Cognitive mechanisms of inhibitory control deficits in autism spectrum disorder / Lauren M. SCHMITT in Journal of Child Psychology and Psychiatry, 59-5 (May 2018)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 59-5 (May 2018) . - p.586-595 Titre : Cognitive mechanisms of inhibitory control deficits in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Lauren M. SCHMITT, Auteur ; S. P. WHITE, Auteur ; Edwin H. Jr COOK, Auteur ; J. A. SWEENEY, Auteur ; M. W. MOSCONI, Auteur Article en page(s) : p.586-595 Langues : Anglais (eng) Mots-clés : Autism spectrum disorders  cognitive development  inhibition Index. décimale : PER Périodiques Résumé : BACKGROUND: Inhibitory control deficits are common in autism spectrum disorder (ASD) and associated with more severe repetitive behaviors. Inhibitory control deficits may reflect slower execution of stopping processes, or a reduced ability to delay the onset of behavioral responses in contexts of uncertainty. Previous studies have documented relatively spared stopping processes in ASD, but whether inhibitory control deficits in ASD reflect failures to delay response onset has not been systematically assessed. Further, while improvements in stopping abilities and response slowing are seen through adolescence/early adulthood in health, their development in ASD is less clear. METHODS: A stop-signal test (SST) was administered to 121 individuals with ASD and 76 age and IQ-matched healthy controls (ages 5-28). This test included 'GO trials' in which participants pressed a button when a peripheral target appeared and interleaved 'STOP trials' in which they were cued to inhibit button-presses when a stop-signal appeared at variable times following the GO cue. STOP trial accuracy, RT of the stopping process (SSRT), and reaction time (RT) slowing during GO trials were examined. RESULTS: Relative to controls, individuals with ASD had reduced accuracy on STOP trials. SSRTs were similar across control and ASD participants, but RT slowing was reduced in patients compared to controls. Age-related increases in stopping ability and RT slowing were attenuated in ASD. Reduced stopping accuracy and RT slowing were associated with more severe repetitive behaviors in ASD. DISCUSSION: Our findings show that inhibitory control deficits in ASD involve failures to strategically delay behavioral response onset. These results suggest that reduced preparatory behavioral control may underpin inhibitory control deficits as well as repetitive behaviors in ASD. Typical age-related improvements in inhibitory control during late childhood/early adolescence are reduced in ASD, highlighting an important developmental window during which treatments may mitigate cognitive alterations contributing to repetitive behaviors. En ligne : http://dx.doi.org/10.1111/jcpp.12837 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=359 [article] Cognitive mechanisms of inhibitory control deficits in autism spectrum disorder [Texte imprimé et/ou numérique] / Lauren M. SCHMITT, Auteur ; S. P. WHITE, Auteur ; Edwin H. Jr COOK, Auteur ; J. A. SWEENEY, Auteur ; M. W. MOSCONI, Auteur . - p.586-595. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 59-5 (May 2018) . - p.586-595 Mots-clés : Autism spectrum disorders  cognitive development  inhibition Index. décimale : PER Périodiques Résumé : BACKGROUND: Inhibitory control deficits are common in autism spectrum disorder (ASD) and associated with more severe repetitive behaviors. Inhibitory control deficits may reflect slower execution of stopping processes, or a reduced ability to delay the onset of behavioral responses in contexts of uncertainty. Previous studies have documented relatively spared stopping processes in ASD, but whether inhibitory control deficits in ASD reflect failures to delay response onset has not been systematically assessed. Further, while improvements in stopping abilities and response slowing are seen through adolescence/early adulthood in health, their development in ASD is less clear. METHODS: A stop-signal test (SST) was administered to 121 individuals with ASD and 76 age and IQ-matched healthy controls (ages 5-28). This test included 'GO trials' in which participants pressed a button when a peripheral target appeared and interleaved 'STOP trials' in which they were cued to inhibit button-presses when a stop-signal appeared at variable times following the GO cue. STOP trial accuracy, RT of the stopping process (SSRT), and reaction time (RT) slowing during GO trials were examined. RESULTS: Relative to controls, individuals with ASD had reduced accuracy on STOP trials. SSRTs were similar across control and ASD participants, but RT slowing was reduced in patients compared to controls. Age-related increases in stopping ability and RT slowing were attenuated in ASD. Reduced stopping accuracy and RT slowing were associated with more severe repetitive behaviors in ASD. DISCUSSION: Our findings show that inhibitory control deficits in ASD involve failures to strategically delay behavioral response onset. These results suggest that reduced preparatory behavioral control may underpin inhibitory control deficits as well as repetitive behaviors in ASD. Typical age-related improvements in inhibitory control during late childhood/early adolescence are reduced in ASD, highlighting an important developmental window during which treatments may mitigate cognitive alterations contributing to repetitive behaviors. En ligne : http://dx.doi.org/10.1111/jcpp.12837 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=359

