20 résultat(s) recherche sur le mot clé 'genetic'

5-HTTLPR moderates the effect of relational peer victimization on depressive symptoms in adolescent girls / Corina BENJET in Journal of Child Psychology and Psychiatry (51-2, February 2010)

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 51-2 (February 2010) . - p.173-179 Titre : 5-HTTLPR moderates the effect of relational peer victimization on depressive symptoms in adolescent girls Type de document : texte imprimé Auteurs : Corina BENJET, Auteur; Renee THOMPSON, Auteur; Ian H. GOTLIB, Auteur Article en page(s) : p.173-179 Langues : Anglais (eng)   Résumé : Background: Relational peer victimization is associated with internalizing symptoms. Compared to boys, girls are more likely to be both relationally victimized by peers and distressed by the victimization. While previous studies have reported that a functional polymorphism in the promoter region of the serotonin transporter gene (5-HTTLPR) moderates the effect of stressful life events on depressive symptoms, the present study is the first to evaluate the interaction of this polymorphism with relational peer victimization to predict level of depressive symptoms in young girls. Methods: Participants were 78 girls ages 10 to 14 who had no current or past Axis I disorder. Girls were genotyped for 5-HTTLPR; peer victimization was assessed with the Social Experiences Questionnaire, and depressive symptoms with the Children's Depression Inventory. Results: The 5-HTTLPR polymorphism alone did not predict level of depressive symptoms; the interaction of 5-HTTLPR and relational peer victimization, however, was a significant predictor of depressive symptoms. Follow-up analyses indicated that peer victimization significantly predicted level of depressive symptoms only for girls who were homozygous for the short allele, and not for girls homozygous for the long allele or who were heterozygous for the short and long alleles. Conclusions: The findings support the diathesis-stress model of depression: having two 5-HTTLPR short alleles confers vulnerability to depressive symptoms in adolescent girls when they experience relational peer victimization. These findings also suggest that relational peer victimization, at least for girls with genetic vulnerability, is a significant source of stress and should be recognized in the monitoring and prevention of bullying. Mots-clés : Peer-victimization  bullying  depression  genetic-polymorphisms  5-HTTLPR Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/122596842/PDFSTART [article] 5-HTTLPR moderates the effect of relational peer victimization on depressive symptoms in adolescent girls [texte imprimé] / Corina BENJET, Auteur; Renee THOMPSON, Auteur; Ian H. GOTLIB, Auteur . - p.173-179. Langues : Anglais (eng) inJournal of Child Psychology and Psychiatry > 51-2 (February 2010) . - p.173-179   Résumé : Background: Relational peer victimization is associated with internalizing symptoms. Compared to boys, girls are more likely to be both relationally victimized by peers and distressed by the victimization. While previous studies have reported that a functional polymorphism in the promoter region of the serotonin transporter gene (5-HTTLPR) moderates the effect of stressful life events on depressive symptoms, the present study is the first to evaluate the interaction of this polymorphism with relational peer victimization to predict level of depressive symptoms in young girls. Methods: Participants were 78 girls ages 10 to 14 who had no current or past Axis I disorder. Girls were genotyped for 5-HTTLPR; peer victimization was assessed with the Social Experiences Questionnaire, and depressive symptoms with the Children's Depression Inventory. Results: The 5-HTTLPR polymorphism alone did not predict level of depressive symptoms; the interaction of 5-HTTLPR and relational peer victimization, however, was a significant predictor of depressive symptoms. Follow-up analyses indicated that peer victimization significantly predicted level of depressive symptoms only for girls who were homozygous for the short allele, and not for girls homozygous for the long allele or who were heterozygous for the short and long alleles. Conclusions: The findings support the diathesis-stress model of depression: having two 5-HTTLPR short alleles confers vulnerability to depressive symptoms in adolescent girls when they experience relational peer victimization. These findings also suggest that relational peer victimization, at least for girls with genetic vulnerability, is a significant source of stress and should be recognized in the monitoring and prevention of bullying. Mots-clés : Peer-victimization  bullying  depression  genetic-polymorphisms  5-HTTLPR Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/122596842/PDFSTART

Behavior in Prader-Willi syndrome: relationship to genetic subtypes and age / Elisabeth M. DYKENS in Journal of Child Psychology and Psychiatry (49-9, September 2008)

