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Neuronal and glial cell number is altered in a cortical layer-specific manner in autism / C. FALCONE in Autism, 25-8 (November 2021)
[article]
Titre : Neuronal and glial cell number is altered in a cortical layer-specific manner in autism Type de document : Texte imprimé et/ou numérique Auteurs : C. FALCONE, Auteur ; N. Y. MEVISES, Auteur ; T. HONG, Auteur ; B. DUFOUR, Auteur ; X. CHEN, Auteur ; S. C. NOCTOR, Auteur ; V. MARTÍNEZ CERDEÑO, Auteur Article en page(s) : p.2238-2253 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder Autistic Disorder Cell Count Cerebral Cortex Humans Neuroglia Neurons anatomy autism cerebral cortex postmortem Index. décimale : PER Périodiques Résumé : The cerebral cortex affected with autism spectrum disorder presents changes in the number of neurons and glia cells, possibly leading to a dysregulation of brain circuits and affecting behavior. However, little is known about cell number alteration in specific layers of the cortex in autism spectrum disorder. We found an increase in the number of neurons and a decrease in the number of astrocytes in specific layers of the prefrontal cortex in postmortem human brains from autism spectrum disorder cases. We hypothesize that this may be due to a failure in neural stem cells to shift differentiation from neurons to glial cells during prenatal brain development. These data provide key anatomical findings that contribute to the bases of autism spectrum disorder pathogenesis. En ligne : http://dx.doi.org/10.1177/13623613211014408 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=451
in Autism > 25-8 (November 2021) . - p.2238-2253[article] Neuronal and glial cell number is altered in a cortical layer-specific manner in autism [Texte imprimé et/ou numérique] / C. FALCONE, Auteur ; N. Y. MEVISES, Auteur ; T. HONG, Auteur ; B. DUFOUR, Auteur ; X. CHEN, Auteur ; S. C. NOCTOR, Auteur ; V. MARTÍNEZ CERDEÑO, Auteur . - p.2238-2253.
Langues : Anglais (eng)
in Autism > 25-8 (November 2021) . - p.2238-2253
Mots-clés : Autism Spectrum Disorder Autistic Disorder Cell Count Cerebral Cortex Humans Neuroglia Neurons anatomy autism cerebral cortex postmortem Index. décimale : PER Périodiques Résumé : The cerebral cortex affected with autism spectrum disorder presents changes in the number of neurons and glia cells, possibly leading to a dysregulation of brain circuits and affecting behavior. However, little is known about cell number alteration in specific layers of the cortex in autism spectrum disorder. We found an increase in the number of neurons and a decrease in the number of astrocytes in specific layers of the prefrontal cortex in postmortem human brains from autism spectrum disorder cases. We hypothesize that this may be due to a failure in neural stem cells to shift differentiation from neurons to glial cells during prenatal brain development. These data provide key anatomical findings that contribute to the bases of autism spectrum disorder pathogenesis. En ligne : http://dx.doi.org/10.1177/13623613211014408 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=451 Two-dimensional analysis of the supragranular layers in autism spectrum disorder / Aaron T. KARST in Research in Autism Spectrum Disorders, 32 (December 2016)
[article]
Titre : Two-dimensional analysis of the supragranular layers in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Aaron T. KARST, Auteur ; Jeffrey J. HUTSLER, Auteur Article en page(s) : p.96-105 Langues : Anglais (eng) Mots-clés : ASD Autism Cerebral cortex Neuroanatomy Supragranular Index. décimale : PER Périodiques Résumé : Abstract Neurons in the supragranular layers of the human cerebral cortex play an important role in long-range cortico-cortical connections. Alterations to these layers are of special interest in autism spectrum disorder (ASD) as they could play a significant role in altered connectivity between distal regions of cortex. The present study isolated sampling boxes through the use of an automated boundary identification technique. A two-dimensional analysis of the Nissl-stained tissue was then performed to examine whether differences in cell size and number are present in ASD tissue. The analysis focused on layers II and III of association cortex sampled from frontal (BA9), temporal (BA21), and parietal (BA7) regions. In previous studies, both BA9 and BA21 have been linked to alterations in cortical connectivity in ASD. Aside from the expected differences between cortical layers and regions, data analysis revealed that ASD tissue possessed a higher density of cells, the magnitude of which was layer dependent, and that the cell profiles were of a smaller size. The results of this study suggest that cellular abnormalities with respect to cell size and number are present in multiple areas of association cortex, specifically within layers that are involved in long-range connectivity. Additionally, the results comport with previous findings of altered cortical minicolumns in frontal and temporal areas and further suggest that similar irregularities may also be present in parietal areas. En ligne : http://dx.doi.org/10.1016/j.rasd.2016.09.004 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=296
in Research in Autism Spectrum Disorders > 32 (December 2016) . - p.96-105[article] Two-dimensional analysis of the supragranular layers in autism spectrum disorder [Texte imprimé et/ou numérique] / Aaron T. KARST, Auteur ; Jeffrey J. HUTSLER, Auteur . - p.96-105.
