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Neuroanatomy in mouse models of Rett syndrome is related to the severity of Mecp2 mutation and behavioral phenotypes / R. ALLEMANG-GRAND in Molecular Autism, 8 (2017)
[article]
Titre : Neuroanatomy in mouse models of Rett syndrome is related to the severity of Mecp2 mutation and behavioral phenotypes Type de document : Texte imprimé et/ou numérique Auteurs : R. ALLEMANG-GRAND, Auteur ; J. ELLEGOOD, Auteur ; L. SPENCER NOAKES, Auteur ; J. RUSTON, Auteur ; M. JUSTICE, Auteur ; B. J. NIEMAN, Auteur ; J. P. LERCH, Auteur Article en page(s) : 32p. Langues : Anglais (eng) Mots-clés : Magnetic resonance imaging Mecp2 mouse models Neuroanatomy Rett syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome (RTT) is a neurodevelopmental disorder that predominantly affects girls. The majority of RTT cases are caused by de novo mutations in methyl-CpG-binding protein 2 (MECP2), and several mouse models have been created to further understand the disorder. In the current literature, many studies have focused their analyses on the behavioral abnormalities and cellular and molecular impairments that arise from Mecp2 mutations. However, limited efforts have been placed on understanding how Mecp2 mutations disrupt the neuroanatomy and networks of the brain. METHODS: In this study, we examined the neuroanatomy of male and female mice from the Mecp2(tm1Hzo), Mecp2(tm1.1Bird/J), and Mecp2(tm2Bird/J) mouse lines using high-resolution magnetic resonance imaging (MRI) paired with deformation-based morphometry to determine the brain regions susceptible to Mecp2 disruptions. RESULTS: We found that many cortical and subcortical regions were reduced in volume within the brains of mutant mice regardless of mutation type, highlighting regions that are susceptible to Mecp2 disruptions. We also found that the volume within these regions correlated with behavioral metrics. Conversely, regions of the cerebellum were differentially affected by the type of mutation, showing an increase in volume in the mutant Mecp2(tm1Hzo) brain relative to controls and a decrease in the Mecp2(tm1.1Bird/J) and Mecp2(tm2Bird/J) lines. CONCLUSIONS: Our findings demonstrate that the direction and magnitude of the neuroanatomical differences between control and mutant mice carrying Mecp2 mutations are driven by the severity of the mutation and the stage of behavioral impairments. En ligne : http://dx.doi.org/10.1186/s13229-017-0138-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329
in Molecular Autism > 8 (2017) . - 32p.[article] Neuroanatomy in mouse models of Rett syndrome is related to the severity of Mecp2 mutation and behavioral phenotypes [Texte imprimé et/ou numérique] / R. ALLEMANG-GRAND, Auteur ; J. ELLEGOOD, Auteur ; L. SPENCER NOAKES, Auteur ; J. RUSTON, Auteur ; M. JUSTICE, Auteur ; B. J. NIEMAN, Auteur ; J. P. LERCH, Auteur . - 32p.
Langues : Anglais (eng)
in Molecular Autism > 8 (2017) . - 32p.
Mots-clés : Magnetic resonance imaging Mecp2 mouse models Neuroanatomy Rett syndrome Index. décimale : PER Périodiques Résumé : BACKGROUND: Rett syndrome (RTT) is a neurodevelopmental disorder that predominantly affects girls. The majority of RTT cases are caused by de novo mutations in methyl-CpG-binding protein 2 (MECP2), and several mouse models have been created to further understand the disorder. In the current literature, many studies have focused their analyses on the behavioral abnormalities and cellular and molecular impairments that arise from Mecp2 mutations. However, limited efforts have been placed on understanding how Mecp2 mutations disrupt the neuroanatomy and networks of the brain. METHODS: In this study, we examined the neuroanatomy of male and female mice from the Mecp2(tm1Hzo), Mecp2(tm1.1Bird/J), and Mecp2(tm2Bird/J) mouse lines using high-resolution magnetic resonance imaging (MRI) paired with deformation-based morphometry to determine the brain regions susceptible to Mecp2 disruptions. RESULTS: We found that many cortical and subcortical regions were reduced in volume within the brains of mutant mice regardless of mutation type, highlighting regions that are susceptible to Mecp2 disruptions. We also found that the volume within these regions correlated with behavioral metrics. Conversely, regions of the cerebellum were differentially affected by the type of mutation, showing an increase in volume in the mutant Mecp2(tm1Hzo) brain relative to controls and a decrease in the Mecp2(tm1.1Bird/J) and Mecp2(tm2Bird/J) lines. CONCLUSIONS: Our findings demonstrate that the direction and magnitude of the neuroanatomical differences between control and mutant mice carrying Mecp2 mutations are driven by the severity of the mutation and the stage of behavioral impairments. En ligne : http://dx.doi.org/10.1186/s13229-017-0138-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329 Commentary: Mapping the young, resilient brain – reflections on Burt et al. (2016) / Philip SHAW in Journal of Child Psychology and Psychiatry, 57-12 (December 2016)
[article]
Titre : Commentary: Mapping the young, resilient brain – reflections on Burt et al. (2016) Type de document : Texte imprimé et/ou numérique Auteurs : Philip SHAW, Auteur Article en page(s) : p.1465-1466 Langues : Anglais (eng) Mots-clés : Resilience neuroanatomy executive functions Index. décimale : PER Périodiques Résumé : The resilience of many children in the face of adversity has long been a research focus. The study by Burt et al. delineates the neuroanatomy of resilience, using in vivo magnetic resonance images acquired on 1,800 youth. They find that resilient youth had a larger right lateral prefrontal cortex compared to youth who either lacked resilience or did not experience adversity. The size of the right lateral prefrontal cortex was further associated with a likelihood of a maladaptive problem of alcohol use. These findings implicate high-order regulatory processes supported by the right lateral prefrontal cortex as pivotal in resilience. The study also sets the stage for exploring how neuroimaging data, combined with behavioral and genomic information might be used to assess treatment efficacy and identify children who need therapeutic interventions to boost their resilience. En ligne : http://dx.doi.org/10.1111/jcpp.12613 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298