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 49-9 (September 2008) . - p.1001-1008 Titre : Behavior in Prader-Willi syndrome: relationship to genetic subtypes and age Type de document : texte imprimé Auteurs : Elisabeth M. DYKENS, Auteur; Elizabeth ROOF, Auteur Article en page(s) : p.1001-1008 Langues : Anglais (eng)   Résumé : Background: Some behavioral features of Prader-Willi syndrome (PWS) are associated with the major genetic subtypes of this disorder. While most agree that those with maternal uniparental disomy (UPD) have a distinctive cognitive and psychiatric profile, findings are more controversial regarding possible differences among persons who vary in paternal deletion size. Methods: Caregivers of 88 persons with PWS aged 5 to 51 years (M = 22 years) were administered measures of problem behavior, compulsivity, hyperphagia, and adaptive skills. The sample was well characterized as having relatively large, Type I (n = 26) or smaller, Type II (n = 29) deletions, or UPD (n = 33). Results: No significant behavioral differences were found between the Type I versus Type II deletion groups. Within each genetic subtype, however, differences emerged in how advancing age related to behavior. Although age did not emerge as a significant correlate of behavior in the Type II or UPD groups, in the Type I group age was consistently associated with lower problem behaviors, adaptive skills, and externalizing symptoms. Conclusion: Although differences between deletion subtypes were not found, significant within-subtype differences emerged in relationships between age and behavior. Negative associations between age and behavior in the Type I group only may relate to non-imprinted genes that are deleted in Type I but not Type II cases, including CYFIP1. Altered expression of CYFIP1 is seen in other developmental disabilities, including 15q disorders, and haploinsufficiency of CYFIP1 in Type I PWS cases may be associated with age-related phenotypic effects. Findings underscore the importance of a life-span perspective in phenotypic research. Mots-clés : Prader-Willi-syndrome  genetic-subtypes  age  CYFIP1 Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/121356509/PDFSTART [article] Behavior in Prader-Willi syndrome: relationship to genetic subtypes and age [texte imprimé] / Elisabeth M. DYKENS, Auteur; Elizabeth ROOF, Auteur . - p.1001-1008. Langues : Anglais (eng) inJournal of Child Psychology and Psychiatry > 49-9 (September 2008) . - p.1001-1008   Résumé : Background: Some behavioral features of Prader-Willi syndrome (PWS) are associated with the major genetic subtypes of this disorder. While most agree that those with maternal uniparental disomy (UPD) have a distinctive cognitive and psychiatric profile, findings are more controversial regarding possible differences among persons who vary in paternal deletion size. Methods: Caregivers of 88 persons with PWS aged 5 to 51 years (M = 22 years) were administered measures of problem behavior, compulsivity, hyperphagia, and adaptive skills. The sample was well characterized as having relatively large, Type I (n = 26) or smaller, Type II (n = 29) deletions, or UPD (n = 33). Results: No significant behavioral differences were found between the Type I versus Type II deletion groups. Within each genetic subtype, however, differences emerged in how advancing age related to behavior. Although age did not emerge as a significant correlate of behavior in the Type II or UPD groups, in the Type I group age was consistently associated with lower problem behaviors, adaptive skills, and externalizing symptoms. Conclusion: Although differences between deletion subtypes were not found, significant within-subtype differences emerged in relationships between age and behavior. Negative associations between age and behavior in the Type I group only may relate to non-imprinted genes that are deleted in Type I but not Type II cases, including CYFIP1. Altered expression of CYFIP1 is seen in other developmental disabilities, including 15q disorders, and haploinsufficiency of CYFIP1 in Type I PWS cases may be associated with age-related phenotypic effects. Findings underscore the importance of a life-span perspective in phenotypic research. Mots-clés : Prader-Willi-syndrome  genetic-subtypes  age  CYFIP1 Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/121356509/PDFSTART

Brief Report: Relationship Between Non-verbal IQ and Gender in Autism / Ryan BANACH in Journal of Autism and Developmental Disorders (39-1, January 2009)

