Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Détail de l'auteur
Auteur Edwin H. Jr COOK |
Documents disponibles écrits par cet auteur (28)
Faire une suggestion Affiner la recherche
Familiality of behavioral flexibility and response inhibition deficits in autism spectrum disorder (ASD) / Lauren M. SCHMITT in Molecular Autism, 10 (2019)
[article]
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
in Molecular Autism > 10 (2019) . - 47 p.[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 Family-based association testing of OCD-associated SNPs of SLC1A1 in an autism sample / Camille W. BRUNE in Autism Research, 1-2 (April 2008)
[article]
Titre : Family-based association testing of OCD-associated SNPs of SLC1A1 in an autism sample Type de document : Texte imprimé et/ou numérique Auteurs : Camille W. BRUNE, Auteur ; Catherine LORD, Auteur ; Gregory L. HANNA, Auteur ; Eric COURCHESNE, Auteur ; Edwin H. Jr COOK, Auteur ; Bennett L. LEVENTHAL, Auteur ; Soo-Jeong KIM, Auteur Année de publication : 2008 Article en page(s) : p.108-113 Langues : Anglais (eng) Mots-clés : autism SLC1A1 OCD association Index. décimale : PER Périodiques Résumé : Reports identified the neuronal glutamate transporter gene, SLC1A1 (OMIM 133550, chromosome 9p24), as a positional and functional candidate gene for obsessive-compulsive disorder (OCD). The presence of obsessions and compulsions similar to OCD in autism, the identification of this region in a genome-wide linkage analysis of individuals with autism spectrum disorders (ASDs), and the hypothesized role of glutamate in ASDs make SLC1A1 a candidate gene for ASD as well. To test for association between SLC1A1 and autism, we typed three single nucleotide polymorphisms (SNPs, rs301430, rs301979, rs301434) previously associated with OCD in 86 strictly defined trios with autism. Family-Based Association Tests (FBAT) with additive and recessive models were used to check for association. Additionally, an rs301430-rs301979 haplotype identified for OCD was investigated. FBAT revealed nominally significant association between autism and one SNP under a recessive model. The G allele of rs301979 was undertransmitted (equivalent to overtransmission of the C allele under a dominant model) to individuals with autism (Z=-2.47, P=0.01). The G allele was also undertransmitted in the T-G haplotype under the recessive model (Z=-2.41, P=0.02). Both findings were also observed in the male-only sample. However, they did not withstand correction for multiple comparisons. En ligne : http://dx.doi.org/10.1002/aur.11 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=930
in Autism Research > 1-2 (April 2008) . - p.108-113[article] Family-based association testing of OCD-associated SNPs of SLC1A1 in an autism sample [Texte imprimé et/ou numérique] / Camille W. BRUNE, Auteur ; Catherine LORD, Auteur ; Gregory L. HANNA, Auteur ; Eric COURCHESNE, Auteur ; Edwin H. Jr COOK, Auteur ; Bennett L. LEVENTHAL, Auteur ; Soo-Jeong KIM, Auteur . - 2008 . - p.108-113.
Langues : Anglais (eng)
in Autism Research > 1-2 (April 2008) . - p.108-113
Mots-clés : autism SLC1A1 OCD association Index. décimale : PER Périodiques Résumé : Reports identified the neuronal glutamate transporter gene, SLC1A1 (OMIM 133550, chromosome 9p24), as a positional and functional candidate gene for obsessive-compulsive disorder (OCD). The presence of obsessions and compulsions similar to OCD in autism, the identification of this region in a genome-wide linkage analysis of individuals with autism spectrum disorders (ASDs), and the hypothesized role of glutamate in ASDs make SLC1A1 a candidate gene for ASD as well. To test for association between SLC1A1 and autism, we typed three single nucleotide polymorphisms (SNPs, rs301430, rs301979, rs301434) previously associated with OCD in 86 strictly defined trios with autism. Family-Based Association Tests (FBAT) with additive and recessive models were used to check for association. Additionally, an rs301430-rs301979 haplotype identified for OCD was investigated. FBAT revealed nominally significant association between autism and one SNP under a recessive model. The G allele of rs301979 was undertransmitted (equivalent to overtransmission of the C allele under a dominant model) to individuals with autism (Z=-2.47, P=0.01). The G allele was also undertransmitted in the T-G haplotype under the recessive model (Z=-2.41, P=0.02). Both findings were also observed in the male-only sample. However, they did not withstand correction for multiple comparisons. En ligne : http://dx.doi.org/10.1002/aur.11 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=930 Gastrointestinal symptoms in ASD, brain structure of identical twins with ASD / Edwin H. Jr COOK in Autism Research, 2-5 (October 2009)
[article]
Titre : Gastrointestinal symptoms in ASD, brain structure of identical twins with ASD Type de document : Texte imprimé et/ou numérique Auteurs : Edwin H. Jr COOK, Auteur Année de publication : 2009 Article en page(s) : p.285-286 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.95 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=939
in Autism Research > 2-5 (October 2009) . - p.285-286[article] Gastrointestinal symptoms in ASD, brain structure of identical twins with ASD [Texte imprimé et/ou numérique] / Edwin H. Jr COOK, Auteur . - 2009 . - p.285-286.