in Journal of Child Psychology and Psychiatry > 57-12 (December 2016) . - p.1465-1466[article] Commentary: Mapping the young, resilient brain – reflections on Burt et al. (2016) [Texte imprimé et/ou numérique] / Philip SHAW, Auteur . - p.1465-1466.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 57-12 (December 2016) . - p.1465-1466
Mots-clés : Resilience neuroanatomy executive functions Index. décimale : PER Périodiques Résumé : The resilience of many children in the face of adversity has long been a research focus. The study by Burt et al. delineates the neuroanatomy of resilience, using in vivo magnetic resonance images acquired on 1,800 youth. They find that resilient youth had a larger right lateral prefrontal cortex compared to youth who either lacked resilience or did not experience adversity. The size of the right lateral prefrontal cortex was further associated with a likelihood of a maladaptive problem of alcohol use. These findings implicate high-order regulatory processes supported by the right lateral prefrontal cortex as pivotal in resilience. The study also sets the stage for exploring how neuroimaging data, combined with behavioral and genomic information might be used to assess treatment efficacy and identify children who need therapeutic interventions to boost their resilience. En ligne : http://dx.doi.org/10.1111/jcpp.12613 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=298 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 Cortical morphological markers in children with autism: a structural magnetic resonance imaging study of thickness, area, volume, and gyrification / D. Y. YANG in Molecular Autism, 7 (2016)
[article]
Titre : Cortical morphological markers in children with autism: a structural magnetic resonance imaging study of thickness, area, volume, and gyrification Type de document : Texte imprimé et/ou numérique Auteurs : D. Y. YANG, Auteur ; D. BEAM, Auteur ; Kevin A. PELPHREY, Auteur ; Sebiha M. ABDULLAHI, Auteur ; R. J. JOU, Auteur Article en page(s) : 11p. Langues : Anglais (eng) Mots-clés : Age Factors Cerebral Cortex/pathology Child Child Development Disorders, Pervasive/pathology Child, Preschool Gray Matter/pathology Humans Image Processing, Computer-Assisted Magnetic Resonance Imaging Male Neuroimaging Organ Size White Matter/pathology Autism spectrum disorder Brain development Brain structure Neuroanatomy Surface-based morphometry Index. décimale : PER Périodiques Résumé : BACKGROUND: Individuals with autism spectrum disorder (ASD) have been characterized by altered cerebral cortical structures; however, the field has yet to identify consistent markers and prior studies have included mostly adolescents and adults. While there are multiple cortical morphological measures, including cortical thickness, surface area, cortical volume, and cortical gyrification, few single studies have examined all these measures. The current study analyzed all of the four measures and focused on pre-adolescent children with ASD. METHODS: We employed the FreeSurfer pipeline to examine surface-based morphometry in 60 high-functioning boys with ASD (mean age = 8.35 years, range = 4-12 years) and 41 gender-, age-, and IQ-matched typically developing (TD) peers (mean age = 8.83 years), while testing for age-by-diagnosis interaction and between-group differences. RESULTS: During childhood and in specific regions, ASD participants exhibited a lack of normative age-related cortical thinning and volumetric reduction and an abnormal age-related increase in gyrification. Regarding surface area, ASD and TD exhibited statistically comparable age-related development during childhood. Across childhood, ASD relative to TD participants tended to have higher mean levels of gyrification in specific regions. Within ASD, those with higher Social Responsiveness Scale total raw scores tended to have greater age-related increase in gyrification in specific regions during childhood. CONCLUSIONS: ASD is characterized by cortical neuroanatomical abnormalities that are age-, measure-, statistical model-, and region-dependent. The current study is the first to examine the development of all four cortical measures in one of the largest pre-adolescent samples. Strikingly, Neurosynth-based quantitative reverse inference of the surviving clusters suggests that many of the regions identified above are related to social perception, language, self-referential, and action observation networks-those frequently found to be functionally altered in individuals with ASD. The comprehensive, multilevel analyses across a wide range of cortical measures help fill a knowledge gap and present a complex but rich picture of neuroanatomical developmental differences in children with ASD. En ligne : http://dx.doi.org/10.1186/s13229-016-0076-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329
in Molecular Autism > 7 (2016) . - 11p.[article] Cortical morphological markers in children with autism: a structural magnetic resonance imaging study of thickness, area, volume, and gyrification [Texte imprimé et/ou numérique] / D. Y. YANG, Auteur ; D. BEAM, Auteur ; Kevin A. PELPHREY, Auteur ; Sebiha M. ABDULLAHI, Auteur ; R. J. JOU, Auteur . - 11p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 11p.