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 39-1 (January 2009) . - p.188-193 Titre : Brief Report: Relationship Between Non-verbal IQ and Gender in Autism Type de document : texte imprimé Auteurs : Ryan BANACH, Auteur; Ann THOMPSON, Auteur; Peter SZATMARI, Auteur; Jeremy GOLDBERG, Auteur; Lawrence TUFF, Auteur; Lonnie ZWAIGENBAUM, Auteur; William MAHONEY, Auteur Article en page(s) : p.188-193 Langues : Anglais (eng)   Résumé : It has been proposed that females at risk for autism are protected in some way, so that only those with the greatest genetic liability are affected. Consequently, affected male siblings of females with autism should be more impaired than affected male siblings of male probands. One hundred and ninety-four (194) families with a single child with autism (simplex, SPX) and 154 families with more than one child with autism (multiplex, MPX) were examined on measures of severity, including non-verbal IQ. Among SPX families, girls had lower IQ than boys, but no such differences were seen among MPX families. Similarly, the affected brothers of girls with autism were no different from affected brothers of male probands. These data suggest that MPX and SPX families differ with respect to the relationship between gender and IQ. Mots-clés : Autism  IQ  Gender  Genetic Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.springerlink.com/content/b502566456515212/fulltext.pdf [article] Brief Report: Relationship Between Non-verbal IQ and Gender in Autism [texte imprimé] / Ryan BANACH, Auteur; Ann THOMPSON, Auteur; Peter SZATMARI, Auteur; Jeremy GOLDBERG, Auteur; Lawrence TUFF, Auteur; Lonnie ZWAIGENBAUM, Auteur; William MAHONEY, Auteur . - p.188-193. Langues : Anglais (eng) inJournal of Autism and Developmental Disorders > 39-1 (January 2009) . - p.188-193   Résumé : It has been proposed that females at risk for autism are protected in some way, so that only those with the greatest genetic liability are affected. Consequently, affected male siblings of females with autism should be more impaired than affected male siblings of male probands. One hundred and ninety-four (194) families with a single child with autism (simplex, SPX) and 154 families with more than one child with autism (multiplex, MPX) were examined on measures of severity, including non-verbal IQ. Among SPX families, girls had lower IQ than boys, but no such differences were seen among MPX families. Similarly, the affected brothers of girls with autism were no different from affected brothers of male probands. These data suggest that MPX and SPX families differ with respect to the relationship between gender and IQ. Mots-clés : Autism  IQ  Gender  Genetic Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.springerlink.com/content/b502566456515212/fulltext.pdf

Case Report: Retracing Atypical Development: A Preserved Speech Variant of Rett Syndrome / Peter B. MARSCHIK in Journal of Autism and Developmental Disorders (39-6, June 2009)

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 39-6 (June 2009) . - p.958-961 Titre : Case Report: Retracing Atypical Development: A Preserved Speech Variant of Rett Syndrome Type de document : texte imprimé Auteurs : Peter B. MARSCHIK, Auteur; Christa EINSPIELER, Auteur; Andreas OBERLE, Auteur; Franco LACCONE, Auteur; Heinz F. R. PRECHTL, Auteur Article en page(s) : p.958-961 Langues : Anglais (eng)   Résumé : The subject of the present study is the development of a girl with the preserved speech variant of Rett disorder. Our data are based on detailed retrospective and prospective video analyses. Despite achieving developmental milestones, movement quality was already abnormal during the girl's first half year of life. In addition, early hand stereotypies, idiosyncratic vocalizations, asymmetric eye opening, and abnormal facial expressions are early signs proving that this variant of the Rett complex, too, manifests itself within the first months of life. Mots-clés : Autism-spectrum  Development  Genetic-disorder  General-movements  Language  MECP2  Stereotypies Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.springerlink.com/content/f6u6vq4v8w0n86x5/fulltext.pdf [article] Case Report: Retracing Atypical Development: A Preserved Speech Variant of Rett Syndrome [texte imprimé] / Peter B. MARSCHIK, Auteur; Christa EINSPIELER, Auteur; Andreas OBERLE, Auteur; Franco LACCONE, Auteur; Heinz F. R. PRECHTL, Auteur . - p.958-961. Langues : Anglais (eng) inJournal of Autism and Developmental Disorders > 39-6 (June 2009) . - p.958-961   Résumé : The subject of the present study is the development of a girl with the preserved speech variant of Rett disorder. Our data are based on detailed retrospective and prospective video analyses. Despite achieving developmental milestones, movement quality was already abnormal during the girl's first half year of life. In addition, early hand stereotypies, idiosyncratic vocalizations, asymmetric eye opening, and abnormal facial expressions are early signs proving that this variant of the Rett complex, too, manifests itself within the first months of life. Mots-clés : Autism-spectrum  Development  Genetic-disorder  General-movements  Language  MECP2  Stereotypies Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.springerlink.com/content/f6u6vq4v8w0n86x5/fulltext.pdf

Childhood developmental disorders: an academic and clinical convergence point for psychiatry, neurology, psychology and pediatrics / Allan L. REISS in Journal of Child Psychology and Psychiatry (50-1-2, January/February 2009)

