Dépouillements

Developmental malformation of the corpus callosum: a review of typical callosal development and examples of developmental disorders with callosal involvement / L. K. PAUL in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.3-27 Titre : Developmental malformation of the corpus callosum: a review of typical callosal development and examples of developmental disorders with callosal involvement Type de document : Texte imprimé et/ou numérique Auteurs : L. K. PAUL, Auteur Article en page(s) : p.3-27 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This review provides an overview of the involvement of the corpus callosum (CC) in a variety of developmental disorders that are currently defined exclusively by genetics, developmental insult, and/or behavior. I begin with a general review of CC development, connectivity, and function, followed by discussion of the research methods typically utilized to study the callosum. The bulk of the review concentrates on specific developmental disorders, beginning with agenesis of the corpus callosum (AgCC)-the only condition diagnosed exclusively by callosal anatomy. This is followed by a review of several genetic disorders that commonly result in social impairments and/or psychopathology similar to AgCC (neurofibromatosis-1, Turner syndrome, 22q11.2 deletion syndrome, Williams yndrome, and fragile X) and two forms of prenatal injury (premature birth, fetal alcohol syndrome) known to impact callosal development. Finally, I examine callosal involvement in several common developmental disorders defined exclusively by behavioral patterns (developmental language delay, dyslexia, attention-deficit hyperactive disorder, autism spectrum disorders, and Tourette syndrome). En ligne : http://dx.doi.org/10.1007/s11689-010-9059-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Developmental malformation of the corpus callosum: a review of typical callosal development and examples of developmental disorders with callosal involvement [Texte imprimé et/ou numérique] / L. K. PAUL, Auteur . - p.3-27. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.3-27 Index. décimale : PER Périodiques Résumé : This review provides an overview of the involvement of the corpus callosum (CC) in a variety of developmental disorders that are currently defined exclusively by genetics, developmental insult, and/or behavior. I begin with a general review of CC development, connectivity, and function, followed by discussion of the research methods typically utilized to study the callosum. The bulk of the review concentrates on specific developmental disorders, beginning with agenesis of the corpus callosum (AgCC)-the only condition diagnosed exclusively by callosal anatomy. This is followed by a review of several genetic disorders that commonly result in social impairments and/or psychopathology similar to AgCC (neurofibromatosis-1, Turner syndrome, 22q11.2 deletion syndrome, Williams yndrome, and fragile X) and two forms of prenatal injury (premature birth, fetal alcohol syndrome) known to impact callosal development. Finally, I examine callosal involvement in several common developmental disorders defined exclusively by behavioral patterns (developmental language delay, dyslexia, attention-deficit hyperactive disorder, autism spectrum disorders, and Tourette syndrome). En ligne : http://dx.doi.org/10.1007/s11689-010-9059-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

Electrophysiological study of local/global processing in Williams syndrome / A. P. KEY in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.28-38 Titre : Electrophysiological study of local/global processing in Williams syndrome Type de document : Texte imprimé et/ou numérique Auteurs : A. P. KEY, Auteur ; E. M. DYKENS, Auteur Article en page(s) : p.28-38 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Persons with Williams syndrome (WS) demonstrate pronounced deficits in visuo-spatial processing. The purpose of the current study was to examine the preferred level of perceptual analysis in young adults with WS (n = 21) and the role of attention in the processing of hierarchical stimuli. Navon-like letter stimuli were presented to adults with WS and age-matched typical controls in an oddball paradigm where local and global targets could appear with equal probability. Participants received no explicit instruction to direct their attention toward a particular stimulus level. Behavioral and event-related potential (ERP) data were recorded. Behavioral data indicated presence of a global precedence effect in