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 Auteurs : Lauren M. SCHMITT, Auteur ; Stormi P. WHITE, Auteur ; Edwin H. Jr COOK, Auteur ; John A. SWEENEY, Auteur ; Matthew 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] / Lauren M. SCHMITT, Auteur ; Stormi P. WHITE, Auteur ; Edwin H. Jr COOK, Auteur ; John A. SWEENEY, Auteur ; Matthew 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

Cognitive Set Shifting Deficits and Their Relationship to Repetitive Behaviors in Autism Spectrum Disorder / Haylie L. MILLER in Journal of Autism and Developmental Disorders, 45-3 (March 2015)  

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 45-3 (March 2015) . - p.805-815 Titre : Cognitive Set Shifting Deficits and Their Relationship to Repetitive Behaviors in Autism Spectrum Disorder Type de document : texte imprimé Auteurs : Haylie L. MILLER, Auteur ; Michael E. RAGOZZINO, Auteur ; Edwin H. Jr COOK, Auteur ; John A. SWEENEY, Auteur ; Matthew W. MOSCONI, Auteur Article en page(s) : p.805-815 Langues : Anglais (eng) Mots-clés : Cognitive flexibility  Insistence on sameness  Repetitive behavior Index. décimale : PER Périodiques Résumé : The neurocognitive impairments associated with restricted and repetitive behaviors (RRBs) in autism spectrum disorder (ASD) are not yet clear. Prior studies indicate that individuals with ASD show reduced cognitive flexibility, which could reflect difficulty shifting from a previously learned response pattern or a failure to maintain a new response set. We examined different error types on a test of set-shifting completed by 60 individuals with ASD and 55 age- and nonverbal IQ-matched controls. Individuals with ASD were able to initially shift sets, but they exhibited difficulty maintaining new response sets. Difficulty with set maintenance was related to increased severity of RRBs. General difficulty maintaining new response sets and a heightened tendency to revert to old preferences may contribute to RRBs. En ligne : http://dx.doi.org/10.1007/s10803-014-2244-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=258 [article] Cognitive Set Shifting Deficits and Their Relationship to Repetitive Behaviors in Autism Spectrum Disorder [texte imprimé] / Haylie L. MILLER, Auteur ; Michael E. RAGOZZINO, Auteur ; Edwin H. Jr COOK, Auteur ; John A. SWEENEY, Auteur ; Matthew W. MOSCONI, Auteur . - p.805-815. Langues : Anglais (eng) in Journal of Autism and Developmental Disorders > 45-3 (March 2015) . - p.805-815 Mots-clés : Cognitive flexibility  Insistence on sameness  Repetitive behavior Index. décimale : PER Périodiques Résumé : The neurocognitive impairments associated with restricted and repetitive behaviors (RRBs) in autism spectrum disorder (ASD) are not yet clear. Prior studies indicate that individuals with ASD show reduced cognitive flexibility, which could reflect difficulty shifting from a previously learned response pattern or a failure to maintain a new response set. We examined different error types on a test of set-shifting completed by 60 individuals with ASD and 55 age- and nonverbal IQ-matched controls. Individuals with ASD were able to initially shift sets, but they exhibited difficulty maintaining new response sets. Difficulty with set maintenance was related to increased severity of RRBs. General difficulty maintaining new response sets and a heightened tendency to revert to old preferences may contribute to RRBs. En ligne : http://dx.doi.org/10.1007/s10803-014-2244-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=258

Commentary: Making the brain matter in assessing and treating adolescent substance use – a commentary on Conrod and Nikolaou (2016) / Matthew W. MOSCONI in Journal of Child Psychology and Psychiatry, 57-3 (March 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-3 (March 2016) . - p.395-397 Titre : Commentary: Making the brain matter in assessing and treating adolescent substance use – a commentary on Conrod and Nikolaou (2016) Type de document : texte imprimé Auteurs : Matthew W. MOSCONI, Auteur ; Carl W. LEJUEZ, Auteur Article en page(s) : p.395-397 Langues : Anglais (eng) Mots-clés : Substance use Index. décimale : PER Périodiques Résumé : Adolescence represents a period of vulnerability to psychiatric problems due to a range of factors, including advances in social and cognitive abilities, increased levels of autonomy in decision-making and behavioral governance, and greater exposure to opportunities for risk-taking behavior. Adding to these psychological and social challenges, adolescence also is marked by robust maturational changes affecting both the microcircuitry and connectivity between widely distributed brain systems. These changes alter the communication among parallel, distributed brain networks, have implications for one's vulnerability to engage in risk behavior and make the brain particularly susceptible to external perturbations, such as exposure to neurotoxic substances. En ligne : http://dx.doi.org/10.1111/jcpp.12532 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=282 [article] Commentary: Making the brain matter in assessing and treating adolescent substance use – a commentary on Conrod and Nikolaou (2016) [texte imprimé] / Matthew W. MOSCONI, Auteur ; Carl W. LEJUEZ, Auteur . - p.395-397. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-3 (March 2016) . - p.395-397 Mots-clés : Substance use Index. décimale : PER Périodiques Résumé : Adolescence represents a period of vulnerability to psychiatric problems due to a range of factors, including advances in social and cognitive abilities, increased levels of autonomy in decision-making and behavioral governance, and greater exposure to opportunities for risk-taking behavior. Adding to these psychological and social challenges, adolescence also is marked by robust maturational changes affecting both the microcircuitry and connectivity between widely distributed brain systems. These changes alter the communication among parallel, distributed brain networks, have implications for one's vulnerability to engage in risk behavior and make the brain particularly susceptible to external perturbations, such as exposure to neurotoxic substances. En ligne : http://dx.doi.org/10.1111/jcpp.12532 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=282

