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Brief Report: Life History and Neuropathology of a Gifted Man with Asperger Syndrome / Karen M. WEIDENHEIM in Journal of Autism and Developmental Disorders, 42-3 (March 2012)
[article]
Titre : Brief Report: Life History and Neuropathology of a Gifted Man with Asperger Syndrome Type de document : Texte imprimé et/ou numérique Auteurs : Karen M. WEIDENHEIM, Auteur ; Alfonso ESCOBAR, Auteur ; Isabelle RAPIN, Auteur Année de publication : 2012 Article en page(s) : p.460-467 Langues : Anglais (eng) Mots-clés : Autism Asperger syndrome Life history Neuropathology Adult Index. décimale : PER Périodiques Résumé : Despite recent interest in the pathogenesis of the autism spectrum disorders (pervasive developmental disorders), neuropathological descriptions of brains of individuals with well documented clinical information and without potentially confounding symptomatology are exceptionally rare. Asperger syndrome differs from classic autism by lack of cognitive impairment or delay in expressive language acquisition. We examined the 1,570 g brain of a 63 year old otherwise healthy mathematician with an Autistic Spectrum Disorder of Asperger subtype. Except for an atypical gyral pattern and megalencephaly, we detected no specific neuropathologic abnormality. Taken together, the behavioral data and pathological findings in this case are compatible with an early neurodevelopmental process affecting multiple neuroanatomic networks, but without a convincing morphologic signature detectable with routine neuropathologic technology. En ligne : http://dx.doi.org/10.1007/s10803-011-1259-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152
in Journal of Autism and Developmental Disorders > 42-3 (March 2012) . - p.460-467[article] Brief Report: Life History and Neuropathology of a Gifted Man with Asperger Syndrome [Texte imprimé et/ou numérique] / Karen M. WEIDENHEIM, Auteur ; Alfonso ESCOBAR, Auteur ; Isabelle RAPIN, Auteur . - 2012 . - p.460-467.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 42-3 (March 2012) . - p.460-467
Mots-clés : Autism Asperger syndrome Life history Neuropathology Adult Index. décimale : PER Périodiques Résumé : Despite recent interest in the pathogenesis of the autism spectrum disorders (pervasive developmental disorders), neuropathological descriptions of brains of individuals with well documented clinical information and without potentially confounding symptomatology are exceptionally rare. Asperger syndrome differs from classic autism by lack of cognitive impairment or delay in expressive language acquisition. We examined the 1,570 g brain of a 63 year old otherwise healthy mathematician with an Autistic Spectrum Disorder of Asperger subtype. Except for an atypical gyral pattern and megalencephaly, we detected no specific neuropathologic abnormality. Taken together, the behavioral data and pathological findings in this case are compatible with an early neurodevelopmental process affecting multiple neuroanatomic networks, but without a convincing morphologic signature detectable with routine neuropathologic technology. En ligne : http://dx.doi.org/10.1007/s10803-011-1259-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152 Altered posterior cingulate cortical cyctoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism / Adrian L. OBLAK in Autism Research, 4-3 (June 2011)
[article]
Titre : Altered posterior cingulate cortical cyctoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism Type de document : Texte imprimé et/ou numérique Auteurs : Adrian L. OBLAK, Auteur ; Douglas L. ROSENE, Auteur ; Thomas L. KEMPER, Auteur ; Margaret L. BAUMAN, Auteur ; Gene J. BLATT, Auteur Année de publication : 2011 Article en page(s) : p.200-211 Langues : Anglais (eng) Mots-clés : neuropathology gamma-aminobutyric acid neurochemistry ;neuroanatomy Index. décimale : PER Périodiques Résumé : Autism is a developmental disorder with prenatal origins, currently estimated to affect 1 in 91 children in the United States. Social-emotional deficits are a hallmark of autism and early neuropathology studies have indicated involvement of the limbic system. Imaging studies demonstrate abnormal activation of the posterior cingulate cortex (PCC), a component of the limbic system. Abnormal activation has also been noted in the fusiform gyrus (FFG), a region important for facial recognition and a key element in social interaction. A potential imbalance between excitatory and inhibitory interneurons in the cortex may contribute to altered information processing in