Langues : Anglais (eng)
in Research in Autism Spectrum Disorders > 32 (December 2016) . - p.96-105
Mots-clés : ASD Autism Cerebral cortex Neuroanatomy Supragranular Index. décimale : PER Périodiques Résumé : Abstract Neurons in the supragranular layers of the human cerebral cortex play an important role in long-range cortico-cortical connections. Alterations to these layers are of special interest in autism spectrum disorder (ASD) as they could play a significant role in altered connectivity between distal regions of cortex. The present study isolated sampling boxes through the use of an automated boundary identification technique. A two-dimensional analysis of the Nissl-stained tissue was then performed to examine whether differences in cell size and number are present in ASD tissue. The analysis focused on layers II and III of association cortex sampled from frontal (BA9), temporal (BA21), and parietal (BA7) regions. In previous studies, both BA9 and BA21 have been linked to alterations in cortical connectivity in ASD. Aside from the expected differences between cortical layers and regions, data analysis revealed that ASD tissue possessed a higher density of cells, the magnitude of which was layer dependent, and that the cell profiles were of a smaller size. The results of this study suggest that cellular abnormalities with respect to cell size and number are present in multiple areas of association cortex, specifically within layers that are involved in long-range connectivity. Additionally, the results comport with previous findings of altered cortical minicolumns in frontal and temporal areas and further suggest that similar irregularities may also be present in parietal areas. En ligne : http://dx.doi.org/10.1016/j.rasd.2016.09.004 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=296 WDFY3 mutation alters laminar position and morphology of cortical neurons / Zachary A. SCHAAF in Molecular Autism, 13 (2022)
[article]
Titre : WDFY3 mutation alters laminar position and morphology of cortical neurons Type de document : Texte imprimé et/ou numérique Auteurs : Zachary A. SCHAAF, Auteur ; Lyvin TAT, Auteur ; Noemi CANNIZZARO, Auteur ; Ralph GREEN, Auteur ; Thomas RULICKE, Auteur ; Simon HIPPENMEYER, Auteur ; Konstantinos S. ZARBALIS, Auteur Article en page(s) : 27 p. Langues : Anglais (eng) Mots-clés : Adaptor Proteins, Signal Transducing/genetics Animals Autistic Disorder/genetics Autophagy-Related Proteins/genetics Cerebral Cortex/cytology Humans Mice Mutation Neurogenesis/genetics Neurons/cytology Cerebral cortex Dendrites Dendritic spines Excitatory neurons Neuronal migration Wdfy3 Index. décimale : PER Périodiques Résumé : BACKGROUND: Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology. METHODS: Here, in an effort to untangle the origins of NMDs in Wdfy3(lacZ) mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques. RESULTS: We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages. LIMITATIONS: While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation. CONCLUSIONS: Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life. En ligne : http://dx.doi.org/10.1186/s13229-022-00508-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=491
in Molecular Autism > 13 (2022) . - 27 p.[article] WDFY3 mutation alters laminar position and morphology of cortical neurons [Texte imprimé et/ou numérique] / Zachary A. SCHAAF, Auteur ; Lyvin TAT, Auteur ; Noemi CANNIZZARO, Auteur ; Ralph GREEN, Auteur ; Thomas RULICKE, Auteur ; Simon HIPPENMEYER, Auteur ; Konstantinos S. ZARBALIS, Auteur . - 27 p.
Langues : Anglais (eng)
in Molecular Autism > 13 (2022) . - 27 p.
