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Mention de date : June 2010
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2-2 - June 2010 [Texte imprimé et/ou numérique] . - 2010. Langues : Anglais (eng)
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[article]
Titre : Cover essay Type de document : Texte imprimé et/ou numérique Auteurs : J. PIVEN, Auteur Article en page(s) : p.61 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-010-9052-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.61[article] Cover essay [Texte imprimé et/ou numérique] / J. PIVEN, Auteur . - p.61.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.61
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-010-9052-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Somatosensory processing in neurodevelopmental disorders / Carissa J. CASCIO in Journal of Neurodevelopmental Disorders, 2-2 (June 2010)
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[article]
Titre : Somatosensory processing in neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique Auteurs : Carissa J. CASCIO, Auteur Article en page(s) : p.62-9 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The purpose of this article is to review the role of somatosensory perception in typical development, its aberration in a range of neurodevelopmental disorders, and the potential relations between tactile processing abnormalities and central features of each disorder such as motor, communication, and social development. Neurodevelopmental disorders that represent a range of symptoms and etiologies, and for which multiple peer-reviewed articles on somatosensory differences have been published, were chosen to include in the review. Relevant studies in animal models, as well as conditions of early sensory deprivation, are also included. Somatosensory processing plays an important, yet often overlooked, role in typical development and is aberrant in various neurodevelopmental disorders. This is demonstrated in studies of behavior, sensory thresholds, neuroanatomy, and neurophysiology in samples of children with Fragile X syndrome, autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and cerebral palsy (CP). Impaired somatosensory processing is found in a range of neurodevelopmental disorders and is associated with deficits in communication, motor ability, and social skills in these disorders. Given the central role of touch in early development, both experimental and clinical approaches should take into consideration the role of somatosensory processing in the etiology and treatment of neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1007/s11689-010-9046-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.62-9[article] Somatosensory processing in neurodevelopmental disorders [Texte imprimé et/ou numérique] / Carissa J. CASCIO, Auteur . - p.62-9.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.62-9
Index. décimale : PER Périodiques Résumé : The purpose of this article is to review the role of somatosensory perception in typical development, its aberration in a range of neurodevelopmental disorders, and the potential relations between tactile processing abnormalities and central features of each disorder such as motor, communication, and social development. Neurodevelopmental disorders that represent a range of symptoms and etiologies, and for which multiple peer-reviewed articles on somatosensory differences have been published, were chosen to include in the review. Relevant studies in animal models, as well as conditions of early sensory deprivation, are also included. Somatosensory processing plays an important, yet often overlooked, role in typical development and is aberrant in various neurodevelopmental disorders. This is demonstrated in studies of behavior, sensory thresholds, neuroanatomy, and neurophysiology in samples of children with Fragile X syndrome, autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and cerebral palsy (CP). Impaired somatosensory processing is found in a range of neurodevelopmental disorders and is associated with deficits in communication, motor ability, and social skills in these disorders. Given the central role of touch in early development, both experimental and clinical approaches should take into consideration the role of somatosensory processing in the etiology and treatment of neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1007/s11689-010-9046-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
[article]
