiology of autism is discussed herein.En ligne : http://dx.doi.org/10.1186/2040-2392-2-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131
in Molecular Autism > (April 2011) . - 15 p.[article] Further characterization of autoantibodies to GABAergic neurons in the central nervous system produced by a subset of children with autism [Texte imprimé et/ou numérique] / Sharifia WILLS, Auteur ; Christy C. ROSSI, Auteur ; Jeffrey BENNETT, Auteur ; Veronica M. CERDENO, Auteur ; Paul ASHWOOD, Auteur ; David G. AMARAL, Auteur ; Judy VAN DE WATER, Auteur . - 2011 . - 15 p.
Langues : Anglais (eng)
in Molecular Autism > (April 2011) . - 15 p.
Index. décimale : PER Périodiques Résumé : Background
Autism is a neurodevelopmental disorder characterized by impairments in social interaction and deficits in verbal and nonverbal communication, together with the presence of repetitive behaviors or a limited repertoire of activities and interests. The causes of autism are currently unclear. In a previous study, we determined that 21% of children with autism have plasma autoantibodies that are immunoreactive with a population of neurons in the cerebellum that appear to be Golgi cells, which are GABAergic interneurons.
Methods
We have extended this analysis by examining plasma immunoreactivity in the remainder of the brain. To determine cell specificity, double-labeling studies that included one of the calcium-binding proteins that are commonly colocalized in GABAergic neurons (calbindin, parvalbumin or calretinin) were also carried out to determine which GABAergic neurons are immunoreactive. Coronal sections through the rostrocaudal extent of the macaque monkey brain were reacted with plasma from each of seven individuals with autism who had previously demonstrated positive Golgi cell staining, as well as six negative controls. In addition, brain sections from adult male mice were similarly examined.
Results
In each case, specific staining was observed for neurons that had the morphological appearance of interneurons. By double-labeling sections with plasma and with antibodies directed against γ-aminobutyric acid (GABA), we determined that all autoantibody-positive neurons were GABAergic. However, not all GABAergic neurons were autoantibody-positive. Calbindin was colabeled in several of the autoantibody-labeled cells, while parvalbumin colabeling was less frequently observed. Autoantibody-positive cells rarely expressed calretinin. Sections from the mouse brain processed similarly to the primate sections also demonstrated immunoreactivity to interneurons distributed throughout the neocortex and many subcortical regions. Some cell populations stained in the primate (such as the Golgi neurons in the cerebellum) were not as robustly immunoreactive in the mouse brain.
Conclusions
These results suggest that the earlier report of autoantibody immunoreactivity to specific cells in the cerebellum extend to other regions of the brain. Further, these findings confirm the autoantibody-targeted cells to be a subpopulation of GABAergic interneurons. The potential impact of these autoantibodies on GABAergic disruption with respect to the etiology of autism is discussed herein.En ligne : http://dx.doi.org/10.1186/2040-2392-2-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131