Mots-clés : Adaptor Proteins, Signal Transducing/genetics Animals Autistic Disorder/genetics Autophagy-Related Proteins/genetics Cerebral Cortex/cytology Humans Mice Mutation Neurogenesis/genetics Neurons/cytology Cerebral cortex Dendrites Dendritic spines Excitatory neurons Neuronal migration Wdfy3 Index. décimale : PER Périodiques Résumé : BACKGROUND: Proper cerebral cortical development depends on the tightly orchestrated migration of newly born neurons from the inner ventricular and subventricular zones to the outer cortical plate. Any disturbance in this process during prenatal stages may lead to neuronal migration disorders (NMDs), which can vary in extent from focal to global. Furthermore, NMDs show a substantial comorbidity with other neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous work demonstrated focal neuronal migration defects in mice carrying loss-of-function alleles of the recognized autism risk gene WDFY3. However, the cellular origins of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide critical insight into WDFY3-dependent disease pathology. METHODS: Here, in an effort to untangle the origins of NMDs in Wdfy3(lacZ) mice, we employed mosaic analysis with double markers (MADM). MADM technology enabled us to genetically distinctly track and phenotypically analyze mutant and wild-type cells concomitantly in vivo using immunofluorescent techniques. RESULTS: We revealed a cell autonomous requirement of WDFY3 for accurate laminar positioning of cortical projection neurons and elimination of mispositioned cells during early postnatal life. In addition, we identified significant deviations in dendritic arborization, as well as synaptic density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant neurons in Wdfy3-MADM reporter mice at postnatal stages. LIMITATIONS: While Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD pathology that remain inaccessible to investigation in humans, like most animal models, they do not a perfectly replicate all aspects of human ASD biology. The lack of human data makes it indeterminate whether morphological deviations described here apply to ASD patients or some of the other neurodevelopmental conditions associated with WDFY3 mutation. CONCLUSIONS: Our genetic approach revealed several cell autonomous requirements of WDFY3 in neuronal development that could underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions. The results are also consistent with findings in other ASD animal models and patients and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity in postnatal life. En ligne : http://dx.doi.org/10.1186/s13229-022-00508-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=491 Emerging depression in adolescence coincides with accelerated frontal cortical thinning / Marieke G. N. BOS in Journal of Child Psychology and Psychiatry, 59-9 (September 2018)
[article]
Titre : Emerging depression in adolescence coincides with accelerated frontal cortical thinning Type de document : Texte imprimé et/ou numérique Auteurs : Marieke G. N. BOS, Auteur ; Sabine PETERS, Auteur ; Ferdi C. KAMP, Auteur ; Eveline A. CRONE, Auteur ; Christian K. TAMNES, Auteur Article en page(s) : p.994-1002 Langues : Anglais (eng) Mots-clés : Adolescence brain development longitudinal depression MRI cerebral cortex Index. décimale : PER Périodiques Résumé : Background Adolescence is a transition period characterized by heightened emotional reactivity, which for some sets the stage for emerging depressive symptoms. Prior studies suggest that adolescent depression is associated with deviant cortical and subcortical brain structure. Longitudinal studies are, however, currently scarce, but critical to detect which adolescents are at risk for developing depressive symptoms. Methods In this longitudinal study, a community sample of 205 participants underwent magnetic resonance imaging (MRI) in three biennial waves (522 scans) spanning 5 years across ages 8?25 years. Depressive symptomatology was assessed using self-report at the third time point. Mixed models were used to examine the relations between structural brain development, specifically regional change in cortical thickness, surface area and subcortical volumes (hippocampus and amygdala), and depressive symptoms. Results Accelerated frontal lobe cortical thinning was observed in adolescents who developed depressive symptoms at the third time point. This effect remained after controlling for parent-reported affective problems at the first time point. Moreover, the effect was driven by specific lateral orbitofrontal and precentral regions. In addition, differential developmental trajectories of parietal cortical thickness and surface area in several regions were found for participants reporting higher depressive symptomatology, but these results did not survive correction for multiple comparisons. Volumes or developmental volume changes in hippocampus or amygdala were not related to depressive symptoms. Conclusions This study showed that emerging depression is associated with cortical thinning in frontal regions within individuals. These findings move beyond detecting cross-sectional correlations and set the stage for early detection, which may inform future intervention. En ligne : https://doi.org/10.1111/jcpp.12895 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=368
in Journal of Child Psychology and Psychiatry > 59-9 (September 2018) . - p.994-1002[article] Emerging depression in adolescence coincides with accelerated frontal cortical thinning [Texte imprimé et/ou numérique] / Marieke G. N. BOS, Auteur ; Sabine PETERS, Auteur ; Ferdi C. KAMP, Auteur ; Eveline A. CRONE, Auteur ; Christian K. TAMNES, Auteur . - p.994-1002.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 59-9 (September 2018) . - p.994-1002
Mots-clés : Adolescence brain development longitudinal depression MRI cerebral cortex Index. décimale : PER Périodiques Résumé : Background Adolescence is a transition period characterized by heightened emotional reactivity, which for some sets the stage for emerging depressive symptoms. Prior studies suggest that adolescent depression is associated with deviant cortical and subcortical brain structure. Longitudinal studies are, however, currently scarce, but critical to detect which adolescents are at risk for developing depressive symptoms. Methods In this longitudinal study, a community sample of 205 participants underwent magnetic resonance imaging (MRI) in three biennial waves (522 scans) spanning 5 years across ages 8?25 years. Depressive symptomatology was assessed using self-report at the third time point. Mixed models were used to examine the relations between structural brain development, specifically regional change in cortical thickness, surface area and subcortical volumes (hippocampus and amygdala), and depressive symptoms. Results Accelerated frontal lobe cortical thinning was observed in adolescents who developed depressive symptoms at the third time point. This effect remained after controlling for parent-reported affective problems at the first time point. Moreover, the effect was driven by specific lateral orbitofrontal and precentral regions. In addition, differential developmental trajectories of parietal cortical thickness and surface area in several regions were found for participants reporting higher depressive symptomatology, but these results did not survive correction for multiple comparisons. Volumes or developmental volume changes in hippocampus or amygdala were not related to depressive symptoms. Conclusions This study showed that emerging depression is associated with cortical thinning in frontal regions within individuals. These findings move beyond detecting cross-sectional correlations and set the stage for early detection, which may inform future intervention. En ligne : https://doi.org/10.1111/jcpp.12895 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=368