Differentiating social preference and social anxiety phenotypes in fragile X syndrome using an eye gaze analysis: a pilot study / M. P. HONG in Journal of Neurodevelopmental Disorders, 11-1 (December 2019)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 11-1 (December 2019) . - 1 p. Titre : Differentiating social preference and social anxiety phenotypes in fragile X syndrome using an eye gaze analysis: a pilot study Type de document : Texte imprimé et/ou numérique Auteurs : M. P. HONG, Auteur ; E. M. ECKERT, Auteur ; Ernest V. PEDAPATI, Auteur ; R. C. SHAFFER, Auteur ; K. C. DOMINICK, Auteur ; L. K. WINK, Auteur ; J. A. SWEENEY, Auteur ; C. A. ERICKSON, Auteur Article en page(s) : 1 p. Langues : Anglais (eng) Mots-clés : Autism  Eye tracking  Fragile X syndrome  Gaze aversion  Social anxiety  Social interest Index. décimale : PER Périodiques Résumé : BACKGROUND: Fragile X syndrome (FXS) is the leading inherited cause of autism spectrum disorder, but there remains debate regarding the clinical presentation of social deficits in FXS. The aim of this study was to compare individuals with FXS to typically developing controls (TDC) and individuals with idiopathic autism spectrum disorder (ASD) across two social eye tracking paradigms. METHODS: Individuals with FXS and age- and gender-matched TDC and individuals with idiopathic ASD completed emotional face and social preference eye tracking tasks to evaluate gaze aversion and social interest, respectively. Participants completed a battery of cognitive testing and caregiver-reported measures for neurobehavioral characterization. RESULTS: Individuals with FXS exhibited reduced eye and increased mouth gaze to emotional faces compared to TDC. Gaze aversive findings were found to correlate with measures of anxiety, social communication deficits, and behavioral problems. In the social interest task, while individuals with idiopathic ASD showed significantly less social preference, individuals with FXS displayed social preference similar to TDC. CONCLUSIONS: These findings suggest fragile X syndrome social deficits center on social anxiety without the prominent reduction in social interest associated with autism spectrum disorder. Specifically designed eye tracking techniques clarify the nature of social deficits in fragile X syndrome and may have applications to improve phenotyping and evaluate interventions targeting social functioning impairments. En ligne : http://dx.doi.org/10.1186/s11689-019-9262-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386 [article] Differentiating social preference and social anxiety phenotypes in fragile X syndrome using an eye gaze analysis: a pilot study [Texte imprimé et/ou numérique] / M. P. HONG, Auteur ; E. M. ECKERT, Auteur ; Ernest V. PEDAPATI, Auteur ; R. C. SHAFFER, Auteur ; K. C. DOMINICK, Auteur ; L. K. WINK, Auteur ; J. A. SWEENEY, Auteur ; C. A. ERICKSON, Auteur . - 1 p. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 11-1 (December 2019) . - 1 p. Mots-clés : Autism  Eye tracking  Fragile X syndrome  Gaze aversion  Social anxiety  Social interest Index. décimale : PER Périodiques Résumé : BACKGROUND: Fragile X syndrome (FXS) is the leading inherited cause of autism spectrum disorder, but there remains debate regarding the clinical presentation of social deficits in FXS. The aim of this study was to compare individuals with FXS to typically developing controls (TDC) and individuals with idiopathic autism spectrum disorder (ASD) across two social eye tracking paradigms. METHODS: Individuals with FXS and age- and gender-matched TDC and individuals with idiopathic ASD completed emotional face and social preference eye tracking tasks to evaluate gaze aversion and social interest, respectively. Participants completed a battery of cognitive testing and caregiver-reported measures for neurobehavioral characterization. RESULTS: Individuals with FXS exhibited reduced eye and increased mouth gaze to emotional faces compared to TDC. Gaze aversive findings were found to correlate with measures of anxiety, social communication deficits, and behavioral problems. In the social interest task, while individuals with idiopathic ASD showed significantly less social preference, individuals with FXS displayed social preference similar to TDC. CONCLUSIONS: These findings suggest fragile X syndrome social deficits center on social anxiety without the prominent reduction in social interest associated with autism spectrum disorder. Specifically designed eye tracking techniques clarify the nature of social deficits in fragile X syndrome and may have applications to improve phenotyping and evaluate interventions targeting social functioning impairments. En ligne : http://dx.doi.org/10.1186/s11689-019-9262-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386

Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome / L. E. ETHRIDGE in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 38p. Titre : Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome Type de document : Texte imprimé et/ou numérique Auteurs : L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur Article en page(s) : 38p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : [This corrects the article DOI: 10.1186/s13229-017-0140-1.]. En ligne : http://dx.doi.org/10.1186/s13229-017-0150-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330 [article] Erratum to: Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome [Texte imprimé et/ou numérique] / L. E. ETHRIDGE, Auteur ; S. P. WHITE, Auteur ; M. W. MOSCONI, Auteur ; J. WANG, Auteur ; Ernest V. PEDAPATI, Auteur ; C. A. ERICKSON, Auteur ; M. J. BYERLY, Auteur ; J. A. SWEENEY, Auteur . - 38p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 38p. Index. décimale : PER Périodiques Résumé : [This corrects the article DOI: 10.1186/s13229-017-0140-1.]. En ligne : http://dx.doi.org/10.1186/s13229-017-0150-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=330

Familiality of behavioral flexibility and response inhibition deficits in autism spectrum disorder (ASD) / Lauren M. SCHMITT in Molecular Autism, 10 (2019)  

Public ISBD [article]  inMolecular Autism > 10 (2019) . - 47 p. Titre : Familiality of behavioral flexibility and response inhibition deficits in autism spectrum disorder (ASD) Type de document : Texte imprimé et/ou numérique Auteurs : Lauren M. SCHMITT, Auteur ; E. K. BOJANEK, Auteur ; S. P. WHITE, Auteur ; M. E. RAGOZZINO, Auteur ; Edwin H. Jr COOK, Auteur ; J. A. SWEENEY, Auteur ; M. W. MOSCONI, Auteur Article en page(s) : 47 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background: Diminished cognitive control, including reduced behavioral flexibility and behavioral response inhibition, has been repeatedly documented in autism spectrum disorder (ASD). We evaluated behavioral flexibility and response inhibition in probands and their parents using a family trio design to determine the extent to which these cognitive control impairments represent familial traits associated with ASD. Methods: We examined 66 individuals with ASD (probands), 135 unaffected biological parents, and 76 typically developing controls. Participants completed a probabilistic reversal learning task (PRL) and a stop-signal task (SST) to assess behavioral flexibility and response inhibition respectively. Rates of PRL and SST errors were examined across groups, within families, and in relation to clinical and subclinical traits of ASD. Based on prior findings that subclinical broader autism phenotypic (BAP) traits may co-segregate within families and reflect heritable risk factors, we also examined whether cognitive control deficits were more prominent in families in which parents showed BAP features (BAP+). Results: Probands and parents each showed increased rates of PRL and SST errors relative to controls. Error rates across tasks were not related. SST error rates inter-correlated among probands and their parents. PRL errors were more severe in BAP+ parents and their children relative to BAP- parents and their children. For probands of BAP+ parents, PRL and SST error rates were associated with more severe social-communication abnormalities and repetitive behaviors, respectively. Conclusion: Reduced behavioral flexibility and response inhibition are present among probands and their unaffected parents, but represent unique familial deficits associated with ASD that track with separate