persons with WS. However, their ERP responses revealed atypical brain mechanisms underlying attention to local information. During the early perceptual analysis, global targets resulted in reduced P1 and enhanced N150 responses in both participant groups. However, only the typical comparison group demonstrated a larger N150 to local targets. At the more advanced stages of cognitive processing, a larger P3b response to global and local targets was observed in the typical group but not in persons with WS, who instead demonstrated an enhanced P3a to global targets only. The results indicate that in a perceptual task, adults with WS may experience greater than typical global-to-local interference and not allocate sufficient attentional resources to local information. En ligne : http://dx.doi.org/10.1007/s11689-010-9064-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] Electrophysiological study of local/global processing in Williams syndrome [Texte imprimé et/ou numérique] / A. P. KEY, Auteur ; E. M. DYKENS, Auteur . - p.28-38. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.28-38 Index. décimale : PER Périodiques Résumé : Persons with Williams syndrome (WS) demonstrate pronounced deficits in visuo-spatial processing. The purpose of the current study was to examine the preferred level of perceptual analysis in young adults with WS (n = 21) and the role of attention in the processing of hierarchical stimuli. Navon-like letter stimuli were presented to adults with WS and age-matched typical controls in an oddball paradigm where local and global targets could appear with equal probability. Participants received no explicit instruction to direct their attention toward a particular stimulus level. Behavioral and event-related potential (ERP) data were recorded. Behavioral data indicated presence of a global precedence effect in persons with WS. However, their ERP responses revealed atypical brain mechanisms underlying attention to local information. During the early perceptual analysis, global targets resulted in reduced P1 and enhanced N150 responses in both participant groups. However, only the typical comparison group demonstrated a larger N150 to local targets. At the more advanced stages of cognitive processing, a larger P3b response to global and local targets was observed in the typical group but not in persons with WS, who instead demonstrated an enhanced P3a to global targets only. The results indicate that in a perceptual task, adults with WS may experience greater than typical global-to-local interference and not allocate sufficient attentional resources to local information. En ligne : http://dx.doi.org/10.1007/s11689-010-9064-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343

Replication of CNTNAP2 association with nonword repetition and support for FOXP2 association with timed reading and motor activities in a dyslexia family sample / B. PETER in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.39-49 Titre : Replication of CNTNAP2 association with nonword repetition and support for FOXP2 association with timed reading and motor activities in a dyslexia family sample Type de document : Texte imprimé et/ou numérique Auteurs : B. PETER, Auteur ; W. H. RASKIND, Auteur ; M. MATSUSHITA, Auteur ; M. LISOWSKI, Auteur ; T. VU, Auteur ; Virginia W. BERNINGER, Auteur ; E. M. WIJSMAN, Auteur ; Zoran BRKANAC, Auteur Article en page(s) : p.39-49 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Two functionally related genes, FOXP2 and CNTNAP2, influence language abilities in families with rare syndromic and common nonsyndromic forms of impaired language, respectively. We investigated whether these genes are associated with component phenotypes of dyslexia and measures of sequential motor ability. Quantitative transmission disequilibrium testing (QTDT) and linear association modeling were used to evaluate associations with measures of phonological memory (nonword repetition, NWR), expressive language (sentence repetition), reading (real word reading efficiency, RWRE; word attack, WATT), and timed sequential motor activities (rapid alternating place of articulation, RAPA; finger succession in the dominant hand, FS-D) in 188 family trios with a child with dyslexia. Consistent with a prior study of language impairment, QTDT in dyslexia showed evidence of CNTNAP2 single nucleotide polymorphism (SNP) association with NWR. For FOXP2, we provide the first evidence for SNP association with component phenotypes of dyslexia, specifically NWR and RWRE but not WATT. In addition, FOXP2 SNP associations with both RAPA and FS-D were observed. Our results confirm the role of CNTNAP2 in NWR in a dyslexia sample and motivate new questions about the effects of FOXP2 in neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1007/s11689-010-9065-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] Replication of CNTNAP2 association with nonword repetition and support for FOXP2 association with timed reading and motor activities in a dyslexia family sample [Texte imprimé et/ou numérique] / B. PETER, Auteur ; W. H. RASKIND, Auteur ; M. MATSUSHITA, Auteur ; M. LISOWSKI, Auteur ; T. VU, Auteur ; Virginia W. BERNINGER, Auteur ; E. M. WIJSMAN, Auteur ; Zoran BRKANAC, Auteur . - p.39-49. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.39-49 Index. décimale : PER Périodiques Résumé : Two functionally related genes, FOXP2 and CNTNAP2, influence language abilities in families with rare syndromic and common nonsyndromic forms of impaired language, respectively. We investigated whether these genes are associated with component phenotypes of dyslexia and measures of sequential motor ability. Quantitative transmission disequilibrium testing (QTDT) and linear association modeling were used to evaluate associations with measures of phonological memory (nonword repetition, NWR), expressive language (sentence repetition), reading (real word reading efficiency, RWRE; word attack, WATT), and timed sequential motor activities (rapid alternating place of articulation, RAPA; finger succession in the dominant hand, FS-D) in 188 family trios with a child with dyslexia. Consistent with a prior study of language impairment, QTDT in dyslexia showed evidence of CNTNAP2 single nucleotide polymorphism (SNP) association with NWR. For FOXP2, we provide the first evidence for SNP association with component phenotypes of dyslexia, specifically NWR and RWRE but not WATT. In addition, FOXP2 SNP associations with both RAPA and FS-D were observed. Our results confirm the role of CNTNAP2 in NWR in a dyslexia sample and motivate new questions about the effects of FOXP2 in neurodevelopmental disorders. En ligne : http://dx.doi.org/10.1007/s11689-010-9065-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343

Angelman syndrome: advancing the research frontier of neurodevelopmental disorders / B. D. PHILPOT in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.50-6 Titre : Angelman syndrome: advancing the research frontier of neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique Auteurs : B. D. PHILPOT, Auteur ; Charlotte E. THOMPSON, Auteur ; L. FRANCO, Auteur ; C. A. WILLIAMS, Auteur Article en page(s) : p.50-6 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This report is a meeting summary of the 2010 Angelman Syndrome Foundation's scientific symposium on the neuroscience of UBE3A. Angelman syndrome is characterized by loss of speech, severe developmental delay, seizures, and ataxia. These core symptoms are caused by maternal allele disruptions of a single gene-UBE3A. UBE3A encodes an E3 ubiquitin ligase that targets certain proteins for proteasomal degradation. This biology has led to the expectation that the identification of Ube3a protein targets will lead to therapies for Angelman syndrome. The recent discovery of Ube3a substrates such as Arc (activity-regulated cytoskeletal protein) provides new insight into the mechanisms underlying the synaptic function and plasticity deficits caused by the loss of Ube3a. In addition to identifying Ube3a substrates, there have also been recent advances in understanding UBE3A's integrated role in the neuronal repertoire of genes and protein interactions. A developmental picture is now emerging whereby UBE3A gene dosage on chromosome 15 alters synaptic function, with deficiencies leading to Angelman syndrome and overexpression associated with classic autism symptomatology. En ligne : http://dx.doi.org/10.1007/s11689-010-9066-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] Angelman syndrome: advancing the research frontier of neurodevelopmental disorders [Texte imprimé et/ou numérique] / B. D. PHILPOT, Auteur ; Charlotte E. THOMPSON, Auteur ; L. FRANCO, Auteur ; C. A. WILLIAMS, Auteur . - p.50-6. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.50-6 Index. décimale : PER Périodiques Résumé : This report is a meeting summary of the 2010 Angelman Syndrome Foundation's scientific symposium on the neuroscience of UBE3A. Angelman syndrome is characterized by loss of speech, severe developmental delay, seizures, and ataxia. These core symptoms are caused by maternal allele disruptions of a single gene-UBE3A. UBE3A encodes an E3 ubiquitin ligase that targets certain proteins for proteasomal degradation. This biology has led to the expectation that the identification of Ube3a protein targets will lead to therapies for Angelman syndrome. The recent discovery of Ube3a substrates such as Arc (activity-regulated cytoskeletal protein) provides new insight into the mechanisms underlying the synaptic function and plasticity deficits caused by the loss of Ube3a. In addition to identifying Ube3a substrates, there have also been recent advances in understanding UBE3A's integrated role in the neuronal repertoire of genes and protein interactions. A developmental picture is now emerging whereby UBE3A gene dosage on chromosome 15 alters synaptic function, with deficiencies leading to Angelman syndrome and overexpression associated with classic autism symptomatology. En ligne : http://dx.doi.org/10.1007/s11689-010-9066-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343

Clinical assessment of DSM-IV anxiety disorders in fragile X syndrome: prevalence and characterization / L. CORDEIRO in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.57-67 Titre : Clinical assessment of DSM-IV anxiety disorders in fragile X syndrome: prevalence and characterization Type de document : Texte imprimé et/ou numérique Auteurs : L. CORDEIRO, Auteur ; Elizabeth C. BALLINGER, Auteur ; Randi J. HAGERMAN, Auteur ; D. HESSL, Auteur Article en page(s) : p.57-67 Langues : Anglais (eng) Mots-clés : Anxiety  Fragile X syndrome  Intellectual disability  Social phobia  Specific phobia Index. décimale : PER Périodiques Résumé : Fragile X syndrome (FXS) is the most common form of inherited intellectual disability (ID). Anxiety and social withdrawal are considered core features of the FXS phenotype, yet there is limited diagnostic evidence of the prevalence of formal anxiety disorders in FXS. This study assessed the prevalence of anxiety disorders in a sample of 58 males and 39 females with FXS (ages 5.0-33.3 years). Participants' parents completed the Anxiety Disorders Interview Schedule (ADIS-IV), a clinical interview based on DSM-IV criteria, and the Anxiety Depression and Mood Scale (ADAMS), a psychiatric disorders screening instrument normed in ID. We conducted cognitive (IQ) and autism (AUT) assessments and surveyed medication use. Despite a high rate of psychopharmacological treatment, 86.2% of males and 76.9% of females met criteria for an anxiety disorder, with social phobia and specific phobia the most commonly diagnosed. Proband status, gender, and IQ were not significantly related to any anxiety disorders, however significantly higher rates of a few anxiety disorders were found in older age and AUT groups. Significant correlations between ADIS diagnoses and ADAMS scores provided cross-validation of instruments, indicating that the ADIS is suitable for use in FXS. A greater percentage of our sample met criteria for most anxiety disorders than has been reported in other ID groups or the general population. The rate of anxiety compared to general ID suggests that the FMR1 full mutation confers an especially high risk for these disorders, regardless of factors commonly associated with FXS clinical involvement. A thorough clinical assessment and treatment of anxiety should be included in the FXS standard of care. En ligne : http://dx.doi.org/10.1007/s11689-010-9067-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] Clinical assessment of DSM-IV anxiety disorders in fragile X syndrome: prevalence and characterization [Texte imprimé et/ou numérique] / L. CORDEIRO, Auteur ; Elizabeth C. BALLINGER, Auteur ; Randi J. HAGERMAN, Auteur ; D. HESSL, Auteur . - p.57-67. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.57-67 Mots-clés : Anxiety  Fragile X syndrome  Intellectual disability  Social phobia  Specific phobia Index. décimale : PER Périodiques Résumé : Fragile X syndrome (FXS) is the most common form of inherited intellectual disability (ID). Anxiety and social withdrawal are considered core features of the FXS phenotype, yet there is limited diagnostic evidence of the prevalence of formal anxiety disorders in FXS. This study assessed the prevalence of anxiety disorders in a sample of 58 males and 39 females with FXS (ages 5.0-33.3 years). Participants' parents completed the Anxiety Disorders Interview Schedule (ADIS-IV), a clinical interview based on DSM-IV criteria, and the Anxiety Depression and Mood Scale (ADAMS), a psychiatric disorders screening instrument normed in ID. We conducted cognitive (IQ) and autism (AUT) assessments and surveyed medication use. Despite a high rate of psychopharmacological treatment, 86.2% of males and 76.9% of females met criteria for an anxiety disorder, with social phobia and specific phobia the most commonly diagnosed. Proband status, gender, and IQ were not significantly related to any anxiety disorders, however significantly higher rates of a few anxiety disorders were found in older age and AUT groups. Significant correlations between ADIS diagnoses and ADAMS scores provided cross-validation of instruments, indicating that the ADIS is suitable for use in FXS. A greater percentage of our sample met criteria for most anxiety disorders than has been reported in other ID groups or the general population. The rate of anxiety compared to general ID suggests that the FMR1 full mutation confers an especially high risk for these disorders, regardless of factors commonly associated with FXS clinical involvement. A thorough clinical assessment and treatment of anxiety should be included in the FXS standard of care. En ligne : http://dx.doi.org/10.1007/s11689-010-9067-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343

How might stress contribute to increased risk for schizophrenia in children with chromosome 22q11.2 deletion syndrome? / Elliott A. BEATON in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.68-75 Titre : How might stress contribute to increased risk for schizophrenia in children with chromosome 22q11.2 deletion syndrome? Type de document : Texte imprimé et/ou numérique Auteurs : Elliott A. BEATON, Auteur ; T. J. SIMON, Auteur Article en page(s) : p.68-75 Langues : Anglais (eng) Mots-clés : Allostatic load  Children  Cortisol  Developmental disorder  Genotype  Hypothalamic-pituitary-adrenal axis (HPA axis)  Schizophrenia  Socioemotional development  Stress-diathesis  Velo-cardio-facial syndrome (VCFS) Index. décimale : PER Périodiques Résumé : The most common human microdeletion occurs at chromosome 22q11.2. The associated syndrome (22q11.2DS) has a complex and variable phenotype with a high risk of schizophrenia. While the role of stress in the etiopathology of schizophrenia has been under investigation for over 30 years (Walker et al. 2008), the stress-diathesis model has yet to be investigated in children with 22q11.2DS. Children with 22q11.2DS face serious medical, behavioral, and socioemotional challenges from infancy into adulthood. Chronic stress elevates glucocorticoids, decreases immunocompetence, negatively impacts brain development and function, and is associated with psychiatric illness in adulthood. Drawing knowledge from the extant and well-developed anxiety and stress literature will provide invaluable insight into the complex etiopathology of schizophrenia in people with 22q11.2DS while suggesting possible early interventions. Childhood anxiety is treatable and stress coping skills can be developed thereby improving quality of life in the short-term and potentially mitigating the risk of developing psychosis. En ligne : http://dx.doi.org/10.1007/s11689-010-9069-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] How might stress contribute to increased risk for schizophrenia in children with chromosome 22q11.2 deletion syndrome? [Texte imprimé et/ou numérique] / Elliott A. BEATON, Auteur ; T. J. SIMON, Auteur . - p.68-75. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.68-75 Mots-clés : Allostatic load  Children  Cortisol  Developmental disorder  Genotype  Hypothalamic-pituitary-adrenal axis (HPA axis)  Schizophrenia  Socioemotional development  Stress-diathesis  Velo-cardio-facial syndrome (VCFS) Index. décimale : PER Périodiques Résumé : The most common human microdeletion occurs at chromosome 22q11.2. The associated syndrome (22q11.2DS) has a complex and variable phenotype with a high risk of schizophrenia. While the role of stress in the etiopathology of schizophrenia has been under investigation for over 30 years (Walker et al. 2008), the stress-diathesis model has yet to be investigated in children with 22q11.2DS. Children with 22q11.2DS face serious medical, behavioral, and socioemotional challenges from infancy into adulthood. Chronic stress elevates glucocorticoids, decreases immunocompetence, negatively impacts brain development and function, and is associated with psychiatric illness in adulthood. Drawing knowledge from the extant and well-developed anxiety and stress literature will provide invaluable insight into the complex etiopathology of schizophrenia in people with 22q11.2DS while suggesting possible early interventions. Childhood anxiety is treatable and stress coping skills can be developed thereby improving quality of life in the short-term and potentially mitigating the risk of developing psychosis. En ligne : http://dx.doi.org/10.1007/s11689-010-9069-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343