autism. Furthermore, reduced numbers of GABA receptors have previously been reported in the autistic brain. Thionin-stained sections were used to qualitatively assess cytoarchitectonic patterning and quantitatively determine the density of neurons and immunohistochemistry was used to determine the densities of a subset of GABAergic interneurons utilizing parvalbumin-and calbindin-immunoreactivity. In autism, the PCC displayed altered cytoarchitecture with irregularly distributed neurons, poorly demarcated layers IV and V, and increased presence of white matter neurons. In contrast, no neuropathology was observed in the FFG. There was no significant difference in the density of thionin, parvalbumin, or calbindin interneurons in either region and there was a trend towards a reduced density of calbindin neurons in the PCC. This study highlights the presence of abnormal findings in the PCC, which appear to be developmental in nature and could affect the local processing of social–emotional behaviors as well as functioning of interrelated areas. En ligne : http://dx.doi.org/10.1002/aur.188 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=127
in Autism Research > 4-3 (June 2011) . - p.200-211[article] Altered posterior cingulate cortical cyctoarchitecture, but normal density of neurons and interneurons in the posterior cingulate cortex and fusiform gyrus in autism [Texte imprimé et/ou numérique] / Adrian L. OBLAK, Auteur ; Douglas L. ROSENE, Auteur ; Thomas L. KEMPER, Auteur ; Margaret L. BAUMAN, Auteur ; Gene J. BLATT, Auteur . - 2011 . - p.200-211.
Langues : Anglais (eng)
in Autism Research > 4-3 (June 2011) . - p.200-211
Mots-clés : neuropathology gamma-aminobutyric acid neurochemistry ;neuroanatomy Index. décimale : PER Périodiques Résumé : Autism is a developmental disorder with prenatal origins, currently estimated to affect 1 in 91 children in the United States. Social-emotional deficits are a hallmark of autism and early neuropathology studies have indicated involvement of the limbic system. Imaging studies demonstrate abnormal activation of the posterior cingulate cortex (PCC), a component of the limbic system. Abnormal activation has also been noted in the fusiform gyrus (FFG), a region important for facial recognition and a key element in social interaction. A potential imbalance between excitatory and inhibitory interneurons in the cortex may contribute to altered information processing in autism. Furthermore, reduced numbers of GABA receptors have previously been reported in the autistic brain. Thionin-stained sections were used to qualitatively assess cytoarchitectonic patterning and quantitatively determine the density of neurons and immunohistochemistry was used to determine the densities of a subset of GABAergic interneurons utilizing parvalbumin-and calbindin-immunoreactivity. In autism, the PCC displayed altered cytoarchitecture with irregularly distributed neurons, poorly demarcated layers IV and V, and increased presence of white matter neurons. In contrast, no neuropathology was observed in the FFG. There was no significant difference in the density of thionin, parvalbumin, or calbindin interneurons in either region and there was a trend towards a reduced density of calbindin neurons in the PCC. This study highlights the presence of abnormal findings in the PCC, which appear to be developmental in nature and could affect the local processing of social–emotional behaviors as well as functioning of interrelated areas. En ligne : http://dx.doi.org/10.1002/aur.188 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=127 Basal ganglia and autism – a translational perspective / Krishna SUBRAMANIAN in Autism Research, 10-11 (November 2017)
[article]
Titre : Basal ganglia and autism – a translational perspective Type de document : Texte imprimé et/ou numérique Auteurs : Krishna SUBRAMANIAN, Auteur ; Cheryl BRANDENBURG, Auteur ; Fernanda ORSATI, Auteur ; Jean-Jacques SOGHOMONIAN, Auteur ; John P. HUSSMAN, Auteur ; Gene J. BLATT, Auteur Article en page(s) : p.1751-1775 Langues : Anglais (eng) Mots-clés : basal ganglia animal models motor, autism neuroanatomy neuroimaging neuropathology Index. décimale : PER Périodiques Résumé : The basal ganglia are a collection of nuclei below the cortical surface that are involved in both motor and non-motor functions, including higher order cognition, social interactions, speech, and repetitive behaviors. Motor development milestones that are delayed in autism such as gross motor, fine motor and walking can aid in early diagnosis of autism. Neuropathology and neuroimaging