Dépouillements

Journal of Neurodevelopmental Disorders is now a fully open access journal / J. PIVEN in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.1 Titre : Journal of Neurodevelopmental Disorders is now a fully open access journal Type de document : Texte imprimé et/ou numérique Auteurs : J. PIVEN, Auteur Article en page(s) : p.1 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1186/1866-1955-4-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Journal of Neurodevelopmental Disorders is now a fully open access journal [Texte imprimé et/ou numérique] / J. PIVEN, Auteur . - p.1. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.1 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1186/1866-1955-4-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Feasibility, reliability, and clinical validity of the Test of Attentional Performance for Children (KiTAP) in Fragile X syndrome (FXS) / A. KNOX in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.2 Titre : Feasibility, reliability, and clinical validity of the Test of Attentional Performance for Children (KiTAP) in Fragile X syndrome (FXS) Type de document : Texte imprimé et/ou numérique Auteurs : A. KNOX, Auteur ; A. SCHNEIDER, Auteur ; F. ABUCAYAN, Auteur ; C. HERVEY, Auteur ; C. TRAN, Auteur ; D. HESSL, Auteur ; Elizabeth BERRY-KRAVIS, Auteur Article en page(s) : p.2 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention and inhibition are core executive-function deficits in FRagile X syndrome (FXS). This pilot study evaluated the feasibility, reproducibility, and clinical relevance of the KiTAP, a computer-based pictorial measure of attention and inhibition with an enchanted-castle theme, in an FXS cohort. METHODS: The 8-subtest KiTAP battery (as many subtests as each could perform) was given to 36 subjects with FXS, of variable age and cognitive/behavioral functioning, and 29 were retested, with an interval of 2 to 4 weeks between sessions. Subjects were rated by parents on the Aberrant Behavior Checklist-Community Edition (ABC-C) and Behavior Assessment System for Children, Second Edition (BASC-2). Feasibility, ceiling and basal effects, and data range and distribution analyses were used to eliminate outliers and invalid data points. Reproducibility of scores was analyzed using intraclass correlation coefficients (ICCs) and validity/clinical relevance was assessed by correlating KiTAP scores with ABC-C and BASC-2 scores. RESULTS: Most of the participants with FXS were able to complete the Alertness, Distractibility, Flexibility, and Go/NoGo subtests.About 50 to 60% completed the Visual Scanning and Vigilance subtests, and 20 to 25% completed the Sustained Attention and Divided Attention subtests. A panel of seven scores from four subtests were identified as feasible for most subjects, lacked excessive ceiling, basal, or learning effects, exhibited an acceptable range and distribution of scores, had good reproducibility (ICC > 0.7), and correlated with behavioral ratings for hyperactivity or attention (P < 0.01). Only minor differences in performance on the KiTAP were seen between mental age-matched cohorts of subjects with FXS and non-FXS intellectual disability. CONCLUSIONS: The KiTAP can be administered to cohorts with FXS over a wide range of function with valid reproducible scores. With additional validation, it could represent a useful outcome measure for assessment of attention/executive-function abilities in clinical trials targeted to these core deficits in FXS. En ligne : http://dx.doi.org/10.1186/1866-1955-4-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Feasibility, reliability, and clinical validity of the Test of Attentional Performance for Children (KiTAP) in Fragile X syndrome (FXS) [Texte imprimé et/ou numérique] / A. KNOX, Auteur ; A. SCHNEIDER, Auteur ; F. ABUCAYAN, Auteur ; C. HERVEY, Auteur ; C. TRAN, Auteur ; D. HESSL, Auteur ; Elizabeth BERRY-KRAVIS, Auteur . - p.2. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.2 Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention and inhibition are core executive-function deficits in FRagile X syndrome (FXS). This pilot study evaluated the feasibility, reproducibility, and clinical relevance of the KiTAP, a computer-based pictorial measure of attention and inhibition with an enchanted-castle theme, in an FXS cohort. METHODS: The 8-subtest KiTAP battery (as many subtests as each could perform) was given to 36 subjects with FXS, of variable age and cognitive/behavioral functioning, and 29 were retested, with an interval of 2 to 4 weeks between sessions. Subjects were rated by parents on the Aberrant Behavior Checklist-Community Edition (ABC-C) and Behavior Assessment System for Children, Second Edition (BASC-2). Feasibility, ceiling and basal effects, and data range and distribution analyses were used to eliminate outliers and invalid data points. Reproducibility of scores was analyzed using intraclass correlation coefficients (ICCs) and validity/clinical relevance was assessed by correlating KiTAP scores with ABC-C and BASC-2 scores. RESULTS: Most of the participants with FXS were able to complete the Alertness, Distractibility, Flexibility, and Go/NoGo subtests.About 50 to 60% completed the Visual Scanning and Vigilance subtests, and 20 to 25% completed the Sustained Attention and Divided Attention subtests. A panel of seven scores from four subtests were identified as feasible for most subjects, lacked excessive ceiling, basal, or learning effects, exhibited an acceptable range and distribution of scores, had good reproducibility (ICC > 0.7), and correlated with behavioral ratings for hyperactivity or attention (P < 0.01). Only minor differences in performance on the KiTAP were seen between mental age-matched cohorts of subjects with FXS and non-FXS intellectual disability. CONCLUSIONS: The KiTAP can be administered to cohorts with FXS over a wide range of function with valid reproducible scores. With additional validation, it could represent a useful outcome measure for assessment of attention/executive-function abilities in clinical trials targeted to these core deficits in FXS. En ligne : http://dx.doi.org/10.1186/1866-1955-4-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Parental phonological memory contributes to prediction of outcome of late talkers from 20 months to 4 years: a longitudinal study of precursors of specific language impairment / Dorothy V. M. BISHOP in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.3 Titre : Parental phonological memory contributes to prediction of outcome of late talkers from 20 months to 4 years: a longitudinal study of precursors of specific language impairment Type de document : Texte imprimé et/ou numérique Auteurs : Dorothy V. M. BISHOP, Auteur ; G. HOLT, Auteur ; E. LINE, Auteur ; D. MCDONALD, Auteur ; S. MCDONALD, Auteur ; H. WATT, Auteur Article en page(s) : p.3 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Many children who are late talkers go on to develop normal language, but others go on to have longer-term language difficulties. In this study, we considered which factors were predictive of persistent problems in late talkers. METHODS: Parental report of expressive vocabulary at 18 months of age was used to select 26 late talkers and 70 average talkers, who were assessed for language and cognitive ability at 20 months of age. Follow-up at 4 years of age was carried out for 24 late and 58 average talkers. A psychometric test battery was used to categorize children in terms of language status (unimpaired or impaired) and nonverbal ability (normal range or more than 1 SD below average). The vocabulary and non-word repetition skills of the accompanying parent were also assessed. RESULTS: Among the late talkers, seven (29%) met our criteria for specific language impairment (SLI) at 4 years of age, and a further two (8%) had low nonverbal ability. In the group of average talkers, eight (14%) met the criteria for SLI at 4 years, and five other children (8%) had low nonverbal ability. Family history of language problems was slightly better than late-talker status as a predictor of SLI.. The best predictors of SLI at 20 months of age were score on the receptive language scale of the Mullen Scales of Early Learning and the parent's performance on a non-word repetition task. Maternal education was not a significant predictor of outcome. CONCLUSIONS: In this study, around three-quarters of late talkers did not have any language difficulties at 4 years of age, provided there was no family history of language impairment. A family history of language-literacy problems was found to be a significant predictor for persisting problems. Nevertheless, there are children with SLI for whom prediction is difficult because they did not have early language delay. En ligne : http://dx.doi.org/10.1186/1866-1955-4-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Parental phonological memory contributes to prediction of outcome of late talkers from 20 months to 4 years: a longitudinal study of precursors of specific language impairment [Texte imprimé et/ou numérique] / Dorothy V. M. BISHOP, Auteur ; G. HOLT, Auteur ; E. LINE, Auteur ; D. MCDONALD, Auteur ; S. MCDONALD, Auteur ; H. WATT, Auteur . - p.3. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.3 Index. décimale : PER Périodiques Résumé : BACKGROUND: Many children who are late talkers go on to develop normal language, but others go on to have longer-term language difficulties. In this study, we considered which factors were predictive of persistent problems in late talkers. METHODS: Parental report of expressive vocabulary at 18 months of age was used to select 26 late talkers and 70 average talkers, who were assessed for language and cognitive ability at 20 months of age. Follow-up at 4 years of age was carried out for 24 late and 58 average talkers. A psychometric test battery was used to categorize children in terms of language status (unimpaired or impaired) and nonverbal ability (normal range or more than 1 SD below average). The vocabulary and non-word repetition skills of the accompanying parent were also assessed. RESULTS: Among the late talkers, seven (29%) met our criteria for specific language impairment (SLI) at 4 years of age, and a further two (8%) had low nonverbal ability. In the group of average talkers, eight (14%) met the criteria for SLI at 4 years, and five other children (8%) had low nonverbal ability. Family history of language problems was slightly better than late-talker status as a predictor of SLI.. The best predictors of SLI at 20 months of age were score on the receptive language scale of the Mullen Scales of Early Learning and the parent's performance on a non-word repetition task. Maternal education was not a significant predictor of outcome. CONCLUSIONS: In this study, around three-quarters of late talkers did not have any language difficulties at 4 years of age, provided there was no family history of language impairment. A family history of language-literacy problems was found to be a significant predictor for persisting problems. Nevertheless, there are children with SLI for whom prediction is difficult because they did not have early language delay. En ligne : http://dx.doi.org/10.1186/1866-1955-4-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Mechanism of nitrogen metabolism-related parameters and enzyme activities in the pathophysiology of autism / G. A. ABU SHMAIS in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.4 Titre : Mechanism of nitrogen metabolism-related parameters and enzyme activities in the pathophysiology of autism Type de document : Texte imprimé et/ou numérique Auteurs : G. A. ABU SHMAIS, Auteur ; Laila Y. AL-AYADHI, Auteur ; A. M. AL-DBASS, Auteur ; A. K. EL-ANSARY, Auteur Article en page(s) : p.4 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: There is evidence that impaired metabolism play an important role in the etiology of many neuropsychiatric disorders. Although this has not been investigated to date, several recent studies proposed that nitrogen metabolism-related parameters may have a pathophysiological role in autism. METHODS: The study enrolled 20 Saudi boys with autism aged 4 to 12 years and 20 healthy controls matched for age and gender. Levels of creatine, urea, ammonia, gamma-aminobutyric acid (GABA), glutamate:glutamine (Glu:Gln) ratio, and enzymatic activities of glutamate dehydrogenase, 5'-nucleotidase, and adenosine deaminase (ADA) were determined in plasma samples from both groups. RESULTS: We found a significant elevation of creatine, 5'-nucleotidase, GABA, and glutamic acid and a significant decrease in the enzymatic activity of ADA and glutamine level in patients with autism compared with healthy controls. The most significant variation between the two groups was found in the Glu:Gln ratio. CONCLUSION: A raised Glu:Gln ratio together with positive correlations in creatine, GABA, and 5'-nucleotidase levels could contribute to the pathophysiology of autism, and might be useful diagnostic markers. The mechanism through which these parameters might be related to autism is discussed in detail. En ligne : http://dx.doi.org/10.1186/1866-1955-4-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Mechanism of nitrogen metabolism-related parameters and enzyme activities in the pathophysiology of autism [Texte imprimé et/ou numérique] / G. A. ABU SHMAIS, Auteur ; Laila Y. AL-AYADHI, Auteur ; A. M. AL-DBASS, Auteur ; A. K. EL-ANSARY, Auteur . - p.4. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.4 Index. décimale : PER Périodiques Résumé : BACKGROUND: There is evidence that impaired metabolism play an important role in the etiology of many neuropsychiatric disorders. Although this has not been investigated to date, several recent studies proposed that nitrogen metabolism-related parameters may have a pathophysiological role in autism. METHODS: The study enrolled 20 Saudi boys with autism aged 4 to 12 years and 20 healthy controls matched for age and gender. Levels of creatine, urea, ammonia, gamma-aminobutyric acid (GABA), glutamate:glutamine (Glu:Gln) ratio, and enzymatic activities of glutamate dehydrogenase, 5'-nucleotidase, and adenosine deaminase (ADA) were determined in plasma samples from both groups. RESULTS: We found a significant elevation of creatine, 5'-nucleotidase, GABA, and glutamic acid and a significant decrease in the enzymatic activity of ADA and glutamine level in patients with autism compared with healthy controls. The most significant variation between the two groups was found in the Glu:Gln ratio. CONCLUSION: A raised Glu:Gln ratio together with positive correlations in creatine, GABA, and 5'-nucleotidase levels could contribute to the pathophysiology of autism, and might be useful diagnostic markers. The mechanism through which these parameters might be related to autism is discussed in detail. En ligne : http://dx.doi.org/10.1186/1866-1955-4-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