clinical issues. Specifically, behavioral response inhibition impairments are familial in ASD and manifest independently from parental subclinical features. In contrast, behavioral flexibility deficits are selectively present in families with BAP characteristics, suggesting they co-segregate in families with parental subclinical social, communication, and rigid personality traits. Together, these findings provide evidence that behavioral flexibility and response inhibition impairments track differentially with ASD risk mechanisms and related behavioral traits. En ligne : http://dx.doi.org/10.1186/s13229-019-0296-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=414 [article] Familiality of behavioral flexibility and response inhibition deficits in autism spectrum disorder (ASD) [Texte imprimé et/ou numérique] / Lauren M. SCHMITT, Auteur ; E. K. BOJANEK, Auteur ; S. P. WHITE, Auteur ; M. E. RAGOZZINO, Auteur ; Edwin H. Jr COOK, Auteur ; J. A. SWEENEY, Auteur ; M. W. MOSCONI, Auteur . - 47 p. Langues : Anglais (eng) in Molecular Autism > 10 (2019) . - 47 p. Index. décimale : PER Périodiques Résumé : Background: Diminished cognitive control, including reduced behavioral flexibility and behavioral response inhibition, has been repeatedly documented in autism spectrum disorder (ASD). We evaluated behavioral flexibility and response inhibition in probands and their parents using a family trio design to determine the extent to which these cognitive control impairments represent familial traits associated with ASD. Methods: We examined 66 individuals with ASD (probands), 135 unaffected biological parents, and 76 typically developing controls. Participants completed a probabilistic reversal learning task (PRL) and a stop-signal task (SST) to assess behavioral flexibility and response inhibition respectively. Rates of PRL and SST errors were examined across groups, within families, and in relation to clinical and subclinical traits of ASD. Based on prior findings that subclinical broader autism phenotypic (BAP) traits may co-segregate within families and reflect heritable risk factors, we also examined whether cognitive control deficits were more prominent in families in which parents showed BAP features (BAP+). Results: Probands and parents each showed increased rates of PRL and SST errors relative to controls. Error rates across tasks were not related. SST error rates inter-correlated among probands and their parents. PRL errors were more severe in BAP+ parents and their children relative to BAP- parents and their children. For probands of BAP+ parents, PRL and SST error rates were associated with more severe social-communication abnormalities and repetitive behaviors, respectively. Conclusion: Reduced behavioral flexibility and response inhibition are present among probands and their unaffected parents, but represent unique familial deficits associated with ASD that track with separate clinical issues. Specifically, behavioral response inhibition impairments are familial in ASD and manifest independently from parental subclinical features. In contrast, behavioral flexibility deficits are selectively present in families with BAP characteristics, suggesting they co-segregate in families with parental subclinical social, communication, and rigid personality traits. Together, these findings provide evidence that behavioral flexibility and response inhibition impairments track differentially with ASD risk mechanisms and related behavioral traits. En ligne : http://dx.doi.org/10.1186/s13229-019-0296-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=414