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 50-1-2 (January/February 2009) . - p.87-98 Titre : Childhood developmental disorders: an academic and clinical convergence point for psychiatry, neurology, psychology and pediatrics Type de document : texte imprimé Auteurs : Allan L. REISS, Auteur Article en page(s) : p.87-98 Langues : Anglais (eng)   Résumé : Background: Significant advances in understanding brain development and behavior have not been accompanied by revisions of traditional academic structure. Disciplinary isolation and a lack of meaningful interdisciplinary opportunities are persistent barriers in academic medicine. To enhance clinical practice, research, and training for the next generation, academic centers will need to take bold steps that challenge traditional departmental boundaries. Such change is not only desirable but, in fact, necessary to bring about a truly innovative and more effective approach to treating disorders of the developing brain. Methods: I focus on developmental disorders as a convergence point for transcending traditional academic boundaries. First, the current taxonomy of developmental disorders is described with emphasis on how current diagnostic systems inadvertently hinder research progress. Second, I describe the clinical features of autism, a phenomenologically defined condition, and Rett and fragile X syndromes, neurogenetic diseases that are risk factors for autism. Finally, I describe how the fields of psychiatry, psychology, neurology, and pediatrics now have an unprecedented opportunity to promote an interdisciplinary approach to training, research, and clinical practice and, thus, advance a deeper understanding of developmental disorders. Results: Research focused on autism is increasingly demonstrating the heterogeneity of individuals diagnosed by DSM criteria. This heterogeneity hinders the ability of investigators to replicate research results as well as progress towards more effective, etiology-specific interventions. In contrast, fragile X and Rett syndromes are 'real' diseases for which advances in research are rapidly accelerating towards more disease-specific human treatment trials. Conclusions: A major paradigm shift is required to improve our ability to diagnose and treat individuals with developmental disorders. This paradigm shift must take place at all levels – training, research and clinical activity. As clinicians and scientists who are currently constrained by disciplinary-specific history and training, we must move towards redefining ourselves as clinical neuroscientists with shared interests and expertise that permit a more cohesive and effective approach to improving the lives of patients. Mots-clés : Autism  fragile-X-syndrome  Rett-syndrome  interdisciplinary-training  developmental-disorder  brain-development  genetic-risk-factor  neurogenetic-disorder  academic-medicine  clinical-neuroscience  disciplinary-boundaries Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/121671981/PDFSTART [article] Childhood developmental disorders: an academic and clinical convergence point for psychiatry, neurology, psychology and pediatrics [texte imprimé] / Allan L. REISS, Auteur . - p.87-98. Langues : Anglais (eng) inJournal of Child Psychology and Psychiatry > 50-1-2 (January/February 2009) . - p.87-98   Résumé : Background: Significant advances in understanding brain development and behavior have not been accompanied by revisions of traditional academic structure. Disciplinary isolation and a lack of meaningful interdisciplinary opportunities are persistent barriers in academic medicine. To enhance clinical practice, research, and training for the next generation, academic centers will need to take bold steps that challenge traditional departmental boundaries. Such change is not only desirable but, in fact, necessary to bring about a truly innovative and more effective approach to treating disorders of the developing brain. Methods: I focus on developmental disorders as a convergence point for transcending traditional academic boundaries. First, the current taxonomy of developmental disorders is described with emphasis on how current diagnostic systems inadvertently hinder research progress. Second, I describe the clinical features of autism, a phenomenologically defined condition, and Rett and fragile X syndromes, neurogenetic diseases that are risk factors for autism. Finally, I describe how the fields of psychiatry, psychology, neurology, and pediatrics now have an unprecedented opportunity to promote an interdisciplinary approach to training, research, and clinical practice and, thus, advance a deeper understanding of developmental disorders. Results: Research focused on autism is increasingly demonstrating the heterogeneity of individuals diagnosed by DSM criteria. This heterogeneity hinders the ability of investigators to replicate research results as well as progress towards more effective, etiology-specific interventions. In contrast, fragile X and Rett syndromes are 'real' diseases for which advances in research are rapidly accelerating towards more disease-specific human treatment trials. Conclusions: A major paradigm shift is required to improve our ability to diagnose and treat individuals with developmental disorders. This paradigm shift must take place at all levels – training, research and clinical activity. As clinicians and scientists who are currently constrained by disciplinary-specific history and training, we must move towards redefining ourselves as clinical neuroscientists with shared interests and expertise that permit a more cohesive and effective approach to improving the lives of patients. Mots-clés : Autism  fragile-X-syndrome  Rett-syndrome  interdisciplinary-training  developmental-disorder  brain-development  genetic-risk-factor  neurogenetic-disorder  academic-medicine  clinical-neuroscience  disciplinary-boundaries Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/121671981/PDFSTART

Confirmation study of PTEN mutations among individuals with autism or developmental delays/mental retardation and macrocephaly / Kim L. McBRIDE in Autism Research (3-3, June 2010)

