45 recherche sur le mot-clé 'Correlation-dimension'

A dynamical analysis of oscillatory responses in the optic tectum / Sergio NEUENSCHWANDER in Cognitive Brain Research, 1-3 (October 1993)

Public ISBD [article]  inCognitive Brain Research > 1-3 (October 1993) . - p.175-181 Titre : A dynamical analysis of oscillatory responses in the optic tectum Type de document : texte imprimé Auteurs : Sergio NEUENSCHWANDER, Auteur ; Jacques MARTINERIE, Auteur ; Bernard RENAULT, Auteur ; Fransisco J. VARELA, Auteur Année de publication : 1993 Article en page(s) : p.175-181 Langues : Anglais (eng) Mots-clés : Optic-tectum Oscillatory-response Local-field-potential Correlation-dimension Non-linear-forecasting Index. décimale : PER Périodiques Résumé : Multi-unit recordings from the optic tectum of an awake pigeon displaying oscillatory behavior evoked by visual stimulus are highly non-stationary and contain a broad band of frequencies under a time-window analysis. Here we extend these observations by a non-linear dynamical analysis of these oscillatory signals (local fields potentials) in successive epochs during background activity and visual responses. Two numerical estimates have been obtained from the original data every 200 ms: (1) correlation dimension and (2) non-linear forecasting of the trajectories. Results from eight different recording sites analyzed are consistent and indicate, in the average, an increase in complexity of the signal during the oscillatory periods. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=781 [article] A dynamical analysis of oscillatory responses in the optic tectum [texte imprimé] / Sergio NEUENSCHWANDER, Auteur ; Jacques MARTINERIE, Auteur ; Bernard RENAULT, Auteur ; Fransisco J. VARELA, Auteur . - 1993 . - p.175-181. Langues : Anglais (eng) in Cognitive Brain Research > 1-3 (October 1993) . - p.175-181 Mots-clés : Optic-tectum Oscillatory-response Local-field-potential Correlation-dimension Non-linear-forecasting Index. décimale : PER Périodiques Résumé : Multi-unit recordings from the optic tectum of an awake pigeon displaying oscillatory behavior evoked by visual stimulus are highly non-stationary and contain a broad band of frequencies under a time-window analysis. Here we extend these observations by a non-linear dynamical analysis of these oscillatory signals (local fields potentials) in successive epochs during background activity and visual responses. Two numerical estimates have been obtained from the original data every 200 ms: (1) correlation dimension and (2) non-linear forecasting of the trajectories. Results from eight different recording sites analyzed are consistent and indicate, in the average, an increase in complexity of the signal during the oscillatory periods. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=781

Altered medial prefrontal cortex and dorsal raphé activity predict genotype and correlate with abnormal learning behavior in a mouse model of autism-associated 2p16.3 deletion / Rebecca B. HUGHES in Autism Research, 15-4 (April 2022)  

Public ISBD [article]  inAutism Research > 15-4 (April 2022) . - p.614-627 Titre : Altered medial prefrontal cortex and dorsal raphé activity predict genotype and correlate with abnormal learning behavior in a mouse model of autism-associated 2p16.3 deletion Type de document : texte imprimé Auteurs : Rebecca B. HUGHES, Auteur ; Jayde WHITTINGHAM-DOWD, Auteur ; Steven J. CLAPCOTE, Auteur ; Susan J. BROUGHTON, Auteur ; Neil DAWSON, Auteur Article en page(s) : p.614-627 Langues : Anglais (eng) Mots-clés : Animals  Autism Spectrum Disorder/genetics  Autistic Disorder  Disease Models, Animal  Dorsal Raphe Nucleus  Genotype  Humans  Male  Mice  Prefrontal Cortex/diagnostic imaging  Reversal Learning  cognitive neuroscience  copy number variation/copy number variants  frontal lobe  genotype-phenotype correlation  imaging genetics  mouse models  serotonin Index. décimale : PER Périodiques Résumé : 2p16.3 deletion, involving NEUREXIN1 (NRXN1) heterozygous deletion, substantially increases the risk of developing autism and other neurodevelopmental disorders. We have a poor understanding of how NRXN1 heterozygosity impacts on brain function and cognition to increase the risk of developing the disorder. Here we characterize the impact of Nrxn1 heterozygosity on cerebral metabolism, in mice, using (14) C-2-deoxyglucose imaging. We also assess performance in an olfactory-based discrimination and reversal learning (OB-DaRL) task and locomotor activity. We use decision tree classifiers to test the predictive relationship between cerebral metabolism and Nrxn1 genotype. Our data show