Fragile X targeted pharmacotherapy: lessons learned and future directions / C. A. ERICKSON in Journal of Neurodevelopmental Disorders, 9-1 (December 2017)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 9-1 (December 2017) . - p.7 Titre : Fragile X targeted pharmacotherapy: lessons learned and future directions Type de document : Texte imprimé et/ou numérique Auteurs : C. A. ERICKSON, Auteur ; M. H. DAVENPORT, Auteur ; T. L. SCHAEFER, Auteur ; L. K. WINK, Auteur ; Ernest V. PEDAPATI, Auteur ; J. A. SWEENEY, Auteur ; S. E. FITZPATRICK, Auteur ; W. Ted BROWN, Auteur ; Dejan B. BUDIMIROVIC, Auteur ; Randi J. HAGERMAN, Auteur ; D. HESSL, Auteur ; W. E. KAUFMANN, Auteur ; Elizabeth BERRY-KRAVIS, Auteur Article en page(s) : p.7 Langues : Anglais (eng) Mots-clés : Drug development  Fragile X syndrome  Genetic disorder  Targeted treatments  Translational treatment Index. décimale : PER Périodiques Résumé : Our understanding of fragile X syndrome (FXS) pathophysiology continues to improve and numerous potential drug targets have been identified. Yet, current prescribing practices are only symptom-based in order to manage difficult behaviors, as no drug to date is approved for the treatment of FXS. Drugs impacting a diversity of targets in the brain have been studied in recent FXS-specific clinical trials. While many drugs have focused on regulation of enhanced glutamatergic or deficient GABAergic neurotransmission, compounds studied have not been limited to these mechanisms. As a single-gene disorder, it was thought that FXS would have consistent drug targets that could be modulated with pharmacotherapy and lead to significant improvement. Unfortunately, despite promising results in FXS animal models, translational drug treatment development in FXS has largely failed. Future success in this field will depend on learning from past challenges to improve clinical trial design, choose appropriate outcome measures and age range choices, and find readily modulated drug targets. Even with many negative placebo-controlled study results, the field continues to move forward exploring both the new mechanistic drug approaches combined with ways to improve trial execution. This review summarizes the known phenotype and pathophysiology of FXS and past clinical trial rationale and results, and discusses current challenges facing the field and lessons from which to learn for future treatment development efforts. En ligne : http://dx.doi.org/10.1186/s11689-017-9186-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349 [article] Fragile X targeted pharmacotherapy: lessons learned and future directions [Texte imprimé et/ou numérique] / C. A. ERICKSON, Auteur ; M. H. DAVENPORT, Auteur ; T. L. SCHAEFER, Auteur ; L. K. WINK, Auteur ; Ernest V. PEDAPATI, Auteur ; J. A. SWEENEY, Auteur ; S. E. FITZPATRICK, Auteur ; W. Ted BROWN, Auteur ; Dejan B. BUDIMIROVIC, Auteur ; Randi J. HAGERMAN, Auteur ; D. HESSL, Auteur ; W. E. KAUFMANN, Auteur ; Elizabeth BERRY-KRAVIS, Auteur . - p.7. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 9-1 (December 2017) . - p.7 Mots-clés : Drug development  Fragile X syndrome  Genetic disorder  Targeted treatments  Translational treatment Index. décimale : PER Périodiques Résumé : Our understanding of fragile X syndrome (FXS) pathophysiology continues to improve and numerous potential drug targets have been identified. Yet, current prescribing practices are only symptom-based in order to manage difficult behaviors, as no drug to date is approved for the treatment of FXS. Drugs impacting a diversity of targets in the brain have been studied in recent FXS-specific clinical trials. While many drugs have focused on regulation of enhanced glutamatergic or deficient GABAergic neurotransmission, compounds studied have not been limited to these mechanisms. As a single-gene disorder, it was thought that FXS would have consistent drug targets that could be modulated with pharmacotherapy and lead to significant improvement. Unfortunately, despite promising results in FXS animal models, translational drug treatment development in FXS has largely failed. Future success in this field will depend on learning from past challenges to improve clinical trial design, choose appropriate outcome measures and age range choices, and find readily modulated drug targets. Even with many negative placebo-controlled study results, the field continues to move forward exploring both the new mechanistic drug approaches combined with ways to improve trial execution. This review summarizes the known phenotype and pathophysiology of FXS and past clinical trial rationale and results, and discusses current challenges facing the field and lessons from which to learn for future treatment development efforts. En ligne : http://dx.doi.org/10.1186/s11689-017-9186-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=349

Initial action output and feedback-guided motor behaviors in autism spectrum disorder / K. E. UNRUH in Molecular Autism, 12 (2021)  

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Motor Memory Deficits Contribute to Motor Impairments in Autism Spectrum Disorder / K. A. NEELY in Journal of Autism and Developmental Disorders, 49-7 (July 2019)  

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Neural synchronization deficits linked to cortical hyper-excitability and auditory hypersensitivity in fragile X syndrome / L. E. ETHRIDGE in Molecular Autism, 8 (2017)  

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Neurophysiological hyperresponsivity to sensory input in autism spectrum disorders / Y. TAKARAE in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

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Postural orientation and equilibrium processes associated with increased postural sway in autism spectrum disorder (ASD) / Z. WANG in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

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A resting EEG study of neocortical hyperexcitability and altered functional connectivity in fragile X syndrome / J. WANG in Journal of Neurodevelopmental Disorders, 9-1 (December 2017)  

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Resting state EEG abnormalities in autism spectrum disorders / J. WANG in Journal of Neurodevelopmental Disorders, 5-1 (December 2013)  

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