Public ISBD [article]  inAutism Research > 3-3 (June 2010) . - p.137-141 Titre : Confirmation study of PTEN mutations among individuals with autism or developmental delays/mental retardation and macrocephaly Type de document : texte imprimé Auteurs : Kim L. McBRIDE, Auteur; Elizabeth A. VARGA, Auteur; Matthew T. PASTORE, Auteur; Thomas W. PRIOR, Auteur; Kandamurugu MANICKAM, Auteur; Joan F. ATKIN, Auteur; Gail E. HERMAN, Auteur Article en page(s) : p.137-141 Langues : Anglais (eng)   Résumé : There is a strong genetic component to autism spectrum disorders (ASD), but due to significant genetic heterogeneity, individual genetic abnormalities contribute a small percentage to the overall total. Previous studies have demonstrated PTEN mutations in a sizable proportion of individuals with ASD or mental retardation/developmental delays (MR/DD) and macrocephaly that do not have features of Cowden or Bannayan-Riley-Ruvalcaba syndrome. This study was performed to confirm our previous results. We reviewed the charts of individuals who had PTEN clinical sequencing performed at our institution from January 2008 to July 2009. There were 93 subjects tested from our institution during that period. PTEN mutations were found in 2/39 (5.1%) ASD patients and 2/51 (3.9%) MR/DD patients. Three additional patients without mutations had no diagnostic information. Multiple relatives of individuals with a PTEN mutation had macrocephaly, MR, or early onset cancer (breast, renal, and prostate). Of those relatives tested, all had the familial PTEN mutation. None of the affected relatives had previously been diagnosed with Cowden or Bannayan-Riley-Ruvalcaba syndrome. We noted in our previous study several adult relatives without any findings who carried a mutation. Combined with data from our previous cohort, we have found PTEN mutations in 7/99 (7.1%) of individuals with ASD and 8/100 (8.0%) of individuals with MR/DD, all of whom had macrocephaly. We recommend testing for mutations in PTEN for individuals with ASD or MR/DD and macrocephaly. If mutations are found, other family members should be offered testing and the adults offered cancer screening if they have a PTEN mutation. Mots-clés : genetic  Cowden-syndrome  molecular-genetics  PTEN  cancer  autism  developmental-delay Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/123444482/PDFSTART [article] Confirmation study of PTEN mutations among individuals with autism or developmental delays/mental retardation and macrocephaly [texte imprimé] / Kim L. McBRIDE, Auteur; Elizabeth A. VARGA, Auteur; Matthew T. PASTORE, Auteur; Thomas W. PRIOR, Auteur; Kandamurugu MANICKAM, Auteur; Joan F. ATKIN, Auteur; Gail E. HERMAN, Auteur . - p.137-141. Langues : Anglais (eng) inAutism Research > 3-3 (June 2010) . - p.137-141   Résumé : There is a strong genetic component to autism spectrum disorders (ASD), but due to significant genetic heterogeneity, individual genetic abnormalities contribute a small percentage to the overall total. Previous studies have demonstrated PTEN mutations in a sizable proportion of individuals with ASD or mental retardation/developmental delays (MR/DD) and macrocephaly that do not have features of Cowden or Bannayan-Riley-Ruvalcaba syndrome. This study was performed to confirm our previous results. We reviewed the charts of individuals who had PTEN clinical sequencing performed at our institution from January 2008 to July 2009. There were 93 subjects tested from our institution during that period. PTEN mutations were found in 2/39 (5.1%) ASD patients and 2/51 (3.9%) MR/DD patients. Three additional patients without mutations had no diagnostic information. Multiple relatives of individuals with a PTEN mutation had macrocephaly, MR, or early onset cancer (breast, renal, and prostate). Of those relatives tested, all had the familial PTEN mutation. None of the affected relatives had previously been diagnosed with Cowden or Bannayan-Riley-Ruvalcaba syndrome. We noted in our previous study several adult relatives without any findings who carried a mutation. Combined with data from our previous cohort, we have found PTEN mutations in 7/99 (7.1%) of individuals with ASD and 8/100 (8.0%) of individuals with MR/DD, all of whom had macrocephaly. We recommend testing for mutations in PTEN for individuals with ASD or MR/DD and macrocephaly. If mutations are found, other family members should be offered testing and the adults offered cancer screening if they have a PTEN mutation. Mots-clés : genetic  Cowden-syndrome  molecular-genetics  PTEN  cancer  autism  developmental-delay Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/123444482/PDFSTART

Feeling anxious: a twin study of panic/somatic ratings, anxiety sensitivity and heartbeat perception in children / Thalia C. ELEY in Journal of Child Psychology and Psychiatry (48-12, December 2007)