Correction: Endophenotype trait domains for advancing gene discovery in autism spectrum disorder / Matthew W. MOSCONI in Journal of Neurodevelopmental Disorders, 16 (2024)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 16 (2024) Titre : Correction: Endophenotype trait domains for advancing gene discovery in autism spectrum disorder Type de document : texte imprimé Auteurs : Matthew W. MOSCONI, Auteur ; Cassandra J. STEVENS, Auteur ; Kathryn E. UNRUH, Auteur ; Robin SHAFER, Auteur ; Jed T. ELISON, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : https://dx.doi.org/10.1186/s11689-024-09523-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575 [article] Correction: Endophenotype trait domains for advancing gene discovery in autism spectrum disorder [texte imprimé] / Matthew W. MOSCONI, Auteur ; Cassandra J. STEVENS, Auteur ; Kathryn E. UNRUH, Auteur ; Robin SHAFER, Auteur ; Jed T. ELISON, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 16 (2024) Index. décimale : PER Périodiques En ligne : https://dx.doi.org/10.1186/s11689-024-09523-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575

Endophenotype trait domains for advancing gene discovery in autism spectrum disorder / Matthew W. MOSCONI in Journal of Neurodevelopmental Disorders, 15 (2023)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 15 (2023) Titre : Endophenotype trait domains for advancing gene discovery in autism spectrum disorder Type de document : texte imprimé Auteurs : Matthew W. MOSCONI, Auteur ; Cassandra J. STEVENS, Auteur ; Kathryn E. UNRUH, Auteur ; Robin SHAFER, Auteur ; Jed T. ELISON, Auteur Langues : Anglais (eng) Mots-clés : Infant  Humans  Autism Spectrum Disorder/genetics  Endophenotypes  Language  Neurodevelopmental Disorders  Genetic Association Studies Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is associated with a diverse range of etiological processes, including both genetic and non-genetic causes. For a plurality of individuals with ASD, it is likely that the primary causes involve multiple common inherited variants that individually account for only small levels of variation in phenotypic outcomes. This genetic landscape creates a major challenge for detecting small but important pathogenic effects associated with ASD. To address similar challenges, separate fields of medicine have identified endophenotypes, or discrete, quantitative traits that reflect genetic likelihood for a particular clinical condition and leveraged the study of these traits to map polygenic mechanisms and advance more personalized therapeutic strategies for complex diseases. Endophenotypes represent a distinct class of biomarkers useful for understanding genetic contributions to psychiatric and developmental disorders because they are embedded within the causal chain between genotype and clinical phenotype, and they are more proximal to the action of the gene(s) than behavioral traits. Despite their demonstrated power for guiding new understanding of complex genetic structures of clinical conditions, few endophenotypes associated with ASD have been identified and integrated into family genetic studies. In this review, we argue that advancing knowledge of the complex pathogenic processes that contribute to ASD can be accelerated by refocusing attention toward identifying endophenotypic traits reflective of inherited mechanisms. This pivot requires renewed emphasis on study designs with measurement of familial co-variation including infant sibling studies, family trio and quad designs, and analysis of monozygotic and dizygotic twin concordance for select trait dimensions. We also emphasize that clarification of endophenotypic traits necessarily will involve integration of transdiagnostic approaches as candidate traits likely reflect liability for multiple clinical conditions and often are agnostic to diagnostic boundaries. Multiple candidate endophenotypes associated with ASD likelihood are described, and we propose a new focus on the analysis of "endophenotype trait domains" (ETDs), or traits measured across multiple levels (e.g., molecular, cellular, neural system, neuropsychological) along the causal pathway from genes to behavior. To inform our central argument for research efforts toward ETD discovery, we first provide a brief review of the concept of endophenotypes and their application to psychiatry. Next, we highlight key criteria for determining the value of candidate endophenotypes, including unique considerations for the study of ASD. Descriptions of different study designs for assessing endophenotypes in ASD research then are offered, including analysis of how select patterns of results may help prioritize candidate traits in future research. We also present multiple candidate ETDs that collectively cover a breadth of clinical phenomena associated with ASD, including social, language/communication, cognitive control, and sensorimotor processes. These ETDs are described because they represent promising targets for gene discovery related to clinical autistic traits, and they serve as models for analysis of separate candidate domains that may inform understanding of inherited etiological processes associated with ASD as well as overlapping neurodevelopmental disorders. En ligne : https://dx.doi.org/10.1186/s11689-023-09511-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575 [article] Endophenotype trait domains for advancing gene discovery in autism spectrum disorder [texte imprimé] / Matthew W. MOSCONI, Auteur ; Cassandra J. STEVENS, Auteur ; Kathryn E. UNRUH, Auteur ; Robin SHAFER, Auteur ; Jed T. ELISON, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 15 (2023) Mots-clés : Infant  Humans  Autism Spectrum Disorder/genetics  Endophenotypes  Language  Neurodevelopmental Disorders  Genetic Association Studies Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is associated with a diverse range of etiological processes, including both genetic and non-genetic causes. For a plurality of individuals with ASD, it is likely that the primary causes involve multiple common inherited variants that individually account for only small levels of variation in phenotypic outcomes. This genetic landscape creates a major challenge for detecting small but important pathogenic effects associated with ASD. To address similar challenges, separate fields of medicine have identified endophenotypes, or discrete, quantitative traits that reflect genetic likelihood for a particular clinical condition and leveraged the study of these traits to map polygenic mechanisms and advance more personalized therapeutic strategies for complex diseases. Endophenotypes represent a distinct class of biomarkers useful for understanding genetic contributions to psychiatric and developmental disorders because they are embedded within the causal chain between genotype and clinical phenotype, and they are more proximal to the action of the gene(s) than behavioral traits. Despite their demonstrated power for guiding new understanding of complex genetic structures of clinical conditions, few endophenotypes associated with ASD have been identified and integrated into family genetic studies. In this review, we argue that advancing knowledge of the complex pathogenic processes that contribute to ASD can be accelerated by refocusing attention toward identifying endophenotypic traits reflective of inherited mechanisms. This pivot requires renewed emphasis on study designs with measurement of familial co-variation including infant sibling studies, family trio and quad designs, and analysis of monozygotic and dizygotic twin concordance for select trait dimensions. We also emphasize that clarification of endophenotypic traits necessarily will involve integration of transdiagnostic approaches as candidate traits likely reflect liability for multiple clinical conditions and often are agnostic to diagnostic boundaries. Multiple candidate endophenotypes associated with ASD likelihood are described, and we propose a new focus on the analysis of "endophenotype trait domains" (ETDs), or traits measured across multiple levels (e.g., molecular, cellular, neural system, neuropsychological) along the causal pathway from genes to behavior. To inform our central argument for research efforts toward ETD discovery, we first provide a brief review of the concept of endophenotypes and their application to psychiatry. Next, we highlight key criteria for determining the value of candidate endophenotypes, including unique considerations for the study of ASD. Descriptions of different study designs for assessing endophenotypes in ASD research then are offered, including analysis of how select patterns of results may help prioritize candidate traits in future research. We also present multiple candidate ETDs that collectively cover a breadth of clinical phenomena associated with ASD, including social, language/communication, cognitive control, and sensorimotor processes. These ETDs are described because they represent promising targets for gene discovery related to clinical autistic traits, and they serve as models for analysis of separate candidate domains that may inform understanding of inherited etiological processes associated with ASD as well as overlapping neurodevelopmental disorders. En ligne : https://dx.doi.org/10.1186/s11689-023-09511-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=575

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

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

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Functional brain abnormalities associated with comorbid anxiety in autism spectrum disorder / James BARTOLOTTI in Development and Psychopathology, 32-4 (October 2020)  

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

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Motor Functioning and Dyspraxia in Autism Spectrum Disorders / Matthew W. MOSCONI

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Motor Memory Deficits Contribute to Motor Impairments in Autism Spectrum Disorder / Kristina 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 / Lauren E ETHRIDGE in Molecular Autism, 8 (2017)  

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Phenotypic variation in neural sensory processing by deletion size, age, and sex in Phelan-McDermid syndrome / Melody Reese SMITH in Journal of Neurodevelopmental Disorders, 17 (2025)  

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Postural control processes during standing and step initiation in autism spectrum disorder / Erin K. BOJANEK in Journal of Neurodevelopmental Disorders, 12 (2020)  

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

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