that Nrxn1 heterozygosity induces prefrontal cortex (medial prelimbic cortex, mPrL) hypometabolism and a contrasting dorsal raphé nucleus (DRN) hypermetabolism. Metabolism in these regions allows for the predictive classification of Nrxn1 genotype. Consistent with reduced mPrL glucose utilization, prefrontal cortex insulin receptor signaling is decreased in Nrxn1 (+/-) mice. Behaviorally, Nrxn1 (+/-) mice show enhanced learning of a novel discrimination, impaired reversal learning and an increased latency to make correct choices. In addition, male Nrxn1 (+/-) mice show hyperlocomotor activity. Correlative analysis suggests that mPrL hypometabolism contributes to the enhanced novel odor discrimination seen in Nrxn1 (+/-) mice, while DRN hypermetabolism contributes to their increased latency in making correct choices. The data show that Nrxn1 heterozygosity impacts on prefrontal cortex and serotonin system function, which contribute to the cognitive alterations seen in these animals. The data suggest that Nrxn1 (+/-) mice provide a translational model for the cognitive and behavioral alterations seen in autism and other neurodevelopmental disorders associated with 2p16.3 deletion. LAY SUMMARY: Deletion of the chromosomal region 2p16.3, involving reduced NEUREXIN1 gene expression, dramatically increases the risk of developing autism. Here, we show that reduced Neurexin1 expression, in mice, impacts on the prefrontal cortex and impairs cognitive flexibility. The data suggest that 2p16.3 deletion increases the risk of developing autism by impacting on the prefrontal cortex. Mice with the deletion are a useful model for testing new drugs to treat the cognitive flexibility problems experienced by people with autism. En ligne : https://dx.doi.org/10.1002/aur.2685 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 [article] Altered medial prefrontal cortex and dorsal raphé activity predict genotype and correlate with abnormal learning behavior in a mouse model of autism-associated 2p16.3 deletion [texte imprimé] / Rebecca B. HUGHES, Auteur ; Jayde WHITTINGHAM-DOWD, Auteur ; Steven J. CLAPCOTE, Auteur ; Susan J. BROUGHTON, Auteur ; Neil DAWSON, Auteur . - p.614-627. Langues : Anglais (eng) in Autism Research > 15-4 (April 2022) . - p.614-627 Mots-clés : Animals  Autism Spectrum Disorder/genetics  Autistic Disorder  Disease Models, Animal  Dorsal Raphe Nucleus  Genotype  Humans  Male  Mice  Prefrontal Cortex/diagnostic imaging  Reversal Learning  cognitive neuroscience  copy number variation/copy number variants  frontal lobe  genotype-phenotype correlation  imaging genetics  mouse models  serotonin Index. décimale : PER Périodiques Résumé : 2p16.3 deletion, involving NEUREXIN1 (NRXN1) heterozygous deletion, substantially increases the risk of developing autism and other neurodevelopmental disorders. We have a poor understanding of how NRXN1 heterozygosity impacts on brain function and cognition to increase the risk of developing the disorder. Here we characterize the impact of Nrxn1 heterozygosity on cerebral metabolism, in mice, using (14) C-2-deoxyglucose imaging. We also assess performance in an olfactory-based discrimination and reversal learning (OB-DaRL) task and locomotor activity. We use decision tree classifiers to test the predictive relationship between cerebral metabolism and Nrxn1 genotype. Our data show that Nrxn1 heterozygosity induces prefrontal cortex (medial prelimbic cortex, mPrL) hypometabolism and a contrasting dorsal raphé nucleus (DRN) hypermetabolism. Metabolism in these regions allows for the predictive classification of Nrxn1 genotype. Consistent with reduced mPrL glucose utilization, prefrontal cortex insulin receptor signaling is decreased in Nrxn1 (+/-) mice. Behaviorally, Nrxn1 (+/-) mice show enhanced learning of a novel discrimination, impaired reversal learning and an increased latency to make correct choices. In addition, male Nrxn1 (+/-) mice show hyperlocomotor activity. Correlative analysis suggests that mPrL hypometabolism contributes to the enhanced novel odor discrimination seen in Nrxn1 (+/-) mice, while DRN hypermetabolism contributes to their increased latency in making correct choices. The data show that Nrxn1 heterozygosity impacts on prefrontal cortex and serotonin system function, which contribute to the cognitive alterations seen in these animals. The data suggest that Nrxn1 (+/-) mice provide a translational model for the cognitive and behavioral alterations seen in autism and other neurodevelopmental disorders associated with 2p16.3 deletion. LAY SUMMARY: Deletion of the chromosomal region 2p16.3, involving reduced NEUREXIN1 gene expression, dramatically increases the risk of developing autism. Here, we show that reduced Neurexin1 expression, in mice, impacts on the prefrontal cortex and impairs cognitive flexibility. The data suggest that 2p16.3 deletion increases the risk of developing autism by impacting on the prefrontal cortex. Mice with the deletion are a useful model for testing new drugs to treat the cognitive flexibility problems experienced by people with autism. En ligne : https://dx.doi.org/10.1002/aur.2685 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473