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 48-12 (December 2007) . - p.1184–1191 Titre : Feeling anxious: a twin study of panic/somatic ratings, anxiety sensitivity and heartbeat perception in children Type de document : texte imprimé Auteurs : Thalia C. ELEY, Auteur; Alice M. GREGORY, Auteur; David M. CLARK, Auteur; Anke EHLERS, Auteur Article en page(s) : p.1184–1191 Langues : Anglais (eng)   Résumé : Background: Little is known about mechanisms of genetic influence on panic, particularly in childhood. Cognitive theories of panic disorder highlight threatening interpretations of physical sensations, and increased awareness of such sensations. Specifically, anxiety sensitivity (AS) and heartbeat perception (HBP) have been associated with panic in adults and children. We examined genetic and environmental influences on childhood AS, HBP, panic/somatic ratings, and their associations. Methods: Self-ratings of AS and DSM-based anxiety (including panic/somatic items) were obtained from 300 eight-year-old twin pairs (600 individuals), selected for mother-rated child anxiety at age 7. HBP was also assessed. Results: Panic/somatic ratings were significantly correlated with both AS (r = .55) and continuous HBP error scores (r = −.13). AS and HBP scores showed significantly greater correlations with panic/somatic ratings than with all other anxiety scales, except for HBP and school anxiety. Genetic influences on panic/somatic ratings were modest (15%), and moderate for both AS (37%), and HBP (30%). Non-shared environmental influences were substantial. The genetic correlations between panic/somatic ratings and both AS and HBP error scores were .98 (95% CI: .74–1.00) and −.46 (95% CI: −1.00–1.00) respectively. Conclusions: Self-ratings of panic and AS overlap genetically. Future research should consider whether AS mediates genetic risk for panic disorder. Mots-clés : Heartbeat-perception-(HBP)  anxiety-sensitivity  panic-attacks  genetic  twins Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1469-7610.2007.01838.x [article] Feeling anxious: a twin study of panic/somatic ratings, anxiety sensitivity and heartbeat perception in children [texte imprimé] / Thalia C. ELEY, Auteur; Alice M. GREGORY, Auteur; David M. CLARK, Auteur; Anke EHLERS, Auteur . - p.1184–1191. Langues : Anglais (eng) inJournal of Child Psychology and Psychiatry > 48-12 (December 2007) . - p.1184–1191   Résumé : Background: Little is known about mechanisms of genetic influence on panic, particularly in childhood. Cognitive theories of panic disorder highlight threatening interpretations of physical sensations, and increased awareness of such sensations. Specifically, anxiety sensitivity (AS) and heartbeat perception (HBP) have been associated with panic in adults and children. We examined genetic and environmental influences on childhood AS, HBP, panic/somatic ratings, and their associations. Methods: Self-ratings of AS and DSM-based anxiety (including panic/somatic items) were obtained from 300 eight-year-old twin pairs (600 individuals), selected for mother-rated child anxiety at age 7. HBP was also assessed. Results: Panic/somatic ratings were significantly correlated with both AS (r = .55) and continuous HBP error scores (r = −.13). AS and HBP scores showed significantly greater correlations with panic/somatic ratings than with all other anxiety scales, except for HBP and school anxiety. Genetic influences on panic/somatic ratings were modest (15%), and moderate for both AS (37%), and HBP (30%). Non-shared environmental influences were substantial. The genetic correlations between panic/somatic ratings and both AS and HBP error scores were .98 (95% CI: .74–1.00) and −.46 (95% CI: −1.00–1.00) respectively. Conclusions: Self-ratings of panic and AS overlap genetically. Future research should consider whether AS mediates genetic risk for panic disorder. Mots-clés : Heartbeat-perception-(HBP)  anxiety-sensitivity  panic-attacks  genetic  twins Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1469-7610.2007.01838.x

Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods / Anastasia DIMITROPOULOS in Journal of Autism and Developmental Disorders (38-9, October 2008)