A cross-sectional study of the development of volitional control of spatial attention in children with chromosome 22q11.2 deletion syndrome / H. M. SHAPIRO in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.5 Titre : A cross-sectional study of the development of volitional control of spatial attention in children with chromosome 22q11.2 deletion syndrome Type de document : Texte imprimé et/ou numérique Auteurs : H. M. SHAPIRO, Auteur ; Y. TAKARAE, Auteur ; D. J. HARVEY, Auteur ; M. H. CABARAL, Auteur ; T. J. SIMON, Auteur Article en page(s) : p.5 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Chromosome 22q11.2 deletion syndrome (22q11.2DS) results from a 1.5- to 3-megabase deletion on the long arm of chromosome 22 and occurs in approximately 1 in 4000 live births. Previous studies indicate that children with 22q11.2DS are impaired on tasks involving spatial attention. However, the degree to which these impairments are due to volitionally generated (endogenous) or reflexive (exogenous) orienting of attention is unclear. Additionally, the efficacy of these component attention processes throughout child development in 22q11.2DS has yet to be examined. METHODS: Here we compared the performance of a wide age range (7 to 14 years) of children with 22q11.2DS to typically developing (TD) children on a comprehensive visual cueing paradigm to dissociate the contributions of endogenous and exogenous attentional impairments. Paired and two-sample t-tests were used to compare outcome measures within a group or between groups. Additionally, repeated measures regression models were fit to the data in order to examine effects of age on performance. RESULTS: We found that children with 22q11.2DS were impaired on a cueing task with an endogenous cue, but not on the same task with an exogenous cue. Additionally, it was younger children exclusively who were impaired on endogenous cueing when compared to age-matched TD children. Older children with 22q11.2DS performed comparably to age-matched TD peers on the endogenous cueing task. CONCLUSIONS: These results suggest that endogenous but not exogenous orienting of attention is selectively impaired in children with 22q11.2DS. Additionally, the age effect on cueing in children with 22q11.2DS suggests a possible altered developmental trajectory of endogenous cueing. En ligne : http://dx.doi.org/10.1186/1866-1955-4-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] A cross-sectional study of the development of volitional control of spatial attention in children with chromosome 22q11.2 deletion syndrome [Texte imprimé et/ou numérique] / H. M. SHAPIRO, Auteur ; Y. TAKARAE, Auteur ; D. J. HARVEY, Auteur ; M. H. CABARAL, Auteur ; T. J. SIMON, Auteur . - p.5. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.5 Index. décimale : PER Périodiques Résumé : BACKGROUND: Chromosome 22q11.2 deletion syndrome (22q11.2DS) results from a 1.5- to 3-megabase deletion on the long arm of chromosome 22 and occurs in approximately 1 in 4000 live births. Previous studies indicate that children with 22q11.2DS are impaired on tasks involving spatial attention. However, the degree to which these impairments are due to volitionally generated (endogenous) or reflexive (exogenous) orienting of attention is unclear. Additionally, the efficacy of these component attention processes throughout child development in 22q11.2DS has yet to be examined. METHODS: Here we compared the performance of a wide age range (7 to 14 years) of children with 22q11.2DS to typically developing (TD) children on a comprehensive visual cueing paradigm to dissociate the contributions of endogenous and exogenous attentional impairments. Paired and two-sample t-tests were used to compare outcome measures within a group or between groups. Additionally, repeated measures regression models were fit to the data in order to examine effects of age on performance. RESULTS: We found that children with 22q11.2DS were impaired on a cueing task with an endogenous cue, but not on the same task with an exogenous cue. Additionally, it was younger children exclusively who were impaired on endogenous cueing when compared to age-matched TD children. Older children with 22q11.2DS performed comparably to age-matched TD peers on the endogenous cueing task. CONCLUSIONS: These results suggest that endogenous but not exogenous orienting of attention is selectively impaired in children with 22q11.2DS. Additionally, the age effect on cueing in children with 22q11.2DS suggests a possible altered developmental trajectory of endogenous cueing. En ligne : http://dx.doi.org/10.1186/1866-1955-4-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Impaired multiple object tracking in children with chromosome 22q11.2 deletion syndrome / M. H. CABARAL in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.6 Titre : Impaired multiple object tracking in children with chromosome 22q11.2 deletion syndrome Type de document : Texte imprimé et/ou numérique Auteurs : M. H. CABARAL, Auteur ; Elliott A. BEATON, Auteur ; J. STODDARD, Auteur ; T. J. SIMON, Auteur Article en page(s) : p.6 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Chromosome 22q11.2 Deletion Syndrome (22q11.2DS) occurs in approximately 1:4,000 live births with a complex and variable presentation that includes medical, socioemotional and psychological symptoms with intellectual impairment. Cognitive impairments in spatiotemporal and visuospatial attention have also been reported. However, maintenance of selective attention to dynamic and interacting objects has not been systematically investigated in children with 22q11.2DS. METHODS: We used a multiple object tracking task to assay capacity and resolution performance of children with 22q11.2DS aged 7 to 14 years versus age-matched typically developing (TD) peers. RESULTS: Children with 22q11.2DS but not TD children demonstrated impaired performance when task demands increased due to an increase in the number of targets presented, but not from an increase in object speed. Task performance in children with 22q11.2DS was also unrelated to intelligence or measures of attention deficit hyperactivity disorder. CONCLUSIONS: These findings suggest that children with 22q11.2DS may be particularly susceptible to dynamic crowding of objects with increasing cognitive demands related to monitoring multiple targets reflecting a reduced acuity in spatiotemporal cognitive representation. En ligne : http://dx.doi.org/10.1186/1866-1955-4-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Impaired multiple object tracking in children with chromosome 22q11.2 deletion syndrome [Texte imprimé et/ou numérique] / M. H. CABARAL, Auteur ; Elliott A. BEATON, Auteur ; J. STODDARD, Auteur ; T. J. SIMON, Auteur . - p.6. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.6 Index. décimale : PER Périodiques Résumé : BACKGROUND: Chromosome 22q11.2 Deletion Syndrome (22q11.2DS) occurs in approximately 1:4,000 live births with a complex and variable presentation that includes medical, socioemotional and psychological symptoms with intellectual impairment. Cognitive impairments in spatiotemporal and visuospatial attention have also been reported. However, maintenance of selective attention to dynamic and interacting objects has not been systematically investigated in children with 22q11.2DS. METHODS: We used a multiple object tracking task to assay capacity and resolution performance of children with 22q11.2DS aged 7 to 14 years versus age-matched typically developing (TD) peers. RESULTS: Children with 22q11.2DS but not TD children demonstrated impaired performance when task demands increased due to an increase in the number of targets presented, but not from an increase in object speed. Task performance in children with 22q11.2DS was also unrelated to intelligence or measures of attention deficit hyperactivity disorder. CONCLUSIONS: These findings suggest that children with 22q11.2DS may be particularly susceptible to dynamic crowding of objects with increasing cognitive demands related to monitoring multiple targets reflecting a reduced acuity in spatiotemporal cognitive representation. En ligne : http://dx.doi.org/10.1186/1866-1955-4-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Infant siblings and the investigation of autism risk factors / C. J. NEWSCHAFFER in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.7 Titre : Infant siblings and the investigation of autism risk factors Type de document : Texte imprimé et/ou numérique Auteurs : C. J. NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; M. D. FALLIN, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; D. V. NGUYEN, Auteur ; N. L. LEE, Auteur ; C. A. BERRY, Auteur ; H. FARZADEGAN, Auteur ; H. N. HESS, Auteur ; R. J. LANDA, Auteur ; S. E. LEVY, Auteur ; M. L. MASSOLO, Auteur ; S. C. MEYERER, Auteur ; S. M. MOHAMMED, Auteur ; M. C. OLIVER, Auteur ; S. OZONOFF, Auteur ; J. PANDEY, Auteur ; A. SCHROEDER, Auteur ; K. M. SHEDD-WISE, Auteur Article en page(s) : p.7 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Infant sibling studies have been at the vanguard of autism spectrum disorders (ASD) research over the past decade, providing important new knowledge about the earliest emerging signs of ASD and expanding our understanding of the developmental course of this complex disorder. Studies focused on siblings of children with ASD also have unrealized potential for contributing to ASD etiologic research. Moving targeted time of enrollment back from infancy toward conception creates tremendous opportunities for optimally studying risk factors and risk biomarkers during the pre-, peri- and neonatal periods. By doing so, a traditional sibling study, which already incorporates close developmental follow-up of at-risk infants through the third year of life, is essentially reconfigured as an enriched-risk pregnancy cohort study. This review considers the enriched-risk pregnancy cohort approach of studying infant siblings in the context of current thinking on ASD etiologic mechanisms. It then discusses the key features of this approach and provides a description of the design and implementation strategy of one major ASD enriched-risk pregnancy cohort study: the Early Autism Risk Longitudinal Investigation (EARLI). En ligne : http://dx.doi.org/10.1186/1866-1955-4-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Infant siblings and the investigation of autism risk factors [Texte imprimé et/ou numérique] / C. J. NEWSCHAFFER, Auteur ; Lisa A. CROEN, Auteur ; M. D. FALLIN, Auteur ; I. HERTZ-PICCIOTTO, Auteur ; D. V. NGUYEN, Auteur ; N. L. LEE, Auteur ; C. A. BERRY, Auteur ; H. FARZADEGAN, Auteur ; H. N. HESS, Auteur ; R. J. LANDA, Auteur ; S. E. LEVY, Auteur ; M. L. MASSOLO, Auteur ; S. C. MEYERER, Auteur ; S. M. MOHAMMED, Auteur ; M. C. OLIVER, Auteur ; S. OZONOFF, Auteur ; J. PANDEY, Auteur ; A. SCHROEDER, Auteur ; K. M. SHEDD-WISE, Auteur . - p.7. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.7 Index. décimale : PER Périodiques Résumé : Infant sibling studies have been at the vanguard of autism spectrum disorders (ASD) research over the past decade, providing important new knowledge about the earliest emerging signs of ASD and expanding our understanding of the developmental course of this complex disorder. Studies focused on siblings of children with ASD also have unrealized potential for contributing to ASD etiologic research. Moving targeted time of enrollment back from infancy toward conception creates tremendous opportunities for optimally studying risk factors and risk biomarkers during the pre-, peri- and neonatal periods. By doing so, a traditional sibling study, which already incorporates close developmental follow-up of at-risk infants through the third year of life, is essentially reconfigured as an enriched-risk pregnancy cohort study. This review considers the enriched-risk pregnancy cohort approach of studying infant siblings in the context of current thinking on ASD etiologic mechanisms. It then discusses the key features of this approach and provides a description of the design and implementation strategy of one major ASD enriched-risk pregnancy cohort study: the Early Autism Risk Longitudinal Investigation (EARLI). En ligne : http://dx.doi.org/10.1186/1866-1955-4-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Reduced social preferences in autism: evidence from charitable donations / A. LIN in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.8 Titre : Reduced social preferences in autism: evidence from charitable donations Type de document : Texte imprimé et/ou numérique Auteurs : A. LIN, Auteur ; K. TSAI, Auteur ; A. RANGEL, Auteur ; Ralph ADOLPHS, Auteur Article en page(s) : p.8 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: People with autism have abnormal preferences, ranging from an apparent lack of preference for social stimuli to unusually strong preferences for restricted sets of highly idiosyncratic stimuli. Yet the profile of preferences across social and nonsocial domains has not been mapped out in detail, and the processes responsible remain poorly understood. METHODS: To assess preferences across a range of stimuli, we measured real monetary donations to 50 charities spanning categories pertaining to people, mental health, animals, or the environment. We compared the donations made by 16 high-functioning adults with autism to those made by neurotypical controls matched on age, gender and education. We additionally collected ratings of how people evaluated the different charities. RESULTS: Compared with controls, high-functioning adults with autism donated less overall and also showed a significantly disproportionate reduction in donations to people charities compared with donations to the other charities. Furthermore, whereas controls discriminated strongly between different people charities, choosing to donate a lot of money to some and very little to others, much less discrimination was seen in the autism group. Ratings that probed how participants constructed their preferences did not differ between groups, except for a difference in the perceived impact of pictures and text information about people charities. Strikingly, there were some charities related to mental health, and autism in particular, to which the autism group donated considerably more than did the controls. CONCLUSIONS: People with autism were found to have reduced preference and sensitivity towards charities benefiting other people. The findings provide evidence for a domain-specific impairment in social cognition in autism spectrum disorder, and in particular in linking otherwise intact social knowledge to the construction of value signals on which preferences regarding other people are based. En ligne : http://dx.doi.org/10.1186/1866-1955-4-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Reduced social preferences in autism: evidence from charitable donations [Texte imprimé et/ou numérique] / A. LIN, Auteur ; K. TSAI, Auteur ; A. RANGEL, Auteur ; Ralph ADOLPHS, Auteur . - p.8. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.8 Index. décimale : PER Périodiques Résumé : BACKGROUND: People with autism have abnormal preferences, ranging from an apparent lack of preference for social stimuli to unusually strong preferences for restricted sets of highly idiosyncratic stimuli. Yet the profile of preferences across social and nonsocial domains has not been mapped out in detail, and the processes responsible remain poorly understood. METHODS: To assess preferences across a range of stimuli, we measured real monetary donations to 50 charities spanning categories pertaining to people, mental health, animals, or the environment. We compared the donations made by 16 high-functioning adults with autism to those made by neurotypical controls matched on age, gender and education. We additionally collected ratings of how people evaluated the different charities. RESULTS: Compared with controls, high-functioning adults with autism donated less overall and also showed a significantly disproportionate reduction in donations to people charities compared with donations to the other charities. Furthermore, whereas controls discriminated strongly between different people charities, choosing to donate a lot of money to some and very little to others, much less discrimination was seen in the autism group. Ratings that probed how participants constructed their preferences did not differ between groups, except for a difference in the perceived impact of pictures and text information about people charities. Strikingly, there were some charities related to mental health, and autism in particular, to which the autism group donated considerably more than did the controls. CONCLUSIONS: People with autism were found to have reduced preference and sensitivity towards charities benefiting other people. The findings provide evidence for a domain-specific impairment in social cognition in autism spectrum disorder, and in particular in linking otherwise intact social knowledge to the construction of value signals on which preferences regarding other people are based. En ligne : http://dx.doi.org/10.1186/1866-1955-4-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Response of neural reward regions to food cues in autism spectrum disorders / Carissa J. CASCIO in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.9 Titre : Response of neural reward regions to food cues in autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : Carissa J. CASCIO, Auteur ; J. H. FOSS-FEIG, Auteur ; J. L. HEACOCK, Auteur ; C. R. NEWSOM, Auteur ; R. L. COWAN, Auteur ; M. M. BENNINGFIELD, Auteur ; B. P. ROGERS, Auteur ; A. CAO, Auteur Article en page(s) : p.9 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: One hypothesis for the social deficits that characterize autism spectrum disorders (ASD) is diminished neural reward response to social interaction and attachment. Prior research using established monetary reward paradigms as a test of non-social reward to compare with social reward may involve confounds in the ability of individuals with ASD to utilize symbolic representation of money and the abstraction required to interpret monetary gains. Thus, a useful addition to our understanding of neural reward circuitry in ASD includes a characterization of the neural response to primary rewards. METHOD: We asked 17 children with ASD and 18 children without ASD to abstain from eating for at least four hours before an MRI scan in which they viewed images of high-calorie foods. We assessed the neural reward network for increases in the blood oxygenation level dependent (BOLD) signal in response to the food images RESULTS: We found very similar patterns of increased BOLD signal to these images in the two groups; both groups showed increased BOLD signal in the bilateral amygdala, as well as in the nucleus accumbens, orbitofrontal cortex, and insula. Direct group comparisons revealed that the ASD group showed a stronger response to food cues in bilateral insula along the anterior-posterior gradient and in the anterior cingulate cortex than the control group, whereas there were no neural reward regions that showed higher activation for controls than for ASD. CONCLUSION: These results suggest that neural response to primary rewards is not diminished but in fact shows an aberrant enhancement in children with ASD. En ligne : http://dx.doi.org/10.1186/1866-1955-4-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Response of neural reward regions to food cues in autism spectrum disorders [Texte imprimé et/ou numérique] / Carissa J. CASCIO, Auteur ; J. H. FOSS-FEIG, Auteur ; J. L. HEACOCK, Auteur ; C. R. NEWSOM, Auteur ; R. L. COWAN, Auteur ; M. M. BENNINGFIELD, Auteur ; B. P. ROGERS, Auteur ; A. CAO, Auteur . - p.9. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.9 Index. décimale : PER Périodiques Résumé : BACKGROUND: One hypothesis for the social deficits that characterize autism spectrum disorders (ASD) is diminished neural reward response to social interaction and attachment. Prior research using established monetary reward paradigms as a test of non-social reward to compare with social reward may involve confounds in the ability of individuals with ASD to utilize symbolic representation of money and the abstraction required to interpret monetary gains. Thus, a useful addition to our understanding of neural reward circuitry in ASD includes a characterization of the neural response to primary rewards. METHOD: We asked 17 children with ASD and 18 children without ASD to abstain from eating for at least four hours before an MRI scan in which they viewed images of high-calorie foods. We assessed the neural reward network for increases in the blood oxygenation level dependent (BOLD) signal in response to the food images RESULTS: We found very similar patterns of increased BOLD signal to these images in the two groups; both groups showed increased BOLD signal in the bilateral amygdala, as well as in the nucleus accumbens, orbitofrontal cortex, and insula. Direct group comparisons revealed that the ASD group showed a stronger response to food cues in bilateral insula along the anterior-posterior gradient and in the anterior cingulate cortex than the control group, whereas there were no neural reward regions that showed higher activation for controls than for ASD. CONCLUSION: These results suggest that neural response to primary rewards is not diminished but in fact shows an aberrant enhancement in children with ASD. En ligne : http://dx.doi.org/10.1186/1866-1955-4-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Social 'wanting' dysfunction in autism: neurobiological underpinnings and treatment implications / G. KOHLS in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.10 Titre : Social 'wanting' dysfunction in autism: neurobiological underpinnings and treatment implications Type de document : Texte imprimé et/ou numérique Auteurs : G. KOHLS, Auteur ; C. CHEVALLIER, Auteur ; V. TROIANI, Auteur ; Robert T. SCHULTZ, Auteur Article en page(s) : p.10 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Most behavioral training regimens in autism spectrum disorders (ASD) rely on reward-based reinforcement strategies. Although proven to significantly increase both cognitive and social outcomes and successfully reduce aberrant behaviors, this approach fails to benefit a substantial number of affected individuals. Given the enormous amount of clinical and financial resources devoted to behavioral interventions, there is a surprisingly large gap in our knowledge of the basic reward mechanisms of learning in ASD. Understanding the mechanisms for reward responsiveness and reinforcement-based learning is urgently needed to better inform modifications that might improve current treatments. The fundamental goal of this review is to present a fine-grained literature analysis of reward function in ASD with reference to a validated neurobiological model of reward: the 'wanting'/'liking' framework. Despite some inconsistencies within the available literature, the evaluation across three converging sets of neurobiological data (neuroimaging, electrophysiological recordings, and neurochemical measures) reveals good evidence for disrupted reward-seeking tendencies in ASD, particularly in social contexts. This is most likely caused by dysfunction of the dopaminergic-oxytocinergic 'wanting' circuitry, including the ventral striatum, amygdala, and ventromedial prefrontal cortex. Such a conclusion is consistent with predictions derived from diagnostic criteria concerning the core social phenotype of ASD, which emphasize difficulties with spontaneous self-initiated seeking of social encounters (that is, social motivation). Existing studies suggest that social 'wanting' tendencies vary considerably between individuals with ASD, and that the degree of social motivation is both malleable and predictive of intervention response. Although the topic of reward responsiveness in ASD is very new, with much research still needed, the current data clearly point towards problems with incentive-based motivation and learning, with clear and important implications for treatment. Given the reliance of behavioral interventions on reinforcement-based learning principles, we believe that a systematic focus on the integrity of the reward system in ASD promises to yield many important clues, both to the underlying mechanisms causing ASD and to enhancing the efficacy of existing and new interventions. En ligne : http://dx.doi.org/10.1186/1866-1955-4-10 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Social 'wanting' dysfunction in autism: neurobiological underpinnings and treatment implications [Texte imprimé et/ou numérique] / G. KOHLS, Auteur ; C. CHEVALLIER, Auteur ; V. TROIANI, Auteur ; Robert T. SCHULTZ, Auteur . - p.10. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.10 Index. décimale : PER Périodiques Résumé : Most behavioral training regimens in autism spectrum disorders (ASD) rely on reward-based reinforcement strategies. Although proven to significantly increase both cognitive and social outcomes and successfully reduce aberrant behaviors, this approach fails to benefit a substantial number of affected individuals. Given the enormous amount of clinical and financial resources devoted to behavioral interventions, there is a surprisingly large gap in our knowledge of the basic reward mechanisms of learning in ASD. Understanding the mechanisms for reward responsiveness and reinforcement-based learning is urgently needed to better inform modifications that might improve current treatments. The fundamental goal of this review is to present a fine-grained literature analysis of reward function in ASD with reference to a validated neurobiological model of reward: the 'wanting'/'liking' framework. Despite some inconsistencies within the available literature, the evaluation across three converging sets of neurobiological data (neuroimaging, electrophysiological recordings, and neurochemical measures) reveals good evidence for disrupted reward-seeking tendencies in ASD, particularly in social contexts. This is most likely caused by dysfunction of the dopaminergic-oxytocinergic 'wanting' circuitry, including the ventral striatum, amygdala, and ventromedial prefrontal cortex. Such a conclusion is consistent with predictions derived from diagnostic criteria concerning the core social phenotype of ASD, which emphasize difficulties with spontaneous self-initiated seeking of social encounters (that is, social motivation). Existing studies suggest that social 'wanting' tendencies vary considerably between individuals with ASD, and that the degree of social motivation is both malleable and predictive of intervention response. Although the topic of reward responsiveness in ASD is very new, with much research still needed, the current data clearly point towards problems with incentive-based motivation and learning, with clear and important implications for treatment. Given the reliance of behavioral interventions on reinforcement-based learning principles, we believe that a systematic focus on the integrity of the reward system in ASD promises to yield many important clues, both to the underlying mechanisms causing ASD and to enhancing the efficacy of existing and new interventions. En ligne : http://dx.doi.org/10.1186/1866-1955-4-10 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Social attention: a possible early indicator of efficacy in autism clinical trials / G. DAWSON in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.11 Titre : Social attention: a possible early indicator of efficacy in autism clinical trials Type de document : Texte imprimé et/ou numérique Auteurs : G. DAWSON, Auteur ; Raphael BERNIER, Auteur ; R. H. RING, Auteur Article en page(s) : p.11 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : For decades, researchers have sought to clarify the nature of the social communication impairments in autism, highlighting impaired or atypical 'social attention' as a key measurable construct that helps to define the core impairment of social communication. In this paper, we provide an overview of research on social attention impairments in autism and their relation to deficiencies in neural circuitry related to social reward. We offer a framework for considering social attention as a potential moderator or mediator of response to early behavioral intervention, and as an early indicator of efficacy of behavioral and/or pharmacological treatments aimed at addressing the social impairments in autism. En ligne : http://dx.doi.org/10.1186/1866-1955-4-11 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Social attention: a possible early indicator of efficacy in autism clinical trials [Texte imprimé et/ou numérique] / G. DAWSON, Auteur ; Raphael BERNIER, Auteur ; R. H. RING, Auteur . - p.11. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.11 Index. décimale : PER Périodiques Résumé : For decades, researchers have sought to clarify the nature of the social communication impairments in autism, highlighting impaired or atypical 'social attention' as a key measurable construct that helps to define the core impairment of social communication. In this paper, we provide an overview of research on social attention impairments in autism and their relation to deficiencies in neural circuitry related to social reward. We offer a framework for considering social attention as a potential moderator or mediator of response to early behavioral intervention, and as an early indicator of efficacy of behavioral and/or pharmacological treatments aimed at addressing the social impairments in autism. En ligne : http://dx.doi.org/10.1186/1866-1955-4-11 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Comparison of spatial working memory in children with prenatal alcohol exposure and those diagnosed with ADHD; A functional magnetic resonance imaging study / K. L. MALISZA in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.12 Titre : Comparison of spatial working memory in children with prenatal alcohol exposure and those diagnosed with ADHD; A functional magnetic resonance imaging study Type de document : Texte imprimé et/ou numérique Auteurs : K. L. MALISZA, Auteur ; J. L. BUSS, Auteur ; R. B. BOLSTER, Auteur ; P. D. DE GERVAI, Auteur ; L. WOODS-FROHLICH, Auteur ; R. SUMMERS, Auteur ; C. A. CLANCY, Auteur ; A. E. CHUDLEY, Auteur ; S. LONGSTAFFE, Auteur Article en page(s) : p.12 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Alcohol related neurodevelopmental disorder (ARND) falls under the umbrella of fetal alcohol spectrum disorder (FASD), but individuals do not demonstrate the facial characteristics associated with fetal alcohol syndrome (FAS), making diagnosis difficult. While attentional problems in ARND are similar to those found in attention-deficit/hyperactivity disorder (ADHD), the underlying impairment in attention pathways may be different. METHODS: Functional magnetic resonance imaging (fMRI) of a working memory (1-back) task of 63 children, 10 to 14 years old, diagnosed with ARND and ADHD, as well as typically developing (TD) controls, was conducted at 3 T. Diffusion tensor imaging (DTI) data were also acquired. RESULTS: Activations were observed in posterior parietal and occipital regions in the TD group and in dorsolateral prefrontal and posterior parietal regions in the ARND group, whereas the ADHD group activated only dorsolateral prefrontal regions, during the working memory component of the task (1-back minus 0-back contrast). The increases in frontal and parietal activity were significantly greater in the ARND group compared to the other groups. This increased activity was associated with reduced accuracy and increased response time variability, suggesting that ARND subjects exert greater effort to manage short-term memory load. Significantly greater intra-subject variability, demonstrated by fMRI region-of-interest analysis, in the ADHD and ARND groups compared to the TD group suggests that moment-to-moment lapses in attention contributed to their poorer task performance. Differences in functional activity in ARND subjects with and without a diagnosis of ADHD resulted primarily from reduced activation by the ARND/ADHD + group during the 0-back task. In contrast, children with ADHD alone clearly showed reduced activations during the 1-back task. DTI analysis revealed that the TD group had significantly higher total tract volume and number of fibers than the ARND group. These measures were negatively correlated with errors on the 1-back task, suggesting a link between white matter integrity and task performance. CONCLUSIONS: fMRI activations suggest that the similar behavior of children with ARND and ADHD on a spatial working memory task is the result of different cognitive events. The nature of ADHD in children with ARND appears to differ from that of children with ADHD alone. En ligne : http://dx.doi.org/10.1186/1866-1955-4-12 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Comparison of spatial working memory in children with prenatal alcohol exposure and those diagnosed with ADHD; A functional magnetic resonance imaging study [Texte imprimé et/ou numérique] / K. L. MALISZA, Auteur ; J. L. BUSS, Auteur ; R. B. BOLSTER, Auteur ; P. D. DE GERVAI, Auteur ; L. WOODS-FROHLICH, Auteur ; R. SUMMERS, Auteur ; C. A. CLANCY, Auteur ; A. E. CHUDLEY, Auteur ; S. LONGSTAFFE, Auteur . - p.12. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.12 Index. décimale : PER Périodiques Résumé : BACKGROUND: Alcohol related neurodevelopmental disorder (ARND) falls under the umbrella of fetal alcohol spectrum disorder (FASD), but individuals do not demonstrate the facial characteristics associated with fetal alcohol syndrome (FAS), making diagnosis difficult. While attentional problems in ARND are similar to those found in attention-deficit/hyperactivity disorder (ADHD), the underlying impairment in attention pathways may be different. METHODS: Functional magnetic resonance imaging (fMRI) of a working memory (1-back) task of 63 children, 10 to 14 years old, diagnosed with ARND and ADHD, as well as typically developing (TD) controls, was conducted at 3 T. Diffusion tensor imaging (DTI) data were also acquired. RESULTS: Activations were observed in posterior parietal and occipital regions in the TD group and in dorsolateral prefrontal and posterior parietal regions in the ARND group, whereas the ADHD group activated only dorsolateral prefrontal regions, during the working memory component of the task (1-back minus 0-back contrast). The increases in frontal and parietal activity were significantly greater in the ARND group compared to the other groups. This increased activity was associated with reduced accuracy and increased response time variability, suggesting that ARND subjects exert greater effort to manage short-term memory load. Significantly greater intra-subject variability, demonstrated by fMRI region-of-interest analysis, in the ADHD and ARND groups compared to the TD group suggests that moment-to-moment lapses in attention contributed to their poorer task performance. Differences in functional activity in ARND subjects with and without a diagnosis of ADHD resulted primarily from reduced activation by the ARND/ADHD + group during the 0-back task. In contrast, children with ADHD alone clearly showed reduced activations during the 1-back task. DTI analysis revealed that the TD group had significantly higher total tract volume and number of fibers than the ARND group. These measures were negatively correlated with errors on the 1-back task, suggesting a link between white matter integrity and task performance. CONCLUSIONS: fMRI activations suggest that the similar behavior of children with ARND and ADHD on a spatial working memory task is the result of different cognitive events. The nature of ADHD in children with ARND appears to differ from that of children with ADHD alone. En ligne : http://dx.doi.org/10.1186/1866-1955-4-12 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Adults with autism spectrum disorders exhibit decreased sensitivity to reward parameters when making effort-based decisions / Cara R. DAMIANO in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.13 Titre : Adults with autism spectrum disorders exhibit decreased sensitivity to reward parameters when making effort-based decisions Type de document : Texte imprimé et/ou numérique Auteurs : Cara R. DAMIANO, Auteur ; Joseph ALOI, Auteur ; M. TREADWAY, Auteur ; James W. BODFISH, Auteur ; Gabriel S. DICHTER, Auteur Article en page(s) : p.13 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Efficient effort expenditure to obtain rewards is critical for optimal goal-directed behavior and learning. Clinical observation suggests that individuals with autism spectrum disorders (ASD) may show dysregulated reward-based effort expenditure, but no behavioral study to date has assessed effort-based decision-making in ASD. METHODS: The current study compared a group of adults with ASD to a group of typically developing adults on the Effort Expenditure for Rewards Task (EEfRT), a behavioral measure of effort-based decision-making. In this task, participants were provided with the probability of receiving a monetary reward on a particular trial and asked to choose between either an "easy task" (less motoric effort) for a small, stable reward or a "hard task" (greater motoric effort) for a variable but consistently larger reward. RESULTS: Participants with ASD chose the hard task more frequently than did the control group, yet were less influenced by differences in reward value and probability than the control group. Additionally, effort-based decision-making was related to repetitive behavior symptoms across both groups. CONCLUSIONS: These results suggest that individuals with ASD may be more willing to expend effort to obtain a monetary reward regardless of the reward contingencies. More broadly, results suggest that behavioral choices may be less influenced by information about reward contingencies in individuals with ASD. This atypical pattern of effort-based decision-making may be relevant for understanding the heightened reward motivation for circumscribed interests in ASD. En ligne : http://dx.doi.org/10.1186/1866-1955-4-13 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Adults with autism spectrum disorders exhibit decreased sensitivity to reward parameters when making effort-based decisions [Texte imprimé et/ou numérique] / Cara R. DAMIANO, Auteur ; Joseph ALOI, Auteur ; M. TREADWAY, Auteur ; James W. BODFISH, Auteur ; Gabriel S. DICHTER, Auteur . - p.13. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.13 Index. décimale : PER Périodiques Résumé : BACKGROUND: Efficient effort expenditure to obtain rewards is critical for optimal goal-directed behavior and learning. Clinical observation suggests that individuals with autism spectrum disorders (ASD) may show dysregulated reward-based effort expenditure, but no behavioral study to date has assessed effort-based decision-making in ASD. METHODS: The current study compared a group of adults with ASD to a group of typically developing adults on the Effort Expenditure for Rewards Task (EEfRT), a behavioral measure of effort-based decision-making. In this task, participants were provided with the probability of receiving a monetary reward on a particular trial and asked to choose between either an "easy task" (less motoric effort) for a small, stable reward or a "hard task" (greater motoric effort) for a variable but consistently larger reward. RESULTS: Participants with ASD chose the hard task more frequently than did the control group, yet were less influenced by differences in reward value and probability than the control group. Additionally, effort-based decision-making was related to repetitive behavior symptoms across both groups. CONCLUSIONS: These results suggest that individuals with ASD may be more willing to expend effort to obtain a monetary reward regardless of the reward contingencies. More broadly, results suggest that behavioral choices may be less influenced by information about reward contingencies in individuals with ASD. This atypical pattern of effort-based decision-making may be relevant for understanding the heightened reward motivation for circumscribed interests in ASD. En ligne : http://dx.doi.org/10.1186/1866-1955-4-13 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