An atlas of genetic correlations between gestational age and common psychiatric disorders / Yao YAO in Autism Research, 15-6 (June 2022)  

Public ISBD [article]  inAutism Research > 15-6 (June 2022) . - p.1008-1017 Titre : An atlas of genetic correlations between gestational age and common psychiatric disorders Type de document : texte imprimé Auteurs : Yao YAO, Auteur ; Chun'e LI, Auteur ; Peilin MENG, Auteur ; Bolun CHENG, Auteur ; Shiqiang CHENG, Auteur ; Li LIU, Auteur ; Xuena YANG, Auteur ; Yumeng JIA, Auteur ; Yan WEN, Auteur ; Feng ZHANG, Auteur Article en page(s) : p.1008-1017 Langues : Anglais (eng) Mots-clés : Attention Deficit Disorder with Hyperactivity/genetics  Autism Spectrum Disorder/genetics  Depressive Disorder, Major/genetics  Female  Genetic Predisposition to Disease  Genome-Wide Association Study  Gestational Age  Humans  Infant, Newborn  Mendelian Randomization Analysis  Premature Birth/genetics  Proteomics  genetic correlation  linkage disequilibrium score regression  psychiatric disorders Index. décimale : PER Périodiques Résumé : We aim to systematically explore the potential genetic correlations between five major psychiatric disorders and gestational ages. Genome-wide association study (GWAS) summary datasets of attention deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), schizophrenia (SCZ) and major depressive disorder (MDD) in discovery were downloaded from the Psychiatric GWAS Consortium (PGC) website. Suggestive (Raw p?< 0.05) genetic associations in the discovery phrase were further replicated in independent GWASs which downloaded from PGC, the FinnGen study or Integrative Psychiatric Research (iPSYCH) website. GWASs of gestational duration, preterm and post-term birth were derived from previous studies of infants from the Early Growth Genetics (EGG) Consortium, the iPSYCH study, and the Genomic and Proteomic Network for Preterm Birth Research (GPN). We calculated genetic correlations using linkage disequilibrium score (LDSC) regression. Mendelian randomization (MR) analyses were performed to investigate the causal effects. We identified four suggestive genetic correlations between psychiatric disorders and gestational age factors in discovery LDSC and two replicated in a confirmation LDSC: gestational duration and ADHD (r(g) = -0.1405, FDR p = 0.0406), post-term birth and SCZ (r(g) = -0.2003, FDR p = 0.0042). We also observed causal effect of post-term birth on SCZ by MR (P(Weighted median) = 0.037, P(Inverse variance weighted) = 0.007). Our analysis suggested no significant evidence of horizontal pleiotropy and heterogeneity. This study showed the genetic correlation evidences between gestational age phenotypes and psychiatric disorders, providing novel clues for understanding the pathogenic factors of common psychiatric disorders. LAY SUMMARY: Whereas gestational age factors were reported to be associated with psychiatric disorders, the genetic relationship and causality remain to be revealed. The present study reported the first large-scale genetic correlations investigation of the associations between gestational age phenotypes and psychiatric disorders. Results indicate causal relationships between post-term birth and schizophrenia (SCZ), as well as suggestive genetic correlations between gestational duration and attention deficit/hyperactivity disorder (ADHD). This study provided novel clues for understanding the pathogenic factors of common psychiatric disorders. En ligne : http://dx.doi.org/10.1002/aur.2719 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=476 [article] An atlas of genetic correlations between gestational age and common psychiatric disorders [texte imprimé] / Yao YAO, Auteur ; Chun'e LI, Auteur ; Peilin MENG, Auteur ; Bolun CHENG, Auteur ; Shiqiang CHENG, Auteur ; Li LIU, Auteur ; Xuena YANG, Auteur ; Yumeng JIA, Auteur ; Yan WEN, Auteur ; Feng ZHANG, Auteur . - p.1008-1017. Langues : Anglais (eng) in Autism Research > 15-6 (June 2022) . - p.1008-1017 Mots-clés : Attention Deficit Disorder with Hyperactivity/genetics  Autism Spectrum