Public ISBD [article]  inJournal of Autism and Developmental Disorders > 38-9 (October 2008) . - p.1642-1653 Titre : Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods Type de document : texte imprimé Auteurs : Anastasia DIMITROPOULOS, Auteur; Robert T. SCHULTZ, Auteur Article en page(s) : p.1642-1653 Langues : Anglais (eng)   Résumé : Prader-Willi syndrome (PWS) is a neurodevelopmental disorder characterized by hyperphagia and food preoccupations. Although dysfunction of the hypothalamus likely has a critical role in hyperphagia, it is only one of several regions involved in the regulation of eating. The purpose of this research was to examine food-related neural circuitry using functional magnetic resonance imaging in individuals with PWS and matched controls. Individuals with PWS showed increased activation in neural circuitry known to mediate hunger and motivation (hypothalamus, OFC) in response to high- versus low-calorie foods and in comparison to controls. This suggests neural circuitry for PWS is abnormally activated during hunger, particularly for high-calorie foods, and may mediate abnormally strong hunger states, therefore playing a significant role in PWS-induced hyperphagia. Mots-clés : Prader-Willi-syndrome  fMRI  Hypothalamus  Food-related  Genetic Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.springerlink.com/content/q88350u87311461u/fulltext.pdf [article] Food-related Neural Circuitry in Prader-Willi Syndrome: Response to High- Versus Low-calorie Foods [texte imprimé] / Anastasia DIMITROPOULOS, Auteur; Robert T. SCHULTZ, Auteur . - p.1642-1653. Langues : Anglais (eng) inJournal of Autism and Developmental Disorders > 38-9 (October 2008) . - p.1642-1653   Résumé : Prader-Willi syndrome (PWS) is a neurodevelopmental disorder characterized by hyperphagia and food preoccupations. Although dysfunction of the hypothalamus likely has a critical role in hyperphagia, it is only one of several regions involved in the regulation of eating. The purpose of this research was to examine food-related neural circuitry using functional magnetic resonance imaging in individuals with PWS and matched controls. Individuals with PWS showed increased activation in neural circuitry known to mediate hunger and motivation (hypothalamus, OFC) in response to high- versus low-calorie foods and in comparison to controls. This suggests neural circuitry for PWS is abnormally activated during hunger, particularly for high-calorie foods, and may mediate abnormally strong hunger states, therefore playing a significant role in PWS-induced hyperphagia. Mots-clés : Prader-Willi-syndrome  fMRI  Hypothalamus  Food-related  Genetic Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.springerlink.com/content/q88350u87311461u/fulltext.pdf

Genetic and environmental influences on extreme personality dispositions in adolescent female twins / Michele L. PERGADIA in Journal of Child Psychology and Psychiatry (47-9, September 2006)

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 47-9 (September 2006) . - p.902–909 Titre : Genetic and environmental influences on extreme personality dispositions in adolescent female twins Type de document : texte imprimé Auteurs : Michele L. PERGADIA, Auteur; Andrew C. HEATH, Auteur; Nicholas G. MARTIN, Auteur; Kathleen K. BUCHOLZ, Auteur; Alexandre A. TODOROV, Auteur; Christina N. LESSOV, Auteur; Pamela A.F. MADDEN, Auteur Article en page(s) : p.902–909 Langues : Anglais (eng)   Résumé : Background: The objective was to determine whether the pattern of environmental and genetic influences on deviant personality scores differs from that observed for the normative range of personality, comparing results in adolescent and adult female twins. Methods: A sample of 2,796 female adolescent twins ascertained from birth records provided Junior Eysenck Personality Questionnaire data. The average age of the sample was 17.0 years (S.D. 2.3). Genetic analyses of continuous and extreme personality scores were conducted. Results were compared for 3,178 adult female twins. Results: Genetic analysis of continuous traits in adolescent female twins were similar to findings in adult female twins, with genetic influences accounting for between 37% and 44% of the variance in Extraversion (Ex), Neuroticism (N), and Social Non-Conformity (SNC), with significant evidence of shared environmental influences (19%) found only for SNC in the adult female twins. Analyses of extreme personality characteristics, defined categorically, in the adolescent data and replicated in the adult female data, yielded estimates for high N and high SNC that deviated substantially (p < .05) from those obtained in the continuous trait analyses, and provided suggestive evidence that shared family environment may play a more important role in determining personality deviance than has been previously found when personality is viewed continuously. However, multiple-threshold models that assumed the same genetic and environmental determinants of both normative range variation and extreme scores gave acceptable fits for each personality dimension. Conclusions: The hypothesis of differences in genetic or environmental factors responsible for N and SNC among female twins with scores in the extreme versus normative ranges was partially supported, but not for Ex. Mots-clés : Personality  genetic-analyses  twin-studies  internalizing  externalizing Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1469-7610.2005.01568.x [article] Genetic and environmental influences on extreme personality dispositions in adolescent female twins [texte imprimé] / Michele L. PERGADIA, Auteur; Andrew C. HEATH, Auteur; Nicholas G. MARTIN, Auteur; Kathleen K. BUCHOLZ, Auteur; Alexandre A. TODOROV, Auteur; Christina N. LESSOV, Auteur; Pamela A.F. MADDEN, Auteur . - p.902–909. Langues : Anglais (eng) inJournal of Child Psychology and Psychiatry > 47-9 (September 2006) . - p.902–909   Résumé : Background: The objective was to determine whether the pattern of environmental and genetic influences on deviant personality scores differs from that observed for the normative range of personality, comparing results in adolescent and adult female twins. Methods: A sample of 2,796 female adolescent twins ascertained from birth records provided Junior Eysenck Personality Questionnaire data. The average age of the sample was 17.0 years (S.D. 2.3). Genetic analyses of continuous and extreme personality scores were conducted. Results were compared for 3,178 adult female twins. Results: Genetic analysis of continuous traits in adolescent female twins were similar to findings in adult female twins, with genetic influences accounting for between 37% and 44% of the variance in Extraversion (Ex), Neuroticism (N), and Social Non-Conformity (SNC), with significant evidence of shared environmental influences (19%) found only for SNC in the adult female twins. Analyses of extreme personality characteristics, defined categorically, in the adolescent data and replicated in the adult female data, yielded estimates for high N and high SNC that deviated substantially (p < .05) from those obtained in the continuous trait analyses, and provided suggestive evidence that shared family environment may play a more important role in determining personality deviance than has been previously found when personality is viewed continuously. However, multiple-threshold models that assumed the same genetic and environmental determinants of both normative range variation and extreme scores gave acceptable fits for each personality dimension. Conclusions: The hypothesis of differences in genetic or environmental factors responsible for N and SNC among female twins with scores in the extreme versus normative ranges was partially supported, but not for Ex. Mots-clés : Personality  genetic-analyses  twin-studies  internalizing  externalizing Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www.blackwell-synergy.com/doi/pdf/10.1111/j.1469-7610.2005.01568.x