Langues : Anglais (eng)
in Autism Research > 2-5 (October 2009) . - p.285-286
Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.95 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=939 Gene × Environment effects of serotonin transporter, dopamine receptor D4, and monoamine oxidase A genes with contextual and parenting risk factors on symptoms of oppositional defiant disorder, anxiety, and depression in a community sample of 4-year-old children / John V. LAVIGNE in Development and Psychopathology, 25-2 (May 2013)
[article]
Titre : Gene × Environment effects of serotonin transporter, dopamine receptor D4, and monoamine oxidase A genes with contextual and parenting risk factors on symptoms of oppositional defiant disorder, anxiety, and depression in a community sample of 4-year-old children Type de document : Texte imprimé et/ou numérique Auteurs : John V. LAVIGNE, Auteur ; Laura B. K. HERZING, Auteur ; Edwin H. Jr COOK, Auteur ; Susan A. LEBAILLY, Auteur ; Karen R. GOUZE, Auteur ; Joyce HOPKINS, Auteur ; Fred B. BRYANT, Auteur Article en page(s) : p.555-575 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Genetic factors can play a key role in the multiple level of analyses approach to understanding the development of child psychopathology. The present study examined gene–environment correlations and Gene × Environment interactions for polymorphisms of three target genes, the serotonin transporter gene, the D4 dopamine receptor gene, and the monoamine oxidase A gene in relation to symptoms of anxiety, depression, and oppositional behavior. Saliva samples were collected from 175 non-Hispanic White, 4-year-old children. Psychosocial risk factors included socioeconomic status, life stress, caretaker depression, parental support, hostility, and scaffolding skills. In comparison with the short forms (s/s, s/l) of the serotonin transporter linked polymorphic repeat, the long form (l/l) was associated with greater increases in symptoms of oppositional defiant disorder in interaction with family stress and with greater increases in symptoms of child depression and anxiety in interaction with caretaker depression, family conflict, and socioeconomic status. In boys, low-activity monoamine oxidase A gene was associated with increases in child anxiety and depression in interaction with caretaker depression, hostility, family conflict, and family stress. The results highlight the important of gene–environment interplay in the development of symptoms of child psychopathology in young children. En ligne : http://dx.doi.org/10.1017/S0954579412001241 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=199
in Development and Psychopathology > 25-2 (May 2013) . - p.555-575[article] Gene × Environment effects of serotonin transporter, dopamine receptor D4, and monoamine oxidase A genes with contextual and parenting risk factors on symptoms of oppositional defiant disorder, anxiety, and depression in a community sample of 4-year-old children [Texte imprimé et/ou numérique] / John V. LAVIGNE, Auteur ; Laura B. K. HERZING, Auteur ; Edwin H. Jr COOK, Auteur ; Susan A. LEBAILLY, Auteur ; Karen R. GOUZE, Auteur ; Joyce HOPKINS, Auteur ; Fred B. BRYANT, Auteur . - p.555-575.
Langues : Anglais (eng)
in Development and Psychopathology > 25-2 (May 2013) . - p.555-575
Index. décimale : PER Périodiques Résumé : Genetic factors can play a key role in the multiple level of analyses approach to understanding the development of child psychopathology. The present study examined gene–environment correlations and Gene × Environment interactions for polymorphisms of three target genes, the serotonin transporter gene, the D4 dopamine receptor gene, and the monoamine oxidase A gene in relation to symptoms of anxiety, depression, and oppositional behavior. Saliva samples were collected from 175 non-Hispanic White, 4-year-old children. Psychosocial risk factors included socioeconomic status, life stress, caretaker depression, parental support, hostility, and scaffolding skills. In comparison with the short forms (s/s, s/l) of the serotonin transporter linked polymorphic repeat, the long form (l/l) was associated with greater increases in symptoms of oppositional defiant disorder in interaction with family stress and with greater increases in symptoms of child depression and anxiety in interaction with caretaker depression, family conflict, and socioeconomic status. In boys, low-activity monoamine oxidase A gene was associated with increases in child anxiety and depression in interaction with caretaker depression, hostility, family conflict, and family stress. The results highlight the important of gene–environment interplay in the development of symptoms of child psychopathology in young children. En ligne : http://dx.doi.org/10.1017/S0954579412001241 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=199 A genotype resource for postmortem brain samples from the Autism Tissue Program / Richard F. WINTLE in Autism Research, 4-2 (April 2011)
[article]
