Discrete Cortical Neuropathology in Autism Spectrum Disorders / Neha UPPAL

Public ISBD in The Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM Titre : Discrete Cortical Neuropathology in Autism Spectrum Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Neha UPPAL, Auteur ; Patrick R. HOF, Auteur Année de publication : 2013 Importance : p.313-325 Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Autism spectrum disorders (ASD) are the most inheritable of psychiatric disorders, although precise genetic alterations have only been identified in about 20% of cases. The major impact of the condition on the development and social integration of affected children has led to a marked increase in research efforts focusing on the possible roles of neuropathological processes underlying it. This chapter provides an overview of the literature on the cortical neuropathology of ASD. Postmortem studies are pivotal for cell-level exploration, especially in the context of brain regions which consistently show altered patterns of activation in functional magnetic resonance imaging studies. Cortical alterations known to occur in ASD are reviewed, including abnormalities in neuronal morphology, neurotransmitter systems, and cytoarchitectural organization. We focus in particular on abnormalities of the prefrontal cortex, the inferior frontal cortex, fusiform gyrus, the insular cortex, the cingulate cortex, and the hippocampus. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 in The Neuroscience of Autism Spectrum Disorders / Joseph D. BUXBAUM Discrete Cortical Neuropathology in Autism Spectrum Disorders [Texte imprimé et/ou numérique] / Neha UPPAL, Auteur ; Patrick R. HOF, Auteur . - 2013 . - p.313-325. Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Autism spectrum disorders (ASD) are the most inheritable of psychiatric disorders, although precise genetic alterations have only been identified in about 20% of cases. The major impact of the condition on the development and social integration of affected children has led to a marked increase in research efforts focusing on the possible roles of neuropathological processes underlying it. This chapter provides an overview of the literature on the cortical neuropathology of ASD. Postmortem studies are pivotal for cell-level exploration, especially in the context of brain regions which consistently show altered patterns of activation in functional magnetic resonance imaging studies. Cortical alterations known to occur in ASD are reviewed, including abnormalities in neuronal morphology, neurotransmitter systems, and cytoarchitectural organization. We focus in particular on abnormalities of the prefrontal cortex, the inferior frontal cortex, fusiform gyrus, the insular cortex, the cingulate cortex, and the hippocampus. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189

Exemplaires

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Neuropathology of the posteroinferior occipitotemporal gyrus in children with autism / Neha UPPAL in Molecular Autism, (February 2014)  

Public ISBD [article]  inMolecular Autism > (February 2014) Titre : Neuropathology of the posteroinferior occipitotemporal gyrus in children with autism Type de document : Texte imprimé et/ou numérique Auteurs : Neha UPPAL, Auteur ; Isabella GIANATIEMPO, Auteur ; Bridget WICINSKI, Auteur ; James SCHMEIDLER, Auteur ; Helmut HEINSEN, Auteur ; Christoph SCHMITZ, Auteur ; Joseph D. BUXBAUM, Auteur ; Patrick R. HOF, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : While most neuropathologic studies focus on regions involved in behavioral abnormalities in autism, it is also important to identify whether areas that appear functionally normal are devoid of pathologic alterations. In this study we analyzed the posteroinferior occipitotemporal gyrus, an extrastriate area not considered to be affected in autism. This area borders the fusiform gyrus, which is known to exhibit functional and cellular abnormalities in autism.FINDINGS:No studies have implicated posteroinferior occipitotemporal gyrus dysfunction in autism, leading us to hypothesize that neuropathology would not occur in this area. We indeed observed no significant differences in pyramidal neuron number or size in layers III, V, and VI in seven pairs of autism and controls. These findings are consistent with the hypothesis that neuropathology is unique to areas involved in stereotypies and social and emotional behaviors, and support the specificity of the localization of pathology in the fusiform gyrus. En ligne : http://dx.doi.org/10.1186/2040-2392-5-17 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227 [article] Neuropathology of the posteroinferior occipitotemporal gyrus in children with autism [Texte imprimé et/ou numérique] / Neha UPPAL, Auteur ; Isabella GIANATIEMPO, Auteur ; Bridget WICINSKI, Auteur ; James SCHMEIDLER, Auteur ; Helmut HEINSEN, Auteur ; Christoph SCHMITZ, Auteur ; Joseph D. BUXBAUM, Auteur ; Patrick R. HOF, Auteur. Langues : Anglais (eng) in Molecular Autism > (February 2014) Index. décimale : PER Périodiques Résumé : While most neuropathologic studies focus on regions involved in behavioral abnormalities in autism, it is also important to identify whether areas that appear functionally normal are devoid of pathologic alterations. In this study we analyzed the posteroinferior occipitotemporal gyrus, an extrastriate area not considered to be affected in autism. This area borders the fusiform gyrus, which is known to exhibit functional and cellular abnormalities in autism.FINDINGS:No studies have implicated posteroinferior occipitotemporal gyrus dysfunction in autism, leading us to hypothesize that neuropathology would not occur in this area. We indeed observed no significant differences in pyramidal neuron number or size in layers III, V, and VI in seven pairs of autism and controls. These findings are consistent with the hypothesis that neuropathology is unique to areas involved in stereotypies and social and emotional behaviors, and support the specificity of the localization of pathology in the fusiform gyrus. En ligne : http://dx.doi.org/10.1186/2040-2392-5-17 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227

