Cumulative Risk of the Oxytocin Receptor Gene Interacts with Prenatal Exposure to Oxytocin Receptor Antagonist to Predict Children's Social Communication Development / Edwa FRIEDLANDER in Autism Research, 12-7 (July 2019)  

Public ISBD [article]  inAutism Research > 12-7 (July 2019) . - p.1087-1100 Titre : Cumulative Risk of the Oxytocin Receptor Gene Interacts with Prenatal Exposure to Oxytocin Receptor Antagonist to Predict Children's Social Communication Development Type de document : texte imprimé Auteurs : Edwa FRIEDLANDER, Auteur ; Nurit YIRMIYA, Auteur ; Efrat LAIBA, Auteur ; Ayelet HAREL-GADASSI, Auteur ; Maya YAARI, Auteur ; Ohad FELDSTEIN, Auteur ; David MANKUTA, Auteur ; Salomon ISRAEL, Auteur Année de publication : 2019 Article en page(s) : p.1087-1100 Langues : Anglais (eng) Mots-clés : Oxtr  autism spectrum disorder  gene-environment interaction  oxytocin  oxytocin receptor antagonist  oxytocin receptor gene Index. décimale : PER Périodiques Résumé : Compelling evidence for the far-reaching role of oxytocin (OT) in social cognition and affiliative behaviors set the basis for examining the association between genetic variation in the OT receptor (OXTR) gene and risk for autism spectrum disorder (ASD). In the current study, gene-environment interaction between OXTR and prenatal exposure to either OT or OXTR antagonist (OXTRA) in predicting early social communication development was examined. One hundred and fifty-three children (age: M = 4.32, SD = 1.07) were assigned to four groups based on prenatal history: children whose mothers prenatally received OXTRA and Nifedipine to delay preterm labor (n = 27); children whose mothers received Nifedipine only to delay preterm labor (n = 35); children whose mothers received OT for labor augmentation (n = 56), and a no intervention group (n = 35). Participants completed a developmental assessment of intelligence quotient (IQ), adaptive behavior, and social communication abilities. DNA was extracted via buccal swab. A genetic risk score was calculated based on four OXTR single nucleotide polymorphisms (rs53576, rs237887, rs1042778, and rs2254298) previously reported to be associated with ASD symptomatology. OXTRrisk-allele dosage was associated with more severe autism diagnostics observation schedule (ADOS) scores only in the OXTRA group. In contrast, in the Nifedipine, OT, and no intervention groups, OXTRrisk-allele dosage was not associated with children's ADOS scores. These findings highlight the importance of both genetic and environmental pathways of OT in signaling early social development and raise the need for further research in this field. Autism Res 2019, 12: 1087-1100. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: In the current study, we examined if the association between prenatal exposure to an oxytocin receptor antagonist (OXTRA) and autism spectrum disorder (ASD) related impairments are dependent on an individual's genetic background for the oxytocin receptor gene (OXTR). Children who carried a greater number of risk alleles for the OXTR gene and whose mothers received OXTRA to delay preterm labor showed more ASD-related impairments. The results highlight the importance of both genetic and environmental pathways of oxytocin in shaping early social development. En ligne : http://dx.doi.org/10.1002/aur.2111 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402 [article] Cumulative Risk of the Oxytocin Receptor Gene Interacts with Prenatal Exposure to Oxytocin Receptor Antagonist to Predict Children's Social Communication Development [texte imprimé] / Edwa FRIEDLANDER, Auteur ; Nurit YIRMIYA, Auteur ; Efrat LAIBA, Auteur ; Ayelet HAREL-GADASSI, Auteur ; Maya YAARI, Auteur ; Ohad FELDSTEIN, Auteur ; David MANKUTA, Auteur ; Salomon ISRAEL, Auteur . - 2019 . - p.1087-1100. Langues : Anglais (eng) in Autism Research > 12-7 (July 2019) . - p.1087-1100 Mots-clés : Oxtr  autism spectrum disorder  gene-environment interaction  oxytocin  oxytocin receptor antagonist  oxytocin receptor gene Index. décimale : PER Périodiques Résumé : Compelling evidence for the far-reaching role of oxytocin (OT) in social cognition and affiliative behaviors set the basis for examining the association between genetic variation in the OT receptor (OXTR) gene and risk for autism spectrum disorder (ASD). In the current study, gene-environment interaction between OXTR and prenatal exposure to either OT or OXTR antagonist (OXTRA) in predicting early social communication development was examined. One hundred and fifty-three children (age: M = 4.32, SD = 1.07) were assigned to four groups based on prenatal history: children whose mothers prenatally received OXTRA and Nifedipine to delay preterm labor (n = 27); children whose mothers received Nifedipine only to delay preterm labor (n = 35); children whose mothers received OT for labor augmentation (n = 56), and a no intervention group (n = 35). Participants completed a developmental assessment of intelligence quotient (IQ), adaptive behavior, and social communication abilities. DNA was extracted via buccal swab. A genetic risk score was calculated based on four OXTR single nucleotide polymorphisms (rs53576, rs237887, rs1042778, and rs2254298) previously reported to be associated with ASD symptomatology. OXTRrisk-allele dosage was associated with more severe autism diagnostics observation schedule (ADOS) scores only in the OXTRA group. In contrast, in the Nifedipine, OT, and no intervention groups, OXTRrisk-allele dosage was not associated with children's ADOS scores. These findings highlight the importance of both genetic and environmental pathways of OT in signaling early social development and raise the need for further research in this field. Autism Res 2019, 12: 1087-1100. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: In the current study, we examined if the association between prenatal exposure to an oxytocin receptor antagonist (OXTRA) and autism spectrum disorder (ASD) related impairments are dependent on an individual's genetic background for the oxytocin receptor gene (OXTR). Children who carried a greater number of risk alleles for the OXTR gene and whose mothers received OXTRA to delay preterm labor showed more ASD-related impairments. The results highlight the importance of both genetic and environmental pathways of oxytocin in shaping early social development. En ligne : http://dx.doi.org/10.1002/aur.2111 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402