Titre : Aging in fragile X syndrome Type de document : Texte imprimé et/ou numérique Auteurs : A. UTARI, Auteur ; E. ADAMS, Auteur ; Elizabeth BERRY-KRAVIS, Auteur ; Alyssa D. CHAVEZ, Auteur ; F. SCAGGS, Auteur ; L. NGOTRAN, Auteur ; A. BOYD, Auteur ; D. HESSL, Auteur ; L. W. GANE, Auteur ; F. TASSONE, Auteur ; N. TARTAGLIA, Auteur ; M. A. LEEHEY, Auteur ; Randi J. HAGERMAN, Auteur Article en page(s) : p.70-76 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Many studies have focused on the behavior and cognitive problems in young patients with fragile X syndrome (FXS), but there are no studies about the problems in aging for those with FXS. The discovery of the fragile X-associated tremor ataxia syndrome (FXTAS), a neurodegenerative disorder related to elevated FMR1-mRNA, in elderly men and some women with the premutation, intensified the need for aging studies in FXS. Approximately 40% of males with FXS have repeat size mosaicism and as a result, some of these individuals also have elevated levels of FMR1-mRNA which theoretically puts them at risk for FXTAS. Here, we have surveyed all of the aging patients with FXS that we have followed over the years to clarify the medical complications of aging seen in those with FXS. Data was collected from 62 individuals with the FXS full mutation (44 males; 18 females) who were at least 40 years old at their most recent clinical examination. We found that the five most frequent medical problems in these patients were neurological problems (38.7%), gastrointestinal problems (30.6%), obesity (28.8%), hypertension (24.2%) and heart problems (24.2%). Movement disorders were significantly different between males and females (38.6% vs.10.2%, p = 0.029). We did not find any differences in medical problems between those with a full mutation and those with mosaicism. Identification of medical problems associated with aging in FXS is important to establish appropriate recommendations for medical screening and treatment considerations. En ligne : http://dx.doi.org/10.1007/s11689-010-9047-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.70-76[article] Aging in fragile X syndrome [Texte imprimé et/ou numérique] / A. UTARI, Auteur ; E. ADAMS, Auteur ; Elizabeth BERRY-KRAVIS, Auteur ; Alyssa D. CHAVEZ, Auteur ; F. SCAGGS, Auteur ; L. NGOTRAN, Auteur ; A. BOYD, Auteur ; D. HESSL, Auteur ; L. W. GANE, Auteur ; F. TASSONE, Auteur ; N. TARTAGLIA, Auteur ; M. A. LEEHEY, Auteur ; Randi J. HAGERMAN, Auteur . - p.70-76.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.70-76
Index. décimale : PER Périodiques Résumé : Many studies have focused on the behavior and cognitive problems in young patients with fragile X syndrome (FXS), but there are no studies about the problems in aging for those with FXS. The discovery of the fragile X-associated tremor ataxia syndrome (FXTAS), a neurodegenerative disorder related to elevated FMR1-mRNA, in elderly men and some women with the premutation, intensified the need for aging studies in FXS. Approximately 40% of males with FXS have repeat size mosaicism and as a result, some of these individuals also have elevated levels of FMR1-mRNA which theoretically puts them at risk for FXTAS. Here, we have surveyed all of the aging patients with FXS that we have followed over the years to clarify the medical complications of aging seen in those with FXS. Data was collected from 62 individuals with the FXS full mutation (44 males; 18 females) who were at least 40 years old at their most recent clinical examination. We found that the five most frequent medical problems in these patients were neurological problems (38.7%), gastrointestinal problems (30.6%), obesity (28.8%), hypertension (24.2%) and heart problems (24.2%). Movement disorders were significantly different between males and females (38.6% vs.10.2%, p = 0.029). We did not find any differences in medical problems between those with a full mutation and those with mosaicism. Identification of medical problems associated with aging in FXS is important to establish appropriate recommendations for medical screening and treatment considerations. En ligne : http://dx.doi.org/10.1007/s11689-010-9047-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 White matter microstructure in 22q11 deletion syndrome: a pilot diffusion tensor imaging and voxel-based morphometry study of children and adolescents / F. SUNDRAM in Journal of Neurodevelopmental Disorders, 2-2 (June 2010)
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[article]
Titre : White matter microstructure in 22q11 deletion syndrome: a pilot diffusion tensor imaging and voxel-based morphometry study of children and adolescents Type de document : Texte imprimé et/ou numérique Auteurs : F. SUNDRAM, Auteur ; Linda E. CAMPBELL, Auteur ; R. AZUMA, Auteur ; Eileen DALY, Auteur ; Oswald J.N. BLOEMEN, Auteur ; Gareth J. BARKER, Auteur ; X. CHITNIS, Auteur ; D. K. JONES, Auteur ; T. VAN AMELSVOORT, Auteur ; K. C. MURPHY, Auteur ; D. G. MURPHY, Auteur Article en page(s) : p.77-92 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Young people with 22q11 Deletion Syndrome (22q11DS) are at substantial risk for developing psychosis and have significant differences in white matter (WM) volume. However, there are few in vivo studies of both WM microstructural integrity (as measured using Diffusion Tensor (DT)-MRI) and WM volume in the same individual. We used DT-MRI and structural MRI (sMRI) with voxel based morphometry (VBM) to compare, respectively, the fractional anisotropy (FA) and WM volume of 11 children and adolescents with 22q11DS and 12 controls. Also, within 22q11DS we related differences in WM to severity