findings in autism cases revealed volumetric changes and altered cell density in select basal ganglia nuclei. Interestingly, in autism, both the basal ganglia and the cerebellum are impacted both in their motor and non-motor domains and recently, found to be connected via the pons through a short disynaptic pathway. In typically developing individuals, the basal ganglia plays an important role in: eye movement, movement coordination, sensory modulation and processing, eye-hand coordination, action chaining, and inhibition control. Genetic models have proved to be useful toward understanding cellular and molecular changes at the synaptic level in the basal ganglia that may in part contribute to these autism-related behaviors. In autism, basal ganglia functions in motor skill acquisition and development are altered, thus disrupting the normal flow of feedback to the cortex. Taken together, there is an abundance of emerging evidence that the basal ganglia likely plays critical roles in maintaining an inhibitory balance between cortical and subcortical structures, critical for normal motor actions and cognitive functions. In autism, this inhibitory balance is disturbed thus impacting key pathways that affect normal cortical network activity. Autism Res 2017, 10: 1751–1775. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary Habit learning, action selection and performance are modulated by the basal ganglia, a collection of groups of neurons located below the cerebral cortex in the brain. In autism, there is emerging evidence that parts of the basal ganglia are structurally and functionally altered disrupting normal information flow. The basal ganglia through its interconnected circuits with the cerebral cortex and the cerebellum can potentially impact various motor and cognitive functions in the autism brain. En ligne : http://dx.doi.org/10.1002/aur.1837 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=322
in Autism Research > 10-11 (November 2017) . - p.1751-1775[article] Basal ganglia and autism – a translational perspective [Texte imprimé et/ou numérique] / Krishna SUBRAMANIAN, Auteur ; Cheryl BRANDENBURG, Auteur ; Fernanda ORSATI, Auteur ; Jean-Jacques SOGHOMONIAN, Auteur ; John P. HUSSMAN, Auteur ; Gene J. BLATT, Auteur . - p.1751-1775.
Langues : Anglais (eng)
in Autism Research > 10-11 (November 2017) . - p.1751-1775
Mots-clés : basal ganglia animal models motor, autism neuroanatomy neuroimaging neuropathology Index. décimale : PER Périodiques Résumé : The basal ganglia are a collection of nuclei below the cortical surface that are involved in both motor and non-motor functions, including higher order cognition, social interactions, speech, and repetitive behaviors. Motor development milestones that are delayed in autism such as gross motor, fine motor and walking can aid in early diagnosis of autism. Neuropathology and neuroimaging findings in autism cases revealed volumetric changes and altered cell density in select basal ganglia nuclei. Interestingly, in autism, both the basal ganglia and the cerebellum are impacted both in their motor and non-motor domains and recently, found to be connected via the pons through a short disynaptic pathway. In typically developing individuals, the basal ganglia plays an important role in: eye movement, movement coordination, sensory modulation and processing, eye-hand coordination, action chaining, and inhibition control. Genetic models have proved to be useful toward understanding cellular and molecular changes at the synaptic level in the basal ganglia that may in part contribute to these autism-related behaviors. In autism, basal ganglia functions in motor skill acquisition and development are altered, thus disrupting the normal flow of feedback to the cortex. Taken together, there is an abundance of emerging evidence that the basal ganglia likely plays critical roles in maintaining an inhibitory balance between cortical and subcortical structures, critical for normal motor actions and cognitive functions. In autism, this inhibitory balance is disturbed thus impacting key pathways that affect normal cortical network activity. Autism Res 2017, 10: 1751–1775. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. Lay Summary Habit learning, action selection and performance are modulated by the basal ganglia, a collection of groups of neurons located below the cerebral cortex in the brain. In autism, there is emerging evidence that parts of the basal ganglia are structurally and functionally altered disrupting normal information flow. The basal ganglia through its interconnected circuits with the cerebral cortex and the cerebellum can potentially impact various motor and cognitive functions in the autism brain. En ligne : http://dx.doi.org/10.1002/aur.1837 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=322 Design and Subject Characteristics in the Federally-Funded Citalopram Trial in Children with Pervasive Developmental Disorders / Lawrence SCAHILL in Journal of Autism and Developmental Disorders, 42-3 (March 2012)