Ultrastructural analyses in the hippocampus CA1 field in Shank3-deficient mice / Neha UPPAL in Molecular Autism, (June 2015)  

Public ISBD [article]  inMolecular Autism > (June 2015) . - p.1-10 Titre : Ultrastructural analyses in the hippocampus CA1 field in Shank3-deficient mice Type de document : Texte imprimé et/ou numérique Auteurs : Neha UPPAL, Auteur ; Rishi PURI, Auteur ; Frank YUK, Auteur ; William G. M. JANSSEN, Auteur ; Ozlem BOZDAGI-GUNAL, Auteur ; Hala HARONY-NICOLAS, Auteur ; Dara L. DICKSTEIN, Auteur ; Joseph D. BUXBAUM, Auteur ; Patrick R. HOF, Auteur Article en page(s) : p.1-10 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The genetics of autism spectrum disorder (hereafter referred to as “autism”) are rapidly unfolding, with a significant increase in the identification of genes implicated in the disorder. Many of these genes are part of a complex landscape of genetic variants that are thought to act together to cause the behavioral phenotype associated with autism. One of the few single-locus causes of autism involves a mutation in the SH3 and multiple ankyrin repeat domains 3 (SHANK3) gene. Previous electrophysiological studies in mice with Shank3 mutations demonstrated impairment in synaptic long-term potentiation, suggesting a potential disruption at the synapse. En ligne : http://dx.doi.org/10.1186/s13229-015-0036-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277 [article] Ultrastructural analyses in the hippocampus CA1 field in Shank3-deficient mice [Texte imprimé et/ou numérique] / Neha UPPAL, Auteur ; Rishi PURI, Auteur ; Frank YUK, Auteur ; William G. M. JANSSEN, Auteur ; Ozlem BOZDAGI-GUNAL, Auteur ; Hala HARONY-NICOLAS, Auteur ; Dara L. DICKSTEIN, Auteur ; Joseph D. BUXBAUM, Auteur ; Patrick R. HOF, Auteur . - p.1-10. Langues : Anglais (eng) in Molecular Autism > (June 2015) . - p.1-10 Index. décimale : PER Périodiques Résumé : The genetics of autism spectrum disorder (hereafter referred to as “autism”) are rapidly unfolding, with a significant increase in the identification of genes implicated in the disorder. Many of these genes are part of a complex landscape of genetic variants that are thought to act together to cause the behavioral phenotype associated with autism. One of the few single-locus causes of autism involves a mutation in the SH3 and multiple ankyrin repeat domains 3 (SHANK3) gene. Previous electrophysiological studies in mice with Shank3 mutations demonstrated impairment in synaptic long-term potentiation, suggesting a potential disruption at the synapse. En ligne : http://dx.doi.org/10.1186/s13229-015-0036-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277

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