of schizotypy, and polymorphism of the catechol-O-methyltransferase (COMT) gene. People with 22q11DS had significantly lower FA in inter-hemispheric and brainstem and frontal, parietal and temporal lobe regions after covarying for IQ. Significant WM volumetric increases were found in the internal capsule, anterior brainstem and frontal and occipital lobes. There was a significant negative correlation between increased schizotypy scores and reduced WM FA in the right posterior limb of internal capsule and the right body and left splenium of corpus callosum. Finally, the Val allele of COMT was associated with a significant reduction in both FA and volume of WM in the frontal lobes, cingulum and corpus callosum. Young people with 22q11DS have significant differences in both WM microstructure and volume. Also, there is preliminary evidence that within 22q11DS, some regional differences in FA are associated with allelic variation in COMT and may perhaps also be associated with schizotypy. En ligne : http://dx.doi.org/10.1007/s11689-010-9043-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.77-92[article] White matter microstructure in 22q11 deletion syndrome: a pilot diffusion tensor imaging and voxel-based morphometry study of children and adolescents [Texte imprimé et/ou numérique] / F. SUNDRAM, Auteur ; Linda E. CAMPBELL, Auteur ; R. AZUMA, Auteur ; Eileen DALY, Auteur ; Oswald J.N. BLOEMEN, Auteur ; Gareth J. BARKER, Auteur ; X. CHITNIS, Auteur ; D. K. JONES, Auteur ; T. VAN AMELSVOORT, Auteur ; K. C. MURPHY, Auteur ; D. G. MURPHY, Auteur . - p.77-92.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.77-92
Index. décimale : PER Périodiques Résumé : Young people with 22q11 Deletion Syndrome (22q11DS) are at substantial risk for developing psychosis and have significant differences in white matter (WM) volume. However, there are few in vivo studies of both WM microstructural integrity (as measured using Diffusion Tensor (DT)-MRI) and WM volume in the same individual. We used DT-MRI and structural MRI (sMRI) with voxel based morphometry (VBM) to compare, respectively, the fractional anisotropy (FA) and WM volume of 11 children and adolescents with 22q11DS and 12 controls. Also, within 22q11DS we related differences in WM to severity of schizotypy, and polymorphism of the catechol-O-methyltransferase (COMT) gene. People with 22q11DS had significantly lower FA in inter-hemispheric and brainstem and frontal, parietal and temporal lobe regions after covarying for IQ. Significant WM volumetric increases were found in the internal capsule, anterior brainstem and frontal and occipital lobes. There was a significant negative correlation between increased schizotypy scores and reduced WM FA in the right posterior limb of internal capsule and the right body and left splenium of corpus callosum. Finally, the Val allele of COMT was associated with a significant reduction in both FA and volume of WM in the frontal lobes, cingulum and corpus callosum. Young people with 22q11DS have significant differences in both WM microstructure and volume. Also, there is preliminary evidence that within 22q11DS, some regional differences in FA are associated with allelic variation in COMT and may perhaps also be associated with schizotypy. En ligne : http://dx.doi.org/10.1007/s11689-010-9043-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 A preliminary study of orbitofrontal activation and hypersociability in Williams Syndrome / M. MIMURA in Journal of Neurodevelopmental Disorders, 2-2 (June 2010)
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[article]
Titre : A preliminary study of orbitofrontal activation and hypersociability in Williams Syndrome Type de document : Texte imprimé et/ou numérique Auteurs : M. MIMURA, Auteur ; F. HOEFT, Auteur ; M. KATO, Auteur ; N. KOBAYASHI, Auteur ; K. SHEAU, Auteur ; J. PIGGOT, Auteur ; D. MILLS, Auteur ; A. GALABURDA, Auteur ; J. R. KORENBERG, Auteur ; Ursula BELLUGI, Auteur ; A. L. REISS, Auteur Article en page(s) : p.93-98 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Individuals with Williams syndrome (WS) demonstrate an abnormally positive social bias. However, the neural substrates of this hypersociability, i.e., positive attribution bias and increased drive toward social interaction, have not fully been elucidated. METHODS: We performed an event-related functional magnetic resonance imaging study while individuals with WS and typically developing controls (TD) matched positive and negative emotional faces. WS compared to TD showed reduced right amygdala activation during presentation of negative faces, as in the previous literature. In addition, WS showed a unique pattern of right orbitofrontal cortex activation. While TD showed medial orbitofrontal cortex activation in response to positive, and lateral orbitofrontal cortex activation to negative, WS showed the opposite pattern. In light of the general notion of a medial/lateral gradient of reward/punishment processing in the orbitofrontal cortex, these findings provide an additional biological explanation for, or correlate of positive attribution bias and hypersociability in WS. En ligne : http://dx.doi.org/10.1007/s11689-009-9041-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.93-98[article] A preliminary study of orbitofrontal activation and hypersociability in Williams Syndrome [Texte imprimé et/ou numérique] / M. MIMURA, Auteur ; F. HOEFT, Auteur ; M. KATO, Auteur ; N. KOBAYASHI, Auteur ; K. SHEAU, Auteur ; J. PIGGOT, Auteur ; D. MILLS, Auteur ; A. GALABURDA, Auteur ; J. R. KORENBERG, Auteur ; Ursula BELLUGI, Auteur ; A. L. REISS, Auteur . - p.93-98.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.93-98