Disorder/genetics  Depressive Disorder, Major/genetics  Female  Genetic Predisposition to Disease  Genome-Wide Association Study  Gestational Age  Humans  Infant, Newborn  Mendelian Randomization Analysis  Premature Birth/genetics  Proteomics  genetic correlation  linkage disequilibrium score regression  psychiatric disorders Index. décimale : PER Périodiques Résumé : We aim to systematically explore the potential genetic correlations between five major psychiatric disorders and gestational ages. Genome-wide association study (GWAS) summary datasets of attention deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), schizophrenia (SCZ) and major depressive disorder (MDD) in discovery were downloaded from the Psychiatric GWAS Consortium (PGC) website. Suggestive (Raw p?< 0.05) genetic associations in the discovery phrase were further replicated in independent GWASs which downloaded from PGC, the FinnGen study or Integrative Psychiatric Research (iPSYCH) website. GWASs of gestational duration, preterm and post-term birth were derived from previous studies of infants from the Early Growth Genetics (EGG) Consortium, the iPSYCH study, and the Genomic and Proteomic Network for Preterm Birth Research (GPN). We calculated genetic correlations using linkage disequilibrium score (LDSC) regression. Mendelian randomization (MR) analyses were performed to investigate the causal effects. We identified four suggestive genetic correlations between psychiatric disorders and gestational age factors in discovery LDSC and two replicated in a confirmation LDSC: gestational duration and ADHD (r(g) = -0.1405, FDR p = 0.0406), post-term birth and SCZ (r(g) = -0.2003, FDR p = 0.0042). We also observed causal effect of post-term birth on SCZ by MR (P(Weighted median) = 0.037, P(Inverse variance weighted) = 0.007). Our analysis suggested no significant evidence of horizontal pleiotropy and heterogeneity. This study showed the genetic correlation evidences between gestational age phenotypes and psychiatric disorders, providing novel clues for understanding the pathogenic factors of common psychiatric disorders. LAY SUMMARY: Whereas gestational age factors were reported to be associated with psychiatric disorders, the genetic relationship and causality remain to be revealed. The present study reported the first large-scale genetic correlations investigation of the associations between gestational age phenotypes and psychiatric disorders. Results indicate causal relationships between post-term birth and schizophrenia (SCZ), as well as suggestive genetic correlations between gestational duration and attention deficit/hyperactivity disorder (ADHD). This study provided novel clues for understanding the pathogenic factors of common psychiatric disorders. En ligne : http://dx.doi.org/10.1002/aur.2719 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=476

Autism spectrum disorder and brain volume link through a set of mTOR-related genes / Martina ARENELLA in Journal of Child Psychology and Psychiatry, 64-7 (July 2023)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 64-7 (July 2023) . - p.1007-1014 Titre : Autism spectrum disorder and brain volume link through a set of mTOR-related genes Type de document : texte imprimé Auteurs : Martina ARENELLA, Auteur ; Nina R. MOTA, Auteur ; Mariel W.A. TEUNISSEN, Auteur ; Han G. BRUNNER, Auteur ; Janita B. BRALTEN, Auteur Article en page(s) : p.1007-1014 Langues : Anglais (eng) Mots-clés : Autism spectrum disorders  genetics  brain volume  mammalian target of rapamycin  stratified genetic correlation Index. décimale : PER Périodiques Résumé : Background Larger than average head and brain sizes are often observed in individuals with autism spectrum disorders (ASDs). ASD and brain volume are both highly heritable, with multiple genetic variants contributing. However, it is unclear whether ASD and brain volume share any genetic mechanisms. Genes from the mammalian target of rapamycin (mTOR) pathway influence brain volume, and variants are found in rare genetic syndromes that include ASD features. Here we investigated whether variants in mTOR-related genes are also associated with ASD and if they constitute a genetic link between large brains and ASD. Methods We extended our analyses between large heads (macrocephaly) and rare de novo mTOR-related variants in an intellectual disability cohort (N = 2,258). Subsequently using Fisher's exact tests we investigated the co-occurrence of mTOR-related de novo variants and ASD in the de-novo-db database (N = 23,098). We next selected common genetic variants within a set of 96 mTOR-related genes in genome-wide