[article]
Titre : Design and Subject Characteristics in the Federally-Funded Citalopram Trial in Children with Pervasive Developmental Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Lawrence SCAHILL, Auteur ; James T. MCCRACKEN, Auteur ; Karen E. BEARSS, Auteur ; Fay ROBINSON, Auteur ; Eric HOLLANDER, Auteur ; Bryan H. KING, Auteur ; Joel D. BREGMAN, Auteur ; Lin SIKICH, Auteur ; Kimberly DUKES, Auteur ; Lisa SULLIVAN, Auteur ; Evdokia ANAGNOSTOU, Auteur ; Craig DONNELLY, Auteur ; Young-Shin KIM, Auteur ; Louise RITZ, Auteur ; Deborah HIRTZ, Auteur ; Ann WAGNER, Auteur Année de publication : 2012 Article en page(s) : p.460-467 Langues : Anglais (eng) Mots-clés : Autism Asperger syndrome Life history Neuropathology Adult Index. décimale : PER Périodiques Résumé : Despite recent interest in the pathogenesis of the autism spectrum disorders (pervasive developmental disorders), neuropathological descriptions of brains of individuals with well documented clinical information and without potentially confounding symptomatology are exceptionally rare. Asperger syndrome differs from classic autism by lack of cognitive impairment or delay in expressive language acquisition. We examined the 1,570 g brain of a 63 year old otherwise healthy mathematician with an Autistic Spectrum Disorder of Asperger subtype. Except for an atypical gyral pattern and megalencephaly, we detected no specific neuropathologic abnormality. Taken together, the behavioral data and pathological findings in this case are compatible with an early neurodevelopmental process affecting multiple neuroanatomic networks, but without a convincing morphologic signature detectable with routine neuropathologic technology. En ligne : http://dx.doi.org/10.1007/s10803-011-1259-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152
in Journal of Autism and Developmental Disorders > 42-3 (March 2012) . - p.460-467[article] Design and Subject Characteristics in the Federally-Funded Citalopram Trial in Children with Pervasive Developmental Disorders [Texte imprimé et/ou numérique] / Lawrence SCAHILL, Auteur ; James T. MCCRACKEN, Auteur ; Karen E. BEARSS, Auteur ; Fay ROBINSON, Auteur ; Eric HOLLANDER, Auteur ; Bryan H. KING, Auteur ; Joel D. BREGMAN, Auteur ; Lin SIKICH, Auteur ; Kimberly DUKES, Auteur ; Lisa SULLIVAN, Auteur ; Evdokia ANAGNOSTOU, Auteur ; Craig DONNELLY, Auteur ; Young-Shin KIM, Auteur ; Louise RITZ, Auteur ; Deborah HIRTZ, Auteur ; Ann WAGNER, Auteur . - 2012 . - p.460-467.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 42-3 (March 2012) . - p.460-467
Mots-clés : Autism Asperger syndrome Life history Neuropathology Adult Index. décimale : PER Périodiques Résumé : Despite recent interest in the pathogenesis of the autism spectrum disorders (pervasive developmental disorders), neuropathological descriptions of brains of individuals with well documented clinical information and without potentially confounding symptomatology are exceptionally rare. Asperger syndrome differs from classic autism by lack of cognitive impairment or delay in expressive language acquisition. We examined the 1,570 g brain of a 63 year old otherwise healthy mathematician with an Autistic Spectrum Disorder of Asperger subtype. Except for an atypical gyral pattern and megalencephaly, we detected no specific neuropathologic abnormality. Taken together, the behavioral data and pathological findings in this case are compatible with an early neurodevelopmental process affecting multiple neuroanatomic networks, but without a convincing morphologic signature detectable with routine neuropathologic technology. En ligne : http://dx.doi.org/10.1007/s10803-011-1259-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152 Elevated GFAP Protein in Anterior Cingulate Cortical White Matter in Males With Autism Spectrum Disorder / Jessica D. CRAWFORD in Autism Research, 8-6 (December 2015)
[article]