Index. décimale : PER Périodiques Résumé : Individuals with Williams syndrome (WS) demonstrate an abnormally positive social bias. However, the neural substrates of this hypersociability, i.e., positive attribution bias and increased drive toward social interaction, have not fully been elucidated. METHODS: We performed an event-related functional magnetic resonance imaging study while individuals with WS and typically developing controls (TD) matched positive and negative emotional faces. WS compared to TD showed reduced right amygdala activation during presentation of negative faces, as in the previous literature. In addition, WS showed a unique pattern of right orbitofrontal cortex activation. While TD showed medial orbitofrontal cortex activation in response to positive, and lateral orbitofrontal cortex activation to negative, WS showed the opposite pattern. In light of the general notion of a medial/lateral gradient of reward/punishment processing in the orbitofrontal cortex, these findings provide an additional biological explanation for, or correlate of positive attribution bias and hypersociability in WS. En ligne : http://dx.doi.org/10.1007/s11689-009-9041-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Enhanced prefrontal serotonin 5-HT(1A) currents in a mouse model of Williams-Beuren syndrome with low innate anxiety / E. PROULX in Journal of Neurodevelopmental Disorders, 2-2 (June 2010)
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[article]
Titre : Enhanced prefrontal serotonin 5-HT(1A) currents in a mouse model of Williams-Beuren syndrome with low innate anxiety Type de document : Texte imprimé et/ou numérique Auteurs : E. PROULX, Auteur ; E. J. YOUNG, Auteur ; L. R. OSBORNE, Auteur ; E. K. LAMBE, Auteur Article en page(s) : p.99-108 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Williams-Beuren syndrome (WBS) is a neurodevelopmental disorder caused by the hemizygous deletion of 28 genes on chromosome 7, including the general transcription factor GTF2IRD1. Mice either hemizygously (Gtf2ird1(+/-)) or homozygously (Gtf2ird1(-/-)) deleted for this transcription factor exhibit low innate anxiety, low aggression and increased social interaction, a phenotype that shares similarities to the high sociability and disinhibition seen in individuals with WBS. Here, we investigated the inhibitory effects of serotonin (5-HT) on the major output neurons of the prefrontal cortex in Gtf2ird1(-/-) mice and their wildtype (WT) siblings. Prefrontal 5-HT receptors are known to modulate anxiety-like behaviors, and the Gtf2ird1(-/-) mice have altered 5-HT metabolism in prefrontal cortex. Using whole cell recording from layer V neurons in acute brain slices of prefrontal cortex, we found that 5-HT elicited significantly larger inhibitory, outward currents in Gtf2ird1(-/-) mice than in WT controls. In both genotypes, these currents were resistant to action potential blockade with TTX and were suppressed by the selective 5-HT(1A) receptor antagonist WAY-100635, suggesting that they are mediated directly by 5-HT(1A) receptors on the recorded neurons. Control experiments suggest a degree of layer and receptor specificity in this enhancement since 5-HT(1A) receptor-mediated responses in layer II/III pyramidal neurons were unchanged as were responses mediated by two other inhibitory receptors in layer V pyramidal neurons. Furthermore, we demonstrate GTF2IRD1 protein expression by neurons in layer V of the prefrontal cortex. Our finding that 5-HT(1A)-mediated responses are selectively enhanced in layer V pyramidal neurons of Gtf2ird1(-/-) mice gives insight into the cellular mechanisms that underlie reduced innate anxiety and increased sociability in these mice, and may be relevant to the low social anxiety and disinhibition in patients with WBS and their sensitivity to serotonergic medicines. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-010-9044-5) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-010-9044-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.99-108[article] Enhanced prefrontal serotonin 5-HT(1A) currents in a mouse model of Williams-Beuren syndrome with low innate anxiety [Texte imprimé et/ou numérique] / E. PROULX, Auteur ; E. J. YOUNG, Auteur ; L. R. OSBORNE, Auteur ; E. K. LAMBE, Auteur . - p.99-108.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.99-108