Titre : A genotype resource for postmortem brain samples from the Autism Tissue Program Type de document : Texte imprimé et/ou numérique Auteurs : Richard F. WINTLE, Auteur ; Anath C. LIONEL, Auteur ; Pingzhao HU, Auteur ; Stephen D. GINSBERG, Auteur ; Dalila PINTO, Auteur ; Bhooma THIRUVAHINDRAPDURAM, Auteur ; John WEI, Auteur ; Christian R. MARSHALL, Auteur ; Jane PICKETT, Auteur ; Edwin H. Jr COOK, Auteur ; Stephen SCHERER, Auteur Année de publication : 2011 Article en page(s) : p.89-97 Langues : Anglais (eng) Mots-clés : autism autism spectrum disorder brain brodmann area 19 copy number variation genome-wide microarray single nucleotide polymorphism Index. décimale : PER Périodiques Résumé : The Autism Tissue Program (ATP), a science program of Autism Speaks, provides researchers with access to well-characterized postmortem brain tissues. Researchers access these tissues through a peer-reviewed, project-based approval process, and obtain related clinical information from a secure, online informatics portal. However, few of these samples have DNA banked from other sources (such as a blood sample from the same individual), hindering genotype–phenotype correlation and interpretation of gene expression data derived from the banked brain tissue. Here, we describe an initiative to extract DNA from Brodmann Area 19, and genotype these samples using both the Affymetrix Genome-Wide Human SNP Array 6.0 and the Illumina Human1M-Duo DNA Analysis BeadChip genome-wide microarray technologies. We additionally verify reported gender, and infer ethnic background from the single nucleotide polymorphism data. We have also used a rigorous, multiple algorithm approach to identify genomic copy number variation (CNV) from these array data. Following an initial proof of principle study using two samples, 52 experimental samples, consisting of 27 subjects with confirmed or suspected autism and related disorders, 5 subjects with cytogenetically visible duplications of 15q, 2 with epilepsy and 18 age-matched normal controls were processed, yielding high-quality genotype data in all cases. The genotype and CNV data are provided via the ATP informatics portal as a resource for the autism research community. En ligne : http://dx.doi.org/10.1002/aur.173 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121
in Autism Research > 4-2 (April 2011) . - p.89-97[article] A genotype resource for postmortem brain samples from the Autism Tissue Program [Texte imprimé et/ou numérique] / Richard F. WINTLE, Auteur ; Anath C. LIONEL, Auteur ; Pingzhao HU, Auteur ; Stephen D. GINSBERG, Auteur ; Dalila PINTO, Auteur ; Bhooma THIRUVAHINDRAPDURAM, Auteur ; John WEI, Auteur ; Christian R. MARSHALL, Auteur ; Jane PICKETT, Auteur ; Edwin H. Jr COOK, Auteur ; Stephen SCHERER, Auteur . - 2011 . - p.89-97.
Langues : Anglais (eng)
in Autism Research > 4-2 (April 2011) . - p.89-97
Mots-clés : autism autism spectrum disorder brain brodmann area 19 copy number variation genome-wide microarray single nucleotide polymorphism Index. décimale : PER Périodiques Résumé : The Autism Tissue Program (ATP), a science program of Autism Speaks, provides researchers with access to well-characterized postmortem brain tissues. Researchers access these tissues through a peer-reviewed, project-based approval process, and obtain related clinical information from a secure, online informatics portal. However, few of these samples have DNA banked from other sources (such as a blood sample from the same individual), hindering genotype–phenotype correlation and interpretation of gene expression data derived from the banked brain tissue. Here, we describe an initiative to extract DNA from Brodmann Area 19, and genotype these samples using both the Affymetrix Genome-Wide Human SNP Array 6.0 and the Illumina Human1M-Duo DNA Analysis BeadChip genome-wide microarray technologies. We additionally verify reported gender, and infer ethnic background from the single nucleotide polymorphism data. We have also used a rigorous, multiple algorithm approach to identify genomic copy number variation (CNV) from these array data. Following an initial proof of principle study using two samples, 52 experimental samples, consisting of 27 subjects with confirmed or suspected autism and related disorders, 5 subjects with cytogenetically visible duplications of 15q, 2 with epilepsy and 18 age-matched normal controls were processed, yielding high-quality genotype data in all cases. The genotype and CNV data are provided via the ATP informatics portal as a resource for the autism research community. En ligne : http://dx.doi.org/10.1002/aur.173 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=121 Habituation to neutral faces; Language regression in ASD / Edwin H. Jr COOK in Autism Research, 2-2 (April 2009)
PermalinkIs there sexual dimorphism of hyperserotonemia in autism spectrum disorder? / Lauren C. SHUFFREY in Autism Research, 10-8 (August 2017)
PermalinkLeveraging blood serotonin as an endophenotype to identify de novo and rare variants involved in autism / R. CHEN in Molecular Autism, 8 (2017)
PermalinkPermalinkPermalinkPermalinkLiterature review: adult structural MRI, postmortem GABA-A protein, 1q21.1 microdeletion/microduplication / Edwin H. Jr COOK in Autism Research, 1-5 (October 2008)
PermalinkLiterature Review: Mitchondrial disorders; Circumscribed interests / Edwin H. Jr COOK in Autism Research, 2-1 (February 2009)
PermalinkLiterature Review: Overlapping genetic association in developmental language disorder and autism; Grey matter in high functioning autism and Asperger's syndrome; Brain activation in self-other face discrimination / Edwin H. Jr COOK in Autism Research, 1-6 (December 2008)
PermalinkLiterature Review: Preference for physical compared to biological motion; Genome-wide association study / Edwin H. Jr COOK in Autism Research, 2-3 (June 2009)
Permalink