Mots-clés : Age Factors Cerebral Cortex/pathology Child Child Development Disorders, Pervasive/pathology Child, Preschool Gray Matter/pathology Humans Image Processing, Computer-Assisted Magnetic Resonance Imaging Male Neuroimaging Organ Size White Matter/pathology Autism spectrum disorder Brain development Brain structure Neuroanatomy Surface-based morphometry Index. décimale : PER Périodiques Résumé : BACKGROUND: Individuals with autism spectrum disorder (ASD) have been characterized by altered cerebral cortical structures; however, the field has yet to identify consistent markers and prior studies have included mostly adolescents and adults. While there are multiple cortical morphological measures, including cortical thickness, surface area, cortical volume, and cortical gyrification, few single studies have examined all these measures. The current study analyzed all of the four measures and focused on pre-adolescent children with ASD. METHODS: We employed the FreeSurfer pipeline to examine surface-based morphometry in 60 high-functioning boys with ASD (mean age = 8.35 years, range = 4-12 years) and 41 gender-, age-, and IQ-matched typically developing (TD) peers (mean age = 8.83 years), while testing for age-by-diagnosis interaction and between-group differences. RESULTS: During childhood and in specific regions, ASD participants exhibited a lack of normative age-related cortical thinning and volumetric reduction and an abnormal age-related increase in gyrification. Regarding surface area, ASD and TD exhibited statistically comparable age-related development during childhood. Across childhood, ASD relative to TD participants tended to have higher mean levels of gyrification in specific regions. Within ASD, those with higher Social Responsiveness Scale total raw scores tended to have greater age-related increase in gyrification in specific regions during childhood. CONCLUSIONS: ASD is characterized by cortical neuroanatomical abnormalities that are age-, measure-, statistical model-, and region-dependent. The current study is the first to examine the development of all four cortical measures in one of the largest pre-adolescent samples. Strikingly, Neurosynth-based quantitative reverse inference of the surviving clusters suggests that many of the regions identified above are related to social perception, language, self-referential, and action observation networks-those frequently found to be functionally altered in individuals with ASD. The comprehensive, multilevel analyses across a wide range of cortical measures help fill a knowledge gap and present a complex but rich picture of neuroanatomical developmental differences in children with ASD. En ligne : http://dx.doi.org/10.1186/s13229-016-0076-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=329 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 Exploring the multidimensional nature of repetitive and restricted behaviors and interests (RRBI) in autism: neuroanatomical correlates and clinical implications / Nicolas TRAUT ; Amandine PEDOUX ; Anna MARUANI ; Anita BEGGIATO ; Monique ELMALEH ; David GERMANAUD ; Anouck AMESTOY ; Myriam LY-LE MOAL ; Christopher CHATHAM ; Lorraine MURTAGH ; Manuel BOUVARD ; Marianne ALISSON ; Marion LEBOYER ; Thomas BOURGERON ; Roberto TORO ; Guillaume DUMAS ; Clara MOREAU ; Richard DELORME in Molecular Autism, 14 (2023)
PermalinkGenetic Effects on Cerebellar Structure Across Mouse Models of Autism Using a Magnetic Resonance Imaging Atlas / Patrick E. STEADMAN in Autism Research, 7-1 (February 2014)
PermalinkNeuroanatomical Phenotypes Are Consistent With Autism-Like Behavioral Phenotypes in the 15q11-13 Duplication Mouse Model / Jacob ELLEGOOD in Autism Research, 8-5 (October 2015)
PermalinkSex differences in brain structure: a twin study on restricted and repetitive behaviors in twin pairs with and without autism / A. VAN'T WESTEINDE in Molecular Autism, 11 (2020)
PermalinkThe autism risk genes MET and PLAUR differentially impact cortical development / Kathie L. EAGLESON in Autism Research, 4-1 (February 2011)
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