Atypical development of the executive attention network in children with chromosome 22q11.2 deletion syndrome / J. STODDARD in Journal of Neurodevelopmental Disorders, 3-1 (March 2011)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.76-85 Titre : Atypical development of the executive attention network in children with chromosome 22q11.2 deletion syndrome Type de document : Texte imprimé et/ou numérique Auteurs : J. STODDARD, Auteur ; L. BECKETT, Auteur ; T. J. SIMON, Auteur Article en page(s) : p.76-85 Langues : Anglais (eng) Mots-clés : Attention networks task  Chromosome 22q11.2 deletion syndrome  Cognitive control Index. décimale : PER Périodiques Résumé : Impairment in the executive control of attention has been found in youth with chromosome 22q11.2 deletion syndrome (22q11.2DS). However, how this impairment is modified by other factors, particularly age, is unknown. Forty-six typically developing and 53 children with 22q11.2DS were tested with the attention networks task (ANT) in this cross-sectional study. We used logarithmic transform and linear modeling to assess age effects on the executive index of the ANT. Mixed modeling accounted for between subject variability, age, handedness, catecholamine-O-transferase (COMT; codon 158) genotype, and gender on performance for all experimental conditions (cue x flanker) and their two-level interactions. Children with 22q11.2DS showed a relative, age-dependent executive index impairment but not orienting or alerting network index impairments. In factorial analysis, age was a major predictor of overall performance. There was a significant effect of the 22q11.2DS on overall performance. Of note, children with 22q11.2DS are specifically vulnerable to incongruent flanker interference, especially at younger ages. We did not find an overall effect of COMT genotype or handedness. Children with 22q11.2DS demonstrated age-related impairment in the executive control of attention. Future investigation will likely reveal that there are different developmental trajectories of executive attentional function likely related to the development of schizophrenia in 22q11.2DS. En ligne : http://dx.doi.org/10.1007/s11689-010-9070-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343 [article] Atypical development of the executive attention network in children with chromosome 22q11.2 deletion syndrome [Texte imprimé et/ou numérique] / J. STODDARD, Auteur ; L. BECKETT, Auteur ; T. J. SIMON, Auteur . - p.76-85. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 3-1 (March 2011) . - p.76-85 Mots-clés : Attention networks task  Chromosome 22q11.2 deletion syndrome  Cognitive control Index. décimale : PER Périodiques Résumé : Impairment in the executive control of attention has been found in youth with chromosome 22q11.2 deletion syndrome (22q11.2DS). However, how this impairment is modified by other factors, particularly age, is unknown. Forty-six typically developing and 53 children with 22q11.2DS were tested with the attention networks task (ANT) in this cross-sectional study. We used logarithmic transform and linear modeling to assess age effects on the executive index of the ANT. Mixed modeling accounted for between subject variability, age, handedness, catecholamine-O-transferase (COMT; codon 158) genotype, and gender on performance for all experimental conditions (cue x flanker) and their two-level interactions. Children with 22q11.2DS showed a relative, age-dependent executive index impairment but not orienting or alerting network index impairments. In factorial analysis, age was a major predictor of overall performance. There was a significant effect of the 22q11.2DS on overall performance. Of note, children with 22q11.2DS are specifically vulnerable to incongruent flanker interference, especially at younger ages. We did not find an overall effect of COMT genotype or handedness. Children with 22q11.2DS demonstrated age-related impairment in the executive control of attention. Future investigation will likely reveal that there are different developmental trajectories of executive attentional function likely related to the development of schizophrenia in 22q11.2DS. En ligne : http://dx.doi.org/10.1007/s11689-010-9070-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=343