Titre : Elevated GFAP Protein in Anterior Cingulate Cortical White Matter in Males With Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Jessica D. CRAWFORD, Auteur ; Michelle J. CHANDLEY, Auteur ; Katalin SZEBENI, Auteur ; Attila SZEBENI, Auteur ; Brandon WATERS, Auteur ; Gregory A. ORDWAY, Auteur Article en page(s) : p.649-657 Langues : Anglais (eng) Mots-clés : cellular neurophysiology neuroanatomy neuropathology Index. décimale : PER Périodiques Résumé : Based on evidence of abnormalities in axon thickness and neuronal disorganization, autism spectrum disorder (ASD) is commonly considered to be a condition resulting from neuronal dysfunction. Yet, recent findings suggest that non-neuronal cell types also contribute to ASD pathology. To investigate the role of glial cells in ASD, a combination of protein and gene expression analyses were used to determine levels of two glial markers, glial fibrillary acidic protein (GFAP) and myelin oligodendrocyte glycoprotein (MOG), in the postmortem brain tissue from control and ASD donors. Levels of GFAP immunoreactivity (ir) were significantly elevated (P?=?0.008) in anterior cingulate cortex (Brodmann area 24; BA24) white matter of ASD donors compared to control donors. In contrast, GFAP-ir levels were similar in BA24 gray matter from ASD and control donors. MOG-ir was also similar in both BA24 white and gray matter from ASD and control donors. In anterior prefrontal cortex (BA10), there were no significant differences in GFAP-ir or MOG-ir in either white or gray matter comparing ASD to control donors. Levels of expression of the genes GFAP and MOG also showed no differences between control and ASD donors in BA24 and BA10 white and gray matter. Collectively, these data imply that ASD is associated with an activation of white matter astrocytes in the anterior cingulate cortex as a result of a yet undefined cellular insult. Research is needed to investigate the molecular pathways that underlie this astrocyte reaction and such research may yield important clues regarding the etiology of ASD. Autism Res 2015, 8: 649–657. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1480 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=278
in Autism Research > 8-6 (December 2015) . - p.649-657[article] Elevated GFAP Protein in Anterior Cingulate Cortical White Matter in Males With Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Jessica D. CRAWFORD, Auteur ; Michelle J. CHANDLEY, Auteur ; Katalin SZEBENI, Auteur ; Attila SZEBENI, Auteur ; Brandon WATERS, Auteur ; Gregory A. ORDWAY, Auteur . - p.649-657.
Langues : Anglais (eng)
in Autism Research > 8-6 (December 2015) . - p.649-657
Mots-clés : cellular neurophysiology neuroanatomy neuropathology Index. décimale : PER Périodiques Résumé : Based on evidence of abnormalities in axon thickness and neuronal disorganization, autism spectrum disorder (ASD) is commonly considered to be a condition resulting from neuronal dysfunction. Yet, recent findings suggest that non-neuronal cell types also contribute to ASD pathology. To investigate the role of glial cells in ASD, a combination of protein and gene expression analyses were used to determine levels of two glial markers, glial fibrillary acidic protein (GFAP) and myelin oligodendrocyte glycoprotein (MOG), in the postmortem brain tissue from control and ASD donors. Levels of GFAP immunoreactivity (ir) were significantly elevated (P?=?0.008) in anterior cingulate cortex (Brodmann area 24; BA24) white matter of ASD donors compared to control donors. In contrast, GFAP-ir levels were similar in BA24 gray matter from ASD and control donors. MOG-ir was also similar in both BA24 white and gray matter from ASD and control donors. In anterior prefrontal cortex (BA10), there were no significant differences in GFAP-ir or MOG-ir in either white or gray matter comparing ASD to control donors. Levels of expression of the genes GFAP and MOG also showed no differences between control and ASD donors in BA24 and BA10 white and gray matter. Collectively, these data imply that ASD is associated with an activation of white matter astrocytes in the anterior cingulate cortex as a result of a yet undefined cellular insult. Research is needed to investigate the molecular pathways that underlie this astrocyte reaction and such research may yield important clues regarding the etiology of ASD. Autism Res 2015, 8: 649–657. © 2015 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1480 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=278 Specific pattern of maturation and differentiation in the formation of cortical tubers in tuberous sclerosis omplex (TSC): evidence from layer-specific marker expression / A. MUHLEBNER in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
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