Heritability of children's prosocial behavior and differential susceptibility to parenting by variation in the dopamine receptor D4 gene / Ariel KNAFO in Development and Psychopathology, 23-1 (January 2011)  

Public ISBD [article]  inDevelopment and Psychopathology > 23-1 (January 2011) . - p.53-67 Titre : Heritability of children's prosocial behavior and differential susceptibility to parenting by variation in the dopamine receptor D4 gene Type de document : texte imprimé Auteurs : Ariel KNAFO, Auteur ; Salomon ISRAEL, Auteur ; Richard P. EBSTEIN, Auteur Année de publication : 2011 Article en page(s) : p.53-67 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Theoretical considerations and new empirical evidence suggest that children's development cannot simply be explained by either genes or environment but that their interaction is important to understanding child behavior. In particular, a genetic polymorphism, the exon III repeat region of the dopamine receptor D4, has been the focus of interest regarding differential susceptibility to parental influence. To study environmental and genetic influences on children's prosocial behavior, 168 twin pairs (mean age = 44 months) participated in an experiment that assessed prosocial behavior via three measures: compliant prosocial behavior elicited in response to social requests, self-initiated prosocial behavior enacted voluntarily, and mothers' rating of children's behavior. Genetic effects accounted for 34% to 53% of the variance in prosocial behavior. The rest of the variance was accounted for by nonshared environment and error. Parenting measures of maternal positivity, negativity, and unexplained punishment did not correlate significantly with children's prosocial behavior. However, when parenting was stratified by presence or absence of the child's dopamine receptor D4 7-repeat allele in an overlapping sample of 167 children to model differential susceptibility to parental influence, a richer picture emerged. Positive parenting related meaningfully to mother-rated prosocial behavior, and unexplained punishment related positively to self-initiated prosocial behavior, but only among children carrying the 7-repeat allele. The findings demonstrate that a molecular genetic strategy, based on genotyping of common polymorphisms and combined with a classic twin approach, provides a richer description of how genes and environment interact to shape children's behavior, and allows for the identification of differential sensitivity to parental influence. En ligne : http://dx.doi.org/10.1017/S0954579410000647 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=117 [article] Heritability of children's prosocial behavior and differential susceptibility to parenting by variation in the dopamine receptor D4 gene [texte imprimé] / Ariel KNAFO, Auteur ; Salomon ISRAEL, Auteur ; Richard P. EBSTEIN, Auteur . - 2011 . - p.53-67. Langues : Anglais (eng) in Development and Psychopathology > 23-1 (January 2011) . - p.53-67 Index. décimale : PER Périodiques Résumé : Theoretical considerations and new empirical evidence suggest that children's development cannot simply be explained by either genes or environment but that their interaction is important to understanding child behavior. In particular, a genetic polymorphism, the exon III repeat region of the dopamine receptor D4, has been the focus of interest regarding differential susceptibility to parental influence. To study environmental and genetic influences on children's prosocial behavior, 168 twin pairs (mean age = 44 months) participated in an experiment that assessed prosocial behavior via three measures: compliant prosocial behavior elicited in response to social requests, self-initiated prosocial behavior enacted voluntarily, and mothers' rating of children's behavior. Genetic effects accounted for 34% to 53% of the variance in prosocial behavior. The rest of the variance was accounted for by nonshared environment and error. Parenting measures of maternal positivity, negativity, and unexplained punishment did not correlate significantly with children's prosocial behavior. However, when parenting was stratified by presence or absence of the child's dopamine receptor D4 7-repeat allele in an overlapping sample of 167 children to model differential susceptibility to parental influence, a richer picture emerged. Positive parenting related meaningfully to mother-rated prosocial behavior, and unexplained punishment related positively to self-initiated prosocial behavior, but only among children carrying the 7-repeat allele. The findings demonstrate that a molecular genetic strategy, based on genotyping of common polymorphisms and combined with a classic twin approach, provides a richer description of how genes and environment interact to shape children's behavior, and allows for the identification of differential sensitivity to parental influence. En ligne : http://dx.doi.org/10.1017/S0954579410000647 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=117