Index. décimale : PER Périodiques Résumé : Williams-Beuren syndrome (WBS) is a neurodevelopmental disorder caused by the hemizygous deletion of 28 genes on chromosome 7, including the general transcription factor GTF2IRD1. Mice either hemizygously (Gtf2ird1(+/-)) or homozygously (Gtf2ird1(-/-)) deleted for this transcription factor exhibit low innate anxiety, low aggression and increased social interaction, a phenotype that shares similarities to the high sociability and disinhibition seen in individuals with WBS. Here, we investigated the inhibitory effects of serotonin (5-HT) on the major output neurons of the prefrontal cortex in Gtf2ird1(-/-) mice and their wildtype (WT) siblings. Prefrontal 5-HT receptors are known to modulate anxiety-like behaviors, and the Gtf2ird1(-/-) mice have altered 5-HT metabolism in prefrontal cortex. Using whole cell recording from layer V neurons in acute brain slices of prefrontal cortex, we found that 5-HT elicited significantly larger inhibitory, outward currents in Gtf2ird1(-/-) mice than in WT controls. In both genotypes, these currents were resistant to action potential blockade with TTX and were suppressed by the selective 5-HT(1A) receptor antagonist WAY-100635, suggesting that they are mediated directly by 5-HT(1A) receptors on the recorded neurons. Control experiments suggest a degree of layer and receptor specificity in this enhancement since 5-HT(1A) receptor-mediated responses in layer II/III pyramidal neurons were unchanged as were responses mediated by two other inhibitory receptors in layer V pyramidal neurons. Furthermore, we demonstrate GTF2IRD1 protein expression by neurons in layer V of the prefrontal cortex. Our finding that 5-HT(1A)-mediated responses are selectively enhanced in layer V pyramidal neurons of Gtf2ird1(-/-) mice gives insight into the cellular mechanisms that underlie reduced innate anxiety and increased sociability in these mice, and may be relevant to the low social anxiety and disinhibition in patients with WBS and their sensitivity to serotonergic medicines. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-010-9044-5) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-010-9044-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 Rapid automatized naming as an index of genetic liability to autism / M. LOSH in Journal of Neurodevelopmental Disorders, 2-2 (June 2010)
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[article]
Titre : Rapid automatized naming as an index of genetic liability to autism Type de document : Texte imprimé et/ou numérique Auteurs : M. LOSH, Auteur ; D. ESSERMAN, Auteur ; J. PIVEN, Auteur Article en page(s) : p.109-16 Langues : Anglais (eng) Mots-clés : Autism Broad autism phenotype Endophenotype Rapid automatized naming Index. décimale : PER Périodiques Résumé : This study investigated rapid automatized naming (RAN) ability in high functioning individuals with autism and parents of individuals with autism. Findings revealed parallel patterns of performance in parents and individuals with autism, where both groups had longer naming times than controls. Significant parent-child correlations were also detected, along with associations with language and personality features of the broad autism phenotype (retrospective reports of early language delay, socially reticent personality). Together, findings point towards RAN as a potential marker of genetic liability to autism. En ligne : http://dx.doi.org/10.1007/s11689-010-9045-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.109-16[article] Rapid automatized naming as an index of genetic liability to autism [Texte imprimé et/ou numérique] / M. LOSH, Auteur ; D. ESSERMAN, Auteur ; J. PIVEN, Auteur . - p.109-16.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.109-16
Mots-clés : Autism Broad autism phenotype Endophenotype Rapid automatized naming Index. décimale : PER Périodiques Résumé : This study investigated rapid automatized naming (RAN) ability in high functioning individuals with autism and parents of individuals with autism. Findings revealed parallel patterns of performance in parents and individuals with autism, where both groups had longer naming times than controls. Significant parent-child correlations were also detected, along with associations with language and personality features of the broad autism phenotype (retrospective reports of early language delay, socially reticent personality). Together, findings point towards RAN as a potential marker of genetic liability to autism. En ligne : http://dx.doi.org/10.1007/s11689-010-9045-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
[article]
Titre : Erratum to: Cover essay Type de document : Texte imprimé et/ou numérique Auteurs : J. PIVEN, Auteur Article en page(s) : p.117 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-010-9050-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.117[article] Erratum to: Cover essay [Texte imprimé et/ou numérique] / J. PIVEN, Auteur . - p.117.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 2-2 (June 2010) . - p.117
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-010-9050-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342