Genetic and environmental influences on the transmission of parental depression to children's depression and conduct disturbance: an extended Children of Twins study / Judy L. SILBERG in Journal of Child Psychology and Psychiatry (51-6, June 2010)

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 51-6 (June 2010) . - p.734-744 Titre : Genetic and environmental influences on the transmission of parental depression to children's depression and conduct disturbance: an extended Children of Twins study Type de document : texte imprimé Auteurs : Judy L. SILBERG, Auteur; Hermine H. MAES, Auteur; Lindon J. EAVES, Auteur Article en page(s) : p.734-744 Langues : Anglais (eng)   Résumé : Background: Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their children's behavioral and emotional functioning is not well understood. The present study was undertaken to determine whether parental depression represents a genuine environmental risk factor in children's psychopathology, or whether children's depression/conduct can be explained as a secondary consequence of the genetic liability transmitted from parents to their offspring. Methods: Children of Twins (COT) data collected on 2,674 adult female and male twins, their spouses, and 2,940 of their children were used to address whether genetic and/or family environmental factors best account for the association between depression in parents and depression and conduct problems in their children. Data collected on juvenile twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated using the statistical program Mx. Results: The most compelling model for the association between parental and juvenile depression was a model of direct environmental risk. Both family environmental and genetic factors accounted for the association between parental depression and child conduct disturbance. Conclusions: These findings illustrate how a genetically mediated behavior such as parental depression can have both an environmental and genetic impact on children's behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic liability influences both parental depression and juvenile conduct disturbance, implicating child conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary, our analyses demonstrate differences in the impact of parental depression on different forms of child psychopathology, and at various stages of development. Mots-clés : Children-of-Twins  parental-depression  juvenile-depression  conduct-disturbance  genetic-risk  family-environment Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/123286549/PDFSTART [article] Genetic and environmental influences on the transmission of parental depression to children's depression and conduct disturbance: an extended Children of Twins study [texte imprimé] / Judy L. SILBERG, Auteur; Hermine H. MAES, Auteur; Lindon J. EAVES, Auteur . - p.734-744. Langues : Anglais (eng) inJournal of Child Psychology and Psychiatry > 51-6 (June 2010) . - p.734-744   Résumé : Background: Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their children's behavioral and emotional functioning is not well understood. The present study was undertaken to determine whether parental depression represents a genuine environmental risk factor in children's psychopathology, or whether children's depression/conduct can be explained as a secondary consequence of the genetic liability transmitted from parents to their offspring. Methods: Children of Twins (COT) data collected on 2,674 adult female and male twins, their spouses, and 2,940 of their children were used to address whether genetic and/or family environmental factors best account for the association between depression in parents and depression and conduct problems in their children. Data collected on juvenile twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated using the statistical program Mx. Results: The most compelling model for the association between parental and juvenile depression was a model of direct environmental risk. Both family environmental and genetic factors accounted for the association between parental depression and child conduct disturbance. Conclusions: These findings illustrate how a genetically mediated behavior such as parental depression can have both an environmental and genetic impact on children's behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic liability influences both parental depression and juvenile conduct disturbance, implicating child conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary, our analyses demonstrate differences in the impact of parental depression on different forms of child psychopathology, and at various stages of development. Mots-clés : Children-of-Twins  parental-depression  juvenile-depression  conduct-disturbance  genetic-risk  family-environment Plan de Classement : PER Périodiques   En ligne depuis le poste de consultation du CID : http://www3.interscience.wiley.com/cgi-bin/fulltext/123286549/PDFSTART