Low CD38 expression in lymphoblastoid cells and haplotypes are both associated with autism in a family-based study / Elad LERER in Autism Research, 3-6 (December 2010)  

Public ISBD [article]  inAutism Research > 3-6 (December 2010) . - p.293-302 Titre : Low CD38 expression in lymphoblastoid cells and haplotypes are both associated with autism in a family-based study Type de document : texte imprimé Auteurs : Elad LERER, Auteur ; Shlomit LEVI, Auteur ; Salomon ISRAEL, Auteur ; Maya YAARI, Auteur ; Lubov NEMANOV, Auteur ; David MANKUTA, Auteur ; Nurit YIRMIYA, Auteur ; Richard P. EBSTEIN, Auteur Année de publication : 2010 Article en page(s) : p.293-302 Langues : Anglais (eng) Mots-clés : autism spectrum disorder (ASD)  CD38;polymorphism  gene expression  real time PCR  haplotype Index. décimale : PER Périodiques Résumé : Background: Impairments in social processes characterize one of the core deficits in autism spectrum disorders (ASD) and accumulating evidence suggests that oxytocin neurotransmission is implicated in mediating social adaptation in ASD. Using a mouse model, CD38, a transmembrane protein expressed in immune cells but also in brain, was found to be critical for social behavior via regulation of oxytocin secretion. This prompted us to both examine CD38 expression in human lymphoblastoid cell lines (LBC) as well as to test association between SNPs across the CD38 gene and ASD. Methods: LBC's were derived from 44 ASD lines and 40 “unaffected” parents. Family-based association (UNPHASED) was examined by genotyping 11 tagging SNPs spanning the CD38 gene identified using HapMap data in 170 trios. An additional SNP (rs3796863) associated in a study by Munesue et al. with ASD was also genotyped. Results: A highly significant reduction in CD38 expression was observed in immortalized lymphocytes derived from ASD subjects compared to their “unaffected” parents (F = 17.2, P = 0.00024, df = 1). Haplotype analysis showed significant association (permutation corrected) between three and seven locus haplotypes and DSM IV ASD in low functioning (IQ<70) subjects. Conclusions: The current report supports a role for CD38 in conferring risk for ASD. Notably, our study shows that this gene is not only associated with low functioning ASD but that CD38 expression is markedly reduced in LBC derived from ASD subjects compared to “unaffected” parents, strengthening the connection between oxytocin and ASD. En ligne : http://dx.doi.org/10.1002/aur.156 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=115 [article] Low CD38 expression in lymphoblastoid cells and haplotypes are both associated with autism in a family-based study [texte imprimé] / Elad LERER, Auteur ; Shlomit LEVI, Auteur ; Salomon ISRAEL, Auteur ; Maya YAARI, Auteur ; Lubov NEMANOV, Auteur ; David MANKUTA, Auteur ; Nurit YIRMIYA, Auteur ; Richard P. EBSTEIN, Auteur . - 2010 . - p.293-302. Langues : Anglais (eng) in Autism Research > 3-6 (December 2010) . - p.293-302 Mots-clés : autism spectrum disorder (ASD)  CD38;polymorphism  gene expression  real time PCR  haplotype Index. décimale : PER Périodiques Résumé : Background: Impairments in social processes characterize one of the core deficits in autism spectrum disorders (ASD) and accumulating evidence suggests that oxytocin neurotransmission is implicated in mediating social adaptation in ASD. Using a mouse model, CD38, a transmembrane protein expressed in immune cells but also in brain, was found to be critical for social behavior via regulation of oxytocin secretion. This prompted us to both examine CD38 expression in human lymphoblastoid cell lines (LBC) as well as to test association between SNPs across the CD38 gene and ASD. Methods: LBC's were derived from 44 ASD lines and 40 “unaffected” parents. Family-based association (UNPHASED) was examined by genotyping 11 tagging SNPs spanning the CD38 gene identified using HapMap data in 170 trios. An additional SNP (rs3796863) associated in a study by Munesue et al. with ASD was also genotyped. Results: A highly significant reduction in CD38 expression was observed in immortalized lymphocytes derived from ASD subjects compared to their “unaffected” parents (F = 17.2, P = 0.00024, df = 1). Haplotype analysis showed significant association (permutation corrected) between three and seven locus haplotypes and DSM IV ASD in low functioning (IQ<70) subjects. Conclusions: The current report supports a role for CD38 in conferring risk for ASD. Notably, our study shows that this gene is not only associated with low functioning ASD but that CD38 expression is markedly reduced in LBC derived from ASD subjects compared to “unaffected” parents, strengthening the connection between oxytocin and ASD. En ligne : http://dx.doi.org/10.1002/aur.156 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=115

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