New approaches to investigating social gestures in autism spectrum disorder / K. T. KISHIDA in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.14 Titre : New approaches to investigating social gestures in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : K. T. KISHIDA, Auteur ; J. LI, Auteur ; J. SCHWIND, Auteur ; P. R. MONTAGUE, Auteur Article en page(s) : p.14 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The combination of economic games and human neuroimaging presents the possibility of using economic probes to identify biomarkers for quantitative features of healthy and diseased cognition. These probes span a range of important cognitive functions, but one new use is in the domain of reciprocating social exchange with other humans - a capacity perturbed in a number of psychopathologies. We summarize the use of a reciprocating exchange game to elicit neural and behavioral signatures for subjects diagnosed with autism spectrum disorder (ASD). Furthermore, we outline early efforts to capture features of social exchange in computational models and use these to identify quantitative behavioral differences between subjects with ASD and matched controls. Lastly, we summarize a number of subsequent studies inspired by the modeling results, which suggest new neural and behavioral signatures that could be used to characterize subtle deficits in information processing during interactions with other humans. En ligne : http://dx.doi.org/10.1186/1866-1955-4-14 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] New approaches to investigating social gestures in autism spectrum disorder [Texte imprimé et/ou numérique] / K. T. KISHIDA, Auteur ; J. LI, Auteur ; J. SCHWIND, Auteur ; P. R. MONTAGUE, Auteur . - p.14. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.14 Index. décimale : PER Périodiques Résumé : The combination of economic games and human neuroimaging presents the possibility of using economic probes to identify biomarkers for quantitative features of healthy and diseased cognition. These probes span a range of important cognitive functions, but one new use is in the domain of reciprocating social exchange with other humans - a capacity perturbed in a number of psychopathologies. We summarize the use of a reciprocating exchange game to elicit neural and behavioral signatures for subjects diagnosed with autism spectrum disorder (ASD). Furthermore, we outline early efforts to capture features of social exchange in computational models and use these to identify quantitative behavioral differences between subjects with ASD and matched controls. Lastly, we summarize a number of subsequent studies inspired by the modeling results, which suggest new neural and behavioral signatures that could be used to characterize subtle deficits in information processing during interactions with other humans. En ligne : http://dx.doi.org/10.1186/1866-1955-4-14 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Association testing of copy number variants in schizophrenia and autism spectrum disorders / Bernard CRESPI in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.15 Titre : Association testing of copy number variants in schizophrenia and autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : Bernard CRESPI, Auteur ; H. J. CROFTS, Auteur Article en page(s) : p.15 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders and schizophrenia have been associated with an overlapping set of copy number variant loci, but the nature and degree of overlap in copy number variants (deletions compared to duplications) between these two disorders remains unclear. METHODS: We systematically evaluated three lines of evidence: (1) the statistical bases for associations of autism spectrum disorders and schizophrenia with a set of the primary CNVs thus far investigated, from previous studies; (2) data from case series studies on the occurrence of these CNVs in autism spectrum disorders, especially among children, and (3) data on the extent to which the CNVs were associated with intellectual disability and developmental, speech, or language delays. We also conducted new analyses of existing data on these CNVs in autism by pooling data from seven case control studies. RESULTS: Four of the CNVs considered, dup 1q21.1, dup 15q11-q13, del 16p11.2, and dup 22q11.21, showed clear statistical evidence as autism risk factors, whereas eight CNVs, del 1q21.1, del 3q29, del 15q11.2, del 15q13.3, dup 16p11.2, dup 16p13.1, del 17p12, and del 22q11.21, were strongly statistically supported as risk factors for schizophrenia. Three of the CNVs, dup 1q21.1, dup 16p11.2, and dup 16p13.1, exhibited statistical support as risk factors for both autism and schizophrenia, although for each of these CNVs statistical significance was nominal for tests involving one of the two disorders. For the CNVs that were statistically associated with schizophrenia but were not statistically associated with autism, a notable number of children with the CNVs have been diagnosed with autism or ASD; children with these CNVs also demonstrate a high incidence of intellectual disability and developmental, speech, or language delays. CONCLUSIONS: These findings suggest that although CNV loci notably overlap between autism and schizophrenia, the degree of strongly statistically supported overlap in specific CNVs at these loci remains limited. These analyses also suggest that relatively severe premorbidity to CNV-associated schizophrenia in children may sometimes be diagnosed as autism spectrum disorder. En ligne : http://dx.doi.org/10.1186/1866-1955-4-15 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Association testing of copy number variants in schizophrenia and autism spectrum disorders [Texte imprimé et/ou numérique] / Bernard CRESPI, Auteur ; H. J. CROFTS, Auteur . - p.15. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.15 Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders and schizophrenia have been associated with an overlapping set of copy number variant loci, but the nature and degree of overlap in copy number variants (deletions compared to duplications) between these two disorders remains unclear. METHODS: We systematically evaluated three lines of evidence: (1) the statistical bases for associations of autism spectrum disorders and schizophrenia with a set of the primary CNVs thus far investigated, from previous studies; (2) data from case series studies on the occurrence of these CNVs in autism spectrum disorders, especially among children, and (3) data on the extent to which the CNVs were associated with intellectual disability and developmental, speech, or language delays. We also conducted new analyses of existing data on these CNVs in autism by pooling data from seven case control studies. RESULTS: Four of the CNVs considered, dup 1q21.1, dup 15q11-q13, del 16p11.2, and dup 22q11.21, showed clear statistical evidence as autism risk factors, whereas eight CNVs, del 1q21.1, del 3q29, del 15q11.2, del 15q13.3, dup 16p11.2, dup 16p13.1, del 17p12, and del 22q11.21, were strongly statistically supported as risk factors for schizophrenia. Three of the CNVs, dup 1q21.1, dup 16p11.2, and dup 16p13.1, exhibited statistical support as risk factors for both autism and schizophrenia, although for each of these CNVs statistical significance was nominal for tests involving one of the two disorders. For the CNVs that were statistically associated with schizophrenia but were not statistically associated with autism, a notable number of children with the CNVs have been diagnosed with autism or ASD; children with these CNVs also demonstrate a high incidence of intellectual disability and developmental, speech, or language delays. CONCLUSIONS: These findings suggest that although CNV loci notably overlap between autism and schizophrenia, the degree of strongly statistically supported overlap in specific CNVs at these loci remains limited. These analyses also suggest that relatively severe premorbidity to CNV-associated schizophrenia in children may sometimes be diagnosed as autism spectrum disorder. En ligne : http://dx.doi.org/10.1186/1866-1955-4-15 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Preserved reward outcome processing in ASD as revealed by event-related potentials / J. C. MCPARTLAND in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.16 Titre : Preserved reward outcome processing in ASD as revealed by event-related potentials Type de document : Texte imprimé et/ou numérique Auteurs : J. C. MCPARTLAND, Auteur ; M. J. CROWLEY, Auteur ; D. R. PERSZYK, Auteur ; C. E. MUKERJI, Auteur ; A. J. NAPLES, Auteur ; J. WU, Auteur ; L. C. MAYES, Auteur Article en page(s) : p.16 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Problems with reward system function have been posited as a primary difficulty in autism spectrum disorders. The current study examined an electrophysiological marker of feedback monitoring, the feedback-related negativity (FRN), during a monetary reward task. The study advanced prior understanding by focusing exclusively on a developmental sample, applying rigorous diagnostic characterization and introducing an experimental paradigm providing more subtly different feedback valence (reward versus non-reward instead of reward versus loss). METHODS: Twenty-six children with autism spectrum disorder and 28 typically developing peers matched on age and full-scale IQ played a guessing game resulting in monetary gain ("win") or neutral outcome ("draw"). ERP components marking early visual processing (N1, P2) and feedback appraisal (FRN) were contrasted between groups in each condition, and their relationships to behavioral measures of social function and dysfunction, social anxiety, and autism symptomatology were explored. RESULTS: FRN was observed on draw trials relative to win trials. Consistent with prior research, children with ASD exhibited a FRN to suboptimal outcomes that was comparable to typical peers. ERP parameters were unrelated to behavioral measures. CONCLUSIONS: Results of the current study indicate typical patterns of feedback monitoring in the context of monetary reward in ASD. The study extends prior findings of normative feedback monitoring to a sample composed exclusively of children and demonstrates that, as in typical development, individuals with autism exhibit a FRN to suboptimal outcomes, irrespective of neutral or negative valence. Results do not support a pervasive problem with reward system function in ASD, instead suggesting any dysfunction lies in more specific domains, such as social perception, or in response to particular feedback-monitoring contexts, such as self-evaluation of one's errors. En ligne : http://dx.doi.org/10.1186/1866-1955-4-16 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Preserved reward outcome processing in ASD as revealed by event-related potentials [Texte imprimé et/ou numérique] / J. C. MCPARTLAND, Auteur ; M. J. CROWLEY, Auteur ; D. R. PERSZYK, Auteur ; C. E. MUKERJI, Auteur ; A. J. NAPLES, Auteur ; J. WU, Auteur ; L. C. MAYES, Auteur . - p.16. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.16 Index. décimale : PER Périodiques Résumé : BACKGROUND: Problems with reward system function have been posited as a primary difficulty in autism spectrum disorders. The current study examined an electrophysiological marker of feedback monitoring, the feedback-related negativity (FRN), during a monetary reward task. The study advanced prior understanding by focusing exclusively on a developmental sample, applying rigorous diagnostic characterization and introducing an experimental paradigm providing more subtly different feedback valence (reward versus non-reward instead of reward versus loss). METHODS: Twenty-six children with autism spectrum disorder and 28 typically developing peers matched on age and full-scale IQ played a guessing game resulting in monetary gain ("win") or neutral outcome ("draw"). ERP components marking early visual processing (N1, P2) and feedback appraisal (FRN) were contrasted between groups in each condition, and their relationships to behavioral measures of social function and dysfunction, social anxiety, and autism symptomatology were explored. RESULTS: FRN was observed on draw trials relative to win trials. Consistent with prior research, children with ASD exhibited a FRN to suboptimal outcomes that was comparable to typical peers. ERP parameters were unrelated to behavioral measures. CONCLUSIONS: Results of the current study indicate typical patterns of feedback monitoring in the context of monetary reward in ASD. The study extends prior findings of normative feedback monitoring to a sample composed exclusively of children and demonstrates that, as in typical development, individuals with autism exhibit a FRN to suboptimal outcomes, irrespective of neutral or negative valence. Results do not support a pervasive problem with reward system function in ASD, instead suggesting any dysfunction lies in more specific domains, such as social perception, or in response to particular feedback-monitoring contexts, such as self-evaluation of one's errors. En ligne : http://dx.doi.org/10.1186/1866-1955-4-16 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Abnormal social reward processing in autism as indexed by pupillary responses to happy faces / L. SEPETA in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.17 Titre : Abnormal social reward processing in autism as indexed by pupillary responses to happy faces Type de document : Texte imprimé et/ou numérique Auteurs : L. SEPETA, Auteur ; N. TSUCHIYA, Auteur ; M. S. DAVIES, Auteur ; M. SIGMAN, Auteur ; Susan Y. BOOKHEIMER, Auteur ; Mirella DAPRETTO, Auteur Article en page(s) : p.17 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Individuals with Autism Spectrum Disorders (ASD) typically show impaired eye contact during social interactions. From a young age, they look less at faces than typically developing (TD) children and tend to avoid direct gaze. However, the reason for this behavior remains controversial; ASD children might avoid eye contact because they perceive the eyes as aversive or because they do not find social engagement through mutual gaze rewarding. METHODS: We monitored pupillary diameter as a measure of autonomic response in children with ASD (n = 20, mean age = 12.4) and TD controls (n = 18, mean age = 13.7) while they looked at faces displaying different emotions. Each face displayed happy, fearful, angry or neutral emotions with the gaze either directed to or averted from the subjects. RESULTS: Overall, children with ASD and TD controls showed similar pupillary responses; however, they differed significantly in their sensitivity to gaze direction for happy faces. Specifically, pupillary diameter increased among TD children when viewing happy faces with direct gaze as compared to those with averted gaze, whereas children with ASD did not show such sensitivity to gaze direction. We found no group differences in fixation that could explain the differential pupillary responses. There was no effect of gaze direction on pupil diameter for negative affect or neutral faces among either the TD or ASD group. CONCLUSIONS: We interpret the increased pupillary diameter to happy faces with direct gaze in TD children to reflect the intrinsic reward value of a smiling face looking directly at an individual. The lack of this effect in children with ASD is consistent with the hypothesis that individuals with ASD may have reduced sensitivity to the reward value of social stimuli. En ligne : http://dx.doi.org/10.1186/1866-1955-4-17 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Abnormal social reward processing in autism as indexed by pupillary responses to happy faces [Texte imprimé et/ou numérique] / L. SEPETA, Auteur ; N. TSUCHIYA, Auteur ; M. S. DAVIES, Auteur ; M. SIGMAN, Auteur ; Susan Y. BOOKHEIMER, Auteur ; Mirella DAPRETTO, Auteur . - p.17. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.17 Index. décimale : PER Périodiques Résumé : BACKGROUND: Individuals with Autism Spectrum Disorders (ASD) typically show impaired eye contact during social interactions. From a young age, they look less at faces than typically developing (TD) children and tend to avoid direct gaze. However, the reason for this behavior remains controversial; ASD children might avoid eye contact because they perceive the eyes as aversive or because they do not find social engagement through mutual gaze rewarding. METHODS: We monitored pupillary diameter as a measure of autonomic response in children with ASD (n = 20, mean age = 12.4) and TD controls (n = 18, mean age = 13.7) while they looked at faces displaying different emotions. Each face displayed happy, fearful, angry or neutral emotions with the gaze either directed to or averted from the subjects. RESULTS: Overall, children with ASD and TD controls showed similar pupillary responses; however, they differed significantly in their sensitivity to gaze direction for happy faces. Specifically, pupillary diameter increased among TD children when viewing happy faces with direct gaze as compared to those with averted gaze, whereas children with ASD did not show such sensitivity to gaze direction. We found no group differences in fixation that could explain the differential pupillary responses. There was no effect of gaze direction on pupil diameter for negative affect or neutral faces among either the TD or ASD group. CONCLUSIONS: We interpret the increased pupillary diameter to happy faces with direct gaze in TD children to reflect the intrinsic reward value of a smiling face looking directly at an individual. The lack of this effect in children with ASD is consistent with the hypothesis that individuals with ASD may have reduced sensitivity to the reward value of social stimuli. En ligne : http://dx.doi.org/10.1186/1866-1955-4-17 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Long-term alterations of striatal parvalbumin interneurons in a rat model of early exposure to alcohol / A. DE GIORGIO in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.18 Titre : Long-term alterations of striatal parvalbumin interneurons in a rat model of early exposure to alcohol Type de document : Texte imprimé et/ou numérique Auteurs : A. DE GIORGIO, Auteur ; S. E. COMPARINI, Auteur ; F. S. INTRA, Auteur ; A. GRANATO, Auteur Article en page(s) : p.18 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Exposure to alcohol in utero is a known cause of mental retardation. Although a certain degree of motor impairment is always associated with fetal alcohol spectrum disorder, little is known about the neurobiological basis of the defective motor control. We have studied the striatal interneurons containing parvalbumin in a rat model of fetal alcohol spectrum disorder. METHODS: Newborn rats received ethanol by inhalation from postnatal day two through six and parvalbumin striatal neurons were labeled by immunohistochemistry on postnatal day 60. The spatial distribution of parvalbumin interneurons was studied using Voronoi spatial tessellation and their dendritic trees were completely reconstructed. RESULTS: Parvalbumin interneurons of ethanol-treated animals showed a clustered spatial distribution similar to that observed in control animals. The dendritic tree of parvalbumin interneurons was significantly reduced in ethanol-treated animals, as compared with controls. CONCLUSIONS: Striatal parvalbumin interneurons are crucial components of the brain network serving motor control. Therefore, the shrinkage of their dendrites could contribute to the motor and cognitive symptoms observed in fetal alcohol spectrum disorder. En ligne : http://dx.doi.org/10.1186/1866-1955-4-18 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Long-term alterations of striatal parvalbumin interneurons in a rat model of early exposure to alcohol [Texte imprimé et/ou numérique] / A. DE GIORGIO, Auteur ; S. E. COMPARINI, Auteur ; F. S. INTRA, Auteur ; A. GRANATO, Auteur . - p.18. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.18 Index. décimale : PER Périodiques Résumé : BACKGROUND: Exposure to alcohol in utero is a known cause of mental retardation. Although a certain degree of motor impairment is always associated with fetal alcohol spectrum disorder, little is known about the neurobiological basis of the defective motor control. We have studied the striatal interneurons containing parvalbumin in a rat model of fetal alcohol spectrum disorder. METHODS: Newborn rats received ethanol by inhalation from postnatal day two through six and parvalbumin striatal neurons were labeled by immunohistochemistry on postnatal day 60. The spatial distribution of parvalbumin interneurons was studied using Voronoi spatial tessellation and their dendritic trees were completely reconstructed. RESULTS: Parvalbumin interneurons of ethanol-treated animals showed a clustered spatial distribution similar to that observed in control animals. The dendritic tree of parvalbumin interneurons was significantly reduced in ethanol-treated animals, as compared with controls. CONCLUSIONS: Striatal parvalbumin interneurons are crucial components of the brain network serving motor control. Therefore, the shrinkage of their dendrites could contribute to the motor and cognitive symptoms observed in fetal alcohol spectrum disorder. En ligne : http://dx.doi.org/10.1186/1866-1955-4-18 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings / Gabriel S. DICHTER in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.19 Titre : Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings Type de document : Texte imprimé et/ou numérique Auteurs : Gabriel S. DICHTER, Auteur ; C. A. DAMIANO, Auteur ; J. A. ALLEN, Auteur Article en page(s) : p.19 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette's syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader-Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies. En ligne : http://dx.doi.org/10.1186/1866-1955-4-19 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings [Texte imprimé et/ou numérique] / Gabriel S. DICHTER, Auteur ; C. A. DAMIANO, Auteur ; J. A. ALLEN, Auteur . - p.19. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.19 Index. décimale : PER Périodiques Résumé : This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette's syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader-Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies. En ligne : http://dx.doi.org/10.1186/1866-1955-4-19 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Reward processing in autism: a thematic series / Gabriel S. DICHTER in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.20 Titre : Reward processing in autism: a thematic series Type de document : Texte imprimé et/ou numérique Auteurs : Gabriel S. DICHTER, Auteur ; Ralph ADOLPHS, Auteur Article en page(s) : p.20 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This thematic series presents theoretical and empirical papers focused on understanding autism from the perspective of reward processing deficits. Although the core symptoms of autism have not traditionally been conceptualized with respect to altered reward-based processes, it is clear that brain reward circuitry plays a critical role in guiding social and nonsocial learning and behavior throughout development. Additionally, brain reward circuitry may respond to social sources of information in ways that are similar to responses to primary rewards, and recent clinical data consistently suggest abnormal behavioral and neurobiologic responses to rewards in autism. This thematic series presents empirical data and review papers that highlight the utility of considering autism from the perspective of reward processing deficits. Our hope is that this novel framework may further elucidate autism pathophysiology, with the ultimate goal of yielding novel insights with potential therapeutic implications. En ligne : http://dx.doi.org/10.1186/1866-1955-4-20 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Reward processing in autism: a thematic series [Texte imprimé et/ou numérique] / Gabriel S. DICHTER, Auteur ; Ralph ADOLPHS, Auteur . - p.20. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.20 Index. décimale : PER Périodiques Résumé : This thematic series presents theoretical and empirical papers focused on understanding autism from the perspective of reward processing deficits. Although the core symptoms of autism have not traditionally been conceptualized with respect to altered reward-based processes, it is clear that brain reward circuitry plays a critical role in guiding social and nonsocial learning and behavior throughout development. Additionally, brain reward circuitry may respond to social sources of information in ways that are similar to responses to primary rewards, and recent clinical data consistently suggest abnormal behavioral and neurobiologic responses to rewards in autism. This thematic series presents empirical data and review papers that highlight the utility of considering autism from the perspective of reward processing deficits. Our hope is that this novel framework may further elucidate autism pathophysiology, with the ultimate goal of yielding novel insights with potential therapeutic implications. En ligne : http://dx.doi.org/10.1186/1866-1955-4-20 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Of mice and monkeys: using non-human primate models to bridge mouse- and human-based investigations of autism spectrum disorders / K. K. WATSON in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.21 Titre : Of mice and monkeys: using non-human primate models to bridge mouse- and human-based investigations of autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : K. K. WATSON, Auteur ; M. L. PLATT, Auteur Article en page(s) : p.21 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The autism spectrum disorders (ASDs) arise from a diverse array of genetic and environmental origins that disrupt the typical developmental trajectory of neural connectivity and synaptogenesis. ASDs are marked by dysfunctional social behavior and cognition, among other deficits. Greater understanding of the biological substrates of typical social behavior in animal models will further our understanding of the etiology of ASDs. Despite the precision and tractability of molecular genetics models of ASDs in rodents, these organisms lack the complexity of human social behavior, thus limiting their impact on understanding ASDs to basic mechanisms. Non-human primates (NHPs) provide an attractive, complementary model for ASDs, due in part to the complexity and dynamics of social structures, reliance on vision for social signaling, and deep homology in brain circuitry mediating social behavior and reward. This knowledge is based on a rich literature, compiled over 50 years of observing primate behavior in the wild, which, in the case of rhesus macaques, is complemented by a large body of research characterizing neuronal activity during cognitive behavior. Several recent developments in this field are directly relevant to ASDs, including how the brain represents the perceptual features of social stimuli, how social information influences attention processes in the brain, and how the value of social interaction is computed. Because the symptoms of ASDs may represent extreme manifestations of traits that vary in intensity within the general population, we will additionally discuss ways in which nonhuman primates also show variation in social behavior and reward sensitivity. In cases where variation in species-typical behavior is analogous to similar variations in human behavior, we believe that study of the neural circuitry underlying this variation will provide important insights into the systems-level mechanisms contributing to ASD pathology. En ligne : http://dx.doi.org/10.1186/1866-1955-4-21 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Of mice and monkeys: using non-human primate models to bridge mouse- and human-based investigations of autism spectrum disorders [Texte imprimé et/ou numérique] / K. K. WATSON, Auteur ; M. L. PLATT, Auteur . - p.21. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.21 Index. décimale : PER Périodiques Résumé : The autism spectrum disorders (ASDs) arise from a diverse array of genetic and environmental origins that disrupt the typical developmental trajectory of neural connectivity and synaptogenesis. ASDs are marked by dysfunctional social behavior and cognition, among other deficits. Greater understanding of the biological substrates of typical social behavior in animal models will further our understanding of the etiology of ASDs. Despite the precision and tractability of molecular genetics models of ASDs in rodents, these organisms lack the complexity of human social behavior, thus limiting their impact on understanding ASDs to basic mechanisms. Non-human primates (NHPs) provide an attractive, complementary model for ASDs, due in part to the complexity and dynamics of social structures, reliance on vision for social signaling, and deep homology in brain circuitry mediating social behavior and reward. This knowledge is based on a rich literature, compiled over 50 years of observing primate behavior in the wild, which, in the case of rhesus macaques, is complemented by a large body of research characterizing neuronal activity during cognitive behavior. Several recent developments in this field are directly relevant to ASDs, including how the brain represents the perceptual features of social stimuli, how social information influences attention processes in the brain, and how the value of social interaction is computed. Because the symptoms of ASDs may represent extreme manifestations of traits that vary in intensity within the general population, we will additionally discuss ways in which nonhuman primates also show variation in social behavior and reward sensitivity. In cases where variation in species-typical behavior is analogous to similar variations in human behavior, we believe that study of the neural circuitry underlying this variation will provide important insights into the systems-level mechanisms contributing to ASD pathology. En ligne : http://dx.doi.org/10.1186/1866-1955-4-21 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Adolescents with prenatal cocaine exposure show subtle alterations in striatal surface morphology and frontal cortical volumes / F. ROUSSOTTE in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.22 Titre : Adolescents with prenatal cocaine exposure show subtle alterations in striatal surface morphology and frontal cortical volumes Type de document : Texte imprimé et/ou numérique Auteurs : F. ROUSSOTTE, Auteur ; L. SODERBERG, Auteur ; T. WARNER, Auteur ; K. NARR, Auteur ; C. LEBEL, Auteur ; M. BEHNKE, Auteur ; F. DAVIS-EYLER, Auteur ; E. SOWELL, Auteur Article en page(s) : p.22 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : BACKGROUND: Published structural neuroimaging studies of prenatal cocaine exposure (PCE) in humans have yielded somewhat inconsistent results, with several studies reporting no significant differences in brain structure between exposed subjects and controls. Here, we sought to clarify some of these discrepancies by applying methodologies that allow for the detection of subtle alterations in brain structure. METHODS: We applied surface-based anatomical modeling methods to magnetic resonance imaging (MRI) data to examine regional changes in the shape and volume of the caudate and putamen in adolescents with prenatal cocaine exposure (n = 40, including 28 exposed participants and 12 unexposed controls, age range 14 to 16 years). We also sought to determine whether changes in regional brain volumes in frontal and subcortical regions occurred in adolescents with PCE compared to control participants. RESULTS: The overall volumes of the caudate and putamen did not significantly differ between PCE participants and controls. However, we found significant (P <0.05, uncorrected) effects of levels of prenatal exposure to cocaine on regional patterns of striatal morphology. Higher levels of prenatal cocaine exposure were associated with expansion of certain striatal subregions and with contraction in others. Volumetric analyses revealed no significant changes in the volume of any subcortical region of interest, but there were subtle group differences in the volumes of some frontal cortical regions, in particular reduced volumes of caudal middle frontal cortices and left lateral orbitofrontal cortex in exposed participants compared to controls. CONCLUSIONS: Prenatal cocaine exposure may lead to subtle and regionally specific patterns of regional dysmorphology in the striatum and volumetric changes in the frontal lobes. The localized and bidirectional nature of effects may explain in part the contradictions in the existing literature. En ligne : http://dx.doi.org/10.1186/1866-1955-4-22 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Adolescents with prenatal cocaine exposure show subtle alterations in striatal surface morphology and frontal cortical volumes [Texte imprimé et/ou numérique] / F. ROUSSOTTE, Auteur ; L. SODERBERG, Auteur ; T. WARNER, Auteur ; K. NARR, Auteur ; C. LEBEL, Auteur ; M. BEHNKE, Auteur ; F. DAVIS-EYLER, Auteur ; E. SOWELL, Auteur . - p.22. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.22 Index. décimale : PER Périodiques Résumé : BACKGROUND: Published structural neuroimaging studies of prenatal cocaine exposure (PCE) in humans have yielded somewhat inconsistent results, with several studies reporting no significant differences in brain structure between exposed subjects and controls. Here, we sought to clarify some of these discrepancies by applying methodologies that allow for the detection of subtle alterations in brain structure. METHODS: We applied surface-based anatomical modeling methods to magnetic resonance imaging (MRI) data to examine regional changes in the shape and volume of the caudate and putamen in adolescents with prenatal cocaine exposure (n = 40, including 28 exposed participants and 12 unexposed controls, age range 14 to 16 years). We also sought to determine whether changes in regional brain volumes in frontal and subcortical regions occurred in adolescents with PCE compared to control participants. RESULTS: The overall volumes of the caudate and putamen did not significantly differ between PCE participants and controls. However, we found significant (P <0.05, uncorrected) effects of levels of prenatal exposure to cocaine on regional patterns of striatal morphology. Higher levels of prenatal cocaine exposure were associated with expansion of certain striatal subregions and with contraction in others. Volumetric analyses revealed no significant changes in the volume of any subcortical region of interest, but there were subtle group differences in the volumes of some frontal cortical regions, in particular reduced volumes of caudal middle frontal cortices and left lateral orbitofrontal cortex in exposed participants compared to controls. CONCLUSIONS: Prenatal cocaine exposure may lead to subtle and regionally specific patterns of regional dysmorphology in the striatum and volumetric changes in the frontal lobes. The localized and bidirectional nature of effects may explain in part the contradictions in the existing literature. En ligne : http://dx.doi.org/10.1186/1866-1955-4-22 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Fragile X syndrome: a pilot proton magnetic resonance spectroscopy study in premutation carriers / B. P. HALLAHAN in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.23 Titre : Fragile X syndrome: a pilot proton magnetic resonance spectroscopy study in premutation carriers Type de document : Texte imprimé et/ou numérique Auteurs : B. P. HALLAHAN, Auteur ; Eileen DALY, Auteur ; A. SIMMONS, Auteur ; C. J. MOORE, Auteur ; K. C. MURPHY, Auteur ; D. D. MURPHY, Auteur Article en page(s) : p.23 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : PURPOSE: There is increasing evidence that neurodevelopmental differences in people with Fragile X syndrome (FraX) may be explained by differences in glutamatergic metabolism. Premutation carriers of FraX were originally considered to be unaffected although several recent reports demonstrate neuroanatomical, cognitive, and emotional differences from controls. However there are few studies on brain metabolism in premutation carriers of FraX. METHODS: We used proton magnetic resonance spectroscopy to compare neuronal integrity of a number of brain metabolites including N-Acetyl Aspartate, Creatine + Phosphocreatinine, Choline, myoInositol, and Glutamate containing substances (Glx) in 17 male premutation carriers of FraX and 16 male healthy control individuals. RESULTS: There was no significant between-group difference in the concentration of any measured brain metabolites. However there was a differential increase in N-acetyl aspartate with aging in premutation FraX individuals compared to controls. CONCLUSIONS: This is the first 1 H-MRS study to examine premutation FraX individuals. Although we demonstrated no difference in the concentration of any of the metabolites examined between the groups, this may be due to the large age ranges included in the two samples. The differential increase in NAA levels with aging may reflect an abnormal synaptic pruning process. En ligne : http://dx.doi.org/10.1186/1866-1955-4-23 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Fragile X syndrome: a pilot proton magnetic resonance spectroscopy study in premutation carriers [Texte imprimé et/ou numérique] / B. P. HALLAHAN, Auteur ; Eileen DALY, Auteur ; A. SIMMONS, Auteur ; C. J. MOORE, Auteur ; K. C. MURPHY, Auteur ; D. D. MURPHY, Auteur . - p.23. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.23 Index. décimale : PER Périodiques Résumé : PURPOSE: There is increasing evidence that neurodevelopmental differences in people with Fragile X syndrome (FraX) may be explained by differences in glutamatergic metabolism. Premutation carriers of FraX were originally considered to be unaffected although several recent reports demonstrate neuroanatomical, cognitive, and emotional differences from controls. However there are few studies on brain metabolism in premutation carriers of FraX. METHODS: We used proton magnetic resonance spectroscopy to compare neuronal integrity of a number of brain metabolites including N-Acetyl Aspartate, Creatine + Phosphocreatinine, Choline, myoInositol, and Glutamate containing substances (Glx) in 17 male premutation carriers of FraX and 16 male healthy control individuals. RESULTS: There was no significant between-group difference in the concentration of any measured brain metabolites. However there was a differential increase in N-acetyl aspartate with aging in premutation FraX individuals compared to controls. CONCLUSIONS: This is the first 1 H-MRS study to examine premutation FraX individuals. Although we demonstrated no difference in the concentration of any of the metabolites examined between the groups, this may be due to the large age ranges included in the two samples. The differential increase in NAA levels with aging may reflect an abnormal synaptic pruning process. En ligne : http://dx.doi.org/10.1186/1866-1955-4-23 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

The effect of intellectual ability on functional activation in a neurodevelopmental disorder: preliminary evidence from multiple fMRI studies in Williams syndrome / J. R. PRYWELLER in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.24 Titre : The effect of intellectual ability on functional activation in a neurodevelopmental disorder: preliminary evidence from multiple fMRI studies in Williams syndrome Type de document : Texte imprimé et/ou numérique Auteurs : J. R. PRYWELLER, Auteur ; S. N. AVERY, Auteur ; J. U. BLACKFORD, Auteur ; E. M. DYKENS, Auteur ; T. A. THORNTON-WELLS, Auteur Article en page(s) : p.24 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : UNLABELLED: BACKGROUND: Williams syndrome (WS) is a rare genetic disorder caused by the deletion of approximately 25 genes at 7q11.23 that involves mild to moderate intellectual disability (ID). When using functional magnetic resonance imaging (fMRI) to compare individuals with ID to typically developing individuals, there is a possibility that differences in IQ contribute to between-group differences in BOLD signal. If IQ is correlated with BOLD signal, then group-level analyses should adjust for IQ, or else IQ should be matched between groups. If, however, IQ is not correlated with BOLD signal, no such adjustment or criteria for matching (and exclusion) based on IQ is necessary. METHODS: In this study, we aimed to test this hypothesis systematically using four extant fMRI datasets in WS. Participants included 29 adult subjects with WS (17 men) demonstrating a wide range of standardized IQ scores (composite IQ mean = 67, SD = 17.2). We extracted average BOLD activation for both cognitive and task-specific anatomically defined regions of interest (ROIs) in each individual and correlated BOLD with composite IQ scores, verbal IQ scores and non-verbal IQ scores in Spearman rank correlation tests. RESULTS: Of the 312 correlations performed, only six correlations (2%) in four ROIs reached statistical significance at a P value < 0.01, but none survived correction for multiple testing. All six correlations were positive. Therefore, none supports the hypothesis that IQ is negatively correlated with BOLD response. CONCLUSIONS: These data suggest that the inclusion of subjects with below normal IQ does not introduce a confounding factor, at least for some types of fMRI studies with low cognitive load. By including subjects who are representative of IQ range for the targeted disorder, findings are more likely to generalize to that population. En ligne : http://dx.doi.org/10.1186/1866-1955-4-24 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] The effect of intellectual ability on functional activation in a neurodevelopmental disorder: preliminary evidence from multiple fMRI studies in Williams syndrome [Texte imprimé et/ou numérique] / J. R. PRYWELLER, Auteur ; S. N. AVERY, Auteur ; J. U. BLACKFORD, Auteur ; E. M. DYKENS, Auteur ; T. A. THORNTON-WELLS, Auteur . - p.24. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.24 Index. décimale : PER Périodiques Résumé : UNLABELLED: BACKGROUND: Williams syndrome (WS) is a rare genetic disorder caused by the deletion of approximately 25 genes at 7q11.23 that involves mild to moderate intellectual disability (ID). When using functional magnetic resonance imaging (fMRI) to compare individuals with ID to typically developing individuals, there is a possibility that differences in IQ contribute to between-group differences in BOLD signal. If IQ is correlated with BOLD signal, then group-level analyses should adjust for IQ, or else IQ should be matched between groups. If, however, IQ is not correlated with BOLD signal, no such adjustment or criteria for matching (and exclusion) based on IQ is necessary. METHODS: In this study, we aimed to test this hypothesis systematically using four extant fMRI datasets in WS. Participants included 29 adult subjects with WS (17 men) demonstrating a wide range of standardized IQ scores (composite IQ mean = 67, SD = 17.2). We extracted average BOLD activation for both cognitive and task-specific anatomically defined regions of interest (ROIs) in each individual and correlated BOLD with composite IQ scores, verbal IQ scores and non-verbal IQ scores in Spearman rank correlation tests. RESULTS: Of the 312 correlations performed, only six correlations (2%) in four ROIs reached statistical significance at a P value < 0.01, but none survived correction for multiple testing. All six correlations were positive. Therefore, none supports the hypothesis that IQ is negatively correlated with BOLD response. CONCLUSIONS: These data suggest that the inclusion of subjects with below normal IQ does not introduce a confounding factor, at least for some types of fMRI studies with low cognitive load. By including subjects who are representative of IQ range for the targeted disorder, findings are more likely to generalize to that population. En ligne : http://dx.doi.org/10.1186/1866-1955-4-24 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Perinatal testosterone exposure and autistic-like traits in the general population: a longitudinal pregnancy-cohort study / Andrew J. O. WHITEHOUSE in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.25 Titre : Perinatal testosterone exposure and autistic-like traits in the general population: a longitudinal pregnancy-cohort study Type de document : Texte imprimé et/ou numérique Auteurs : Andrew J. O. WHITEHOUSE, Auteur ; E. MATTES, Auteur ; M. T. MAYBERY, Auteur ; Cheryl DISSANAYAKE, Auteur ; M. SAWYER, Auteur ; R. M. JONES, Auteur ; C. E. PENNELL, Auteur ; J. A. KEELAN, Auteur ; M. HICKEY, Auteur Article en page(s) : p.25 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : UNLABELLED: BACKGROUND: Increased prenatal testosterone exposure has been hypothesized as a mechanism underlying autism spectrum disorders (ASD). However, no studies have prospectively measured prenatal testosterone exposure and ASD. The current study sought to determine whether testosterone concentrations in umbilical cord blood are associated with a clinical diagnosis of ASD in a small number of children and with autistic-like traits in the general population. METHODS: Umbilical cord blood was collected from 707 children. Samples were analyzed for total (TT) and bioavailable (BioT) testosterone concentrations. Parent report indicated that five individuals had a clinical diagnosis of ASD. Those participants without a diagnosis were approached in early adulthood to complete the Autism-Spectrum Quotient (AQ), a self-report measure of autistic-like traits, with 184 males (M = 20.10 years; SD= 0.65 years) and 190 females (M = 19.92 years; SD=0.68 years) providing data. RESULTS: The BioT and TT concentrations of the five children diagnosed with ASD were within one standard-deviation of the sex-specific means. Spearman's rank-order coefficients revealed no significant correlations between TT levels and scores on any AQ scale among males (rho range: -.01 to .06) or females (rho value range: -.07 to .01). There was also no significant association between BioT or TT concentrations and AQ scores among males (rho value range: -.07 to .08) or females (rho value range: -.06 to .12). Males were more likely than females to have 'high' scores (upper decile) on the AQ scale relating pattern and detail processing. However, the likelihood of a high score on this scale was unrelated to BioT and TT concentrations in both males and females. CONCLUSIONS: These findings indicate that testosterone concentrations from umbilical cord blood are unrelated to autistic-like traits in the general population. However, the findings do not exclude an association between testosterone exposure in early intrauterine life and ASD. En ligne : http://dx.doi.org/10.1186/1866-1955-4-25 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Perinatal testosterone exposure and autistic-like traits in the general population: a longitudinal pregnancy-cohort study [Texte imprimé et/ou numérique] / Andrew J. O. WHITEHOUSE, Auteur ; E. MATTES, Auteur ; M. T. MAYBERY, Auteur ; Cheryl DISSANAYAKE, Auteur ; M. SAWYER, Auteur ; R. M. JONES, Auteur ; C. E. PENNELL, Auteur ; J. A. KEELAN, Auteur ; M. HICKEY, Auteur . - p.25. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.25 Index. décimale : PER Périodiques Résumé : UNLABELLED: BACKGROUND: Increased prenatal testosterone exposure has been hypothesized as a mechanism underlying autism spectrum disorders (ASD). However, no studies have prospectively measured prenatal testosterone exposure and ASD. The current study sought to determine whether testosterone concentrations in umbilical cord blood are associated with a clinical diagnosis of ASD in a small number of children and with autistic-like traits in the general population. METHODS: Umbilical cord blood was collected from 707 children. Samples were analyzed for total (TT) and bioavailable (BioT) testosterone concentrations. Parent report indicated that five individuals had a clinical diagnosis of ASD. Those participants without a diagnosis were approached in early adulthood to complete the Autism-Spectrum Quotient (AQ), a self-report measure of autistic-like traits, with 184 males (M = 20.10 years; SD= 0.65 years) and 190 females (M = 19.92 years; SD=0.68 years) providing data. RESULTS: The BioT and TT concentrations of the five children diagnosed with ASD were within one standard-deviation of the sex-specific means. Spearman's rank-order coefficients revealed no significant correlations between TT levels and scores on any AQ scale among males (rho range: -.01 to .06) or females (rho value range: -.07 to .01). There was also no significant association between BioT or TT concentrations and AQ scores among males (rho value range: -.07 to .08) or females (rho value range: -.06 to .12). Males were more likely than females to have 'high' scores (upper decile) on the AQ scale relating pattern and detail processing. However, the likelihood of a high score on this scale was unrelated to BioT and TT concentrations in both males and females. CONCLUSIONS: These findings indicate that testosterone concentrations from umbilical cord blood are unrelated to autistic-like traits in the general population. However, the findings do not exclude an association between testosterone exposure in early intrauterine life and ASD. En ligne : http://dx.doi.org/10.1186/1866-1955-4-25 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Young adult male carriers of the fragile X premutation exhibit genetically modulated impairments in visuospatial tasks controlled for psychomotor speed / L. M. WONG in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.26 Titre : Young adult male carriers of the fragile X premutation exhibit genetically modulated impairments in visuospatial tasks controlled for psychomotor speed Type de document : Texte imprimé et/ou numérique Auteurs : L. M. WONG, Auteur ; N. J. GOODRICH-HUNSAKER, Auteur ; Y. MCLENNAN, Auteur ; F. TASSONE, Auteur ; D. HARVEY, Auteur ; S. M. RIVERA, Auteur ; T. J. SIMON, Auteur Article en page(s) : p.26 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : UNLABELLED: BACKGROUND: A previous study reported enhanced psychomotor speed, and subtle but significant cognitive impairments, modulated by age and by mutations in the fragile X mental retardation 1 (FMR1) gene in adult female fragile X premutation carriers (fXPCs). Because male carriers, unlike females, do not have a second, unaffected FMR1 allele, male fXPCs should exhibit similar, if not worse, impairments. Understanding male fXPCs is of particular significance because of their increased risk of developing fragile X-associated tremor/ataxia syndrome (FXTAS). METHODS: Male fXPCs (n = 18) and healthy control (HC) adults (n = 26) aged less than 45 years performed two psychomotor speed tasks (manual and oral) and two visuospatial tasks (magnitude comparison and enumeration). In the magnitude comparison task, participants were asked to compare and judge which of two bars was larger. In the enumeration task, participants were shown between one and eight green bars in the center of the screen, and asked to state the total number displayed. Enumeration typically proceeds in one of two modes: subitizing, a fast and accurate process that works only with a small set of items, and counting, which requires accurate serial-object detection and individuation during visual search. We examined the associations between the performance on all tasks and the age, full-scale intelligent quotient, and CGG repeat length of participants. RESULTS: We found that in the magnitude comparison and enumeration tasks, male fXPCs exhibited slower reaction times relative to HCs, even after controlling for simple reaction time. CONCLUSIONS: Our results indicate that male fXPCs as a group show impairments (slower reaction times) in numerical visuospatial tasks, which are consistent with previous findings. This adds to a growing body of literature characterizing the phenotype in fXPCs who are asymptomatic for FXTAS. Future longitudinal studies are needed to determine how these impairments relate to risk of developing FXTAS. En ligne : http://dx.doi.org/10.1186/1866-1955-4-26 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Young adult male carriers of the fragile X premutation exhibit genetically modulated impairments in visuospatial tasks controlled for psychomotor speed [Texte imprimé et/ou numérique] / L. M. WONG, Auteur ; N. J. GOODRICH-HUNSAKER, Auteur ; Y. MCLENNAN, Auteur ; F. TASSONE, Auteur ; D. HARVEY, Auteur ; S. M. RIVERA, Auteur ; T. J. SIMON, Auteur . - p.26. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.26 Index. décimale : PER Périodiques Résumé : UNLABELLED: BACKGROUND: A previous study reported enhanced psychomotor speed, and subtle but significant cognitive impairments, modulated by age and by mutations in the fragile X mental retardation 1 (FMR1) gene in adult female fragile X premutation carriers (fXPCs). Because male carriers, unlike females, do not have a second, unaffected FMR1 allele, male fXPCs should exhibit similar, if not worse, impairments. Understanding male fXPCs is of particular significance because of their increased risk of developing fragile X-associated tremor/ataxia syndrome (FXTAS). METHODS: Male fXPCs (n = 18) and healthy control (HC) adults (n = 26) aged less than 45 years performed two psychomotor speed tasks (manual and oral) and two visuospatial tasks (magnitude comparison and enumeration). In the magnitude comparison task, participants were asked to compare and judge which of two bars was larger. In the enumeration task, participants were shown between one and eight green bars in the center of the screen, and asked to state the total number displayed. Enumeration typically proceeds in one of two modes: subitizing, a fast and accurate process that works only with a small set of items, and counting, which requires accurate serial-object detection and individuation during visual search. We examined the associations between the performance on all tasks and the age, full-scale intelligent quotient, and CGG repeat length of participants. RESULTS: We found that in the magnitude comparison and enumeration tasks, male fXPCs exhibited slower reaction times relative to HCs, even after controlling for simple reaction time. CONCLUSIONS: Our results indicate that male fXPCs as a group show impairments (slower reaction times) in numerical visuospatial tasks, which are consistent with previous findings. This adds to a growing body of literature characterizing the phenotype in fXPCs who are asymptomatic for FXTAS. Future longitudinal studies are needed to determine how these impairments relate to risk of developing FXTAS. En ligne : http://dx.doi.org/10.1186/1866-1955-4-26 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344

Toward epigenetic and gene regulation models of specific language impairment: looking for links among growth, genes, and impairments / M. L. RICE in Journal of Neurodevelopmental Disorders, 4-1 (December 2012)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.27 Titre : Toward epigenetic and gene regulation models of specific language impairment: looking for links among growth, genes, and impairments Type de document : Texte imprimé et/ou numérique Auteurs : M. L. RICE, Auteur Article en page(s) : p.27 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Children with specific language impairment (SLI) are thought to have an inherited form of language impairment that spares other developmental domains. SLI shows strong heritability and recent linkage and association studies have replicated results for candidate genes. Regulatory regions of the genes may be involved. Behavioral growth models of language development of children with SLI reveal that the onset of language is delayed, and the growth trajectories of children with SLI parallel those of younger children without SLI. The rate of language acquisition decelerates in the pre-adolescent period, resulting in immature language levels for the children with SLI that persist into adolescence and beyond. Recent genetic and epigenetic discoveries and models relevant to language impairment are reviewed. T cell regulation of onset, acceleration, and deceleration signaling are described as potential conceptual parallels to the growth timing elements of language acquisition and impairment. A growth signaling disruption (GSD) hypothesis is proposed for SLI, which posits that faulty timing mechanisms at the cellular level, intrinsic to neurocortical functioning essential for language onset and growth regulation, are at the core of the growth outcomes of SLI. The GSD highlights the need to document and account for growth patterns over childhood and suggests needed directions for future investigation. En ligne : http://dx.doi.org/10.1186/1866-1955-4-27 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344 [article] Toward epigenetic and gene regulation models of specific language impairment: looking for links among growth, genes, and impairments [Texte imprimé et/ou numérique] / M. L. RICE, Auteur . - p.27. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 4-1 (December 2012) . - p.27 Index. décimale : PER Périodiques Résumé : Children with specific language impairment (SLI) are thought to have an inherited form of language impairment that spares other developmental domains. SLI shows strong heritability and recent linkage and association studies have replicated results for candidate genes. Regulatory regions of the genes may be involved. Behavioral growth models of language development of children with SLI reveal that the onset of language is delayed, and the growth trajectories of children with SLI parallel those of younger children without SLI. The rate of language acquisition decelerates in the pre-adolescent period, resulting in immature language levels for the children with SLI that persist into adolescence and beyond. Recent genetic and epigenetic discoveries and models relevant to language impairment are reviewed. T cell regulation of onset, acceleration, and deceleration signaling are described as potential conceptual parallels to the growth timing elements of language acquisition and impairment. A growth signaling disruption (GSD) hypothesis is proposed for SLI, which posits that faulty timing mechanisms at the cellular level, intrinsic to neurocortical functioning essential for language onset and growth regulation, are at the core of the growth outcomes of SLI. The GSD highlights the need to document and account for growth patterns over childhood and suggests needed directions for future investigation. En ligne : http://dx.doi.org/10.1186/1866-1955-4-27 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=344