genetic association data of ASD (N = 46,350) to test gene-set association using MAGMA. Lastly, we tested genetic correlation between genome-wide genetic association data of ASD (N = 46,350) and intracranial volume (N = 25,974) globally using linkage disequilibrium score regression as well as mTOR specific by restricting the genetic correlation to the mTOR-related genes using GNOVA. Results Our results show that both macrocephaly and ASD occur above chance level in individuals carrying rare de novo variants in mTOR-related genes. We found a significant mTOR gene-set association with ASD (p = .0029) and an mTOR-stratified positive genetic correlation between ASD and intracranial volume (p = .027), despite the absence of a significant genome-wide correlation (p = .81). Conclusions This work indicates that both rare and common variants in mTOR-related genes are associated with brain volume and ASD and genetically correlate them in the expected direction. We demonstrate that genes involved in mTOR signalling are potential mediators of the relationship between having a large brain and having ASD. En ligne : https://doi.org/10.1111/jcpp.13783 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=508 [article] Autism spectrum disorder and brain volume link through a set of mTOR-related genes [texte imprimé] / Martina ARENELLA, Auteur ; Nina R. MOTA, Auteur ; Mariel W.A. TEUNISSEN, Auteur ; Han G. BRUNNER, Auteur ; Janita B. BRALTEN, Auteur . - p.1007-1014. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 64-7 (July 2023) . - p.1007-1014 Mots-clés : Autism spectrum disorders  genetics  brain volume  mammalian target of rapamycin  stratified genetic correlation Index. décimale : PER Périodiques Résumé : Background Larger than average head and brain sizes are often observed in individuals with autism spectrum disorders (ASDs). ASD and brain volume are both highly heritable, with multiple genetic variants contributing. However, it is unclear whether ASD and brain volume share any genetic mechanisms. Genes from the mammalian target of rapamycin (mTOR) pathway influence brain volume, and variants are found in rare genetic syndromes that include ASD features. Here we investigated whether variants in mTOR-related genes are also associated with ASD and if they constitute a genetic link between large brains and ASD. Methods We extended our analyses between large heads (macrocephaly) and rare de novo mTOR-related variants in an intellectual disability cohort (N = 2,258). Subsequently using Fisher's exact tests we investigated the co-occurrence of mTOR-related de novo variants and ASD in the de-novo-db database (N = 23,098). We next selected common genetic variants within a set of 96 mTOR-related genes in genome-wide genetic association data of ASD (N = 46,350) to test gene-set association using MAGMA. Lastly, we tested genetic correlation between genome-wide genetic association data of ASD (N = 46,350) and intracranial volume (N = 25,974) globally using linkage disequilibrium score regression as well as mTOR specific by restricting the genetic correlation to the mTOR-related genes using GNOVA. Results Our results show that both macrocephaly and ASD occur above chance level in individuals carrying rare de novo variants in mTOR-related genes. We found a significant mTOR gene-set association with ASD (p = .0029) and an mTOR-stratified positive genetic correlation between ASD and intracranial volume (p = .027), despite the absence of a significant genome-wide correlation (p = .81). Conclusions This work indicates that both rare and common variants in mTOR-related genes are associated with brain volume and ASD and genetically correlate them in the expected direction. We demonstrate that genes involved in mTOR signalling are potential mediators of the relationship between having a large brain and having ASD. En ligne : https://doi.org/10.1111/jcpp.13783 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=508

Biological and rearing mother influences on child ADHD symptoms: revisiting the developmental interface between nature and nurture / Gordon T. HAROLD in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1038-1046 Titre : Biological and rearing mother influences on child ADHD symptoms: revisiting the developmental interface between nature and nurture Type de document : texte imprimé Auteurs : Gordon T. HAROLD, Auteur ; Leslie D. LEVE, Auteur ; Douglas BARRETT, Auteur ; Kit K. ELAM, Auteur ; Jenae M. NEIDERHISER, Auteur ; Misaki N. NATSUAKI, Auteur ; Daniel S. SHAW, Auteur ; David REISS, Auteur ; Anita THAPAR, Auteur Article en page(s) : p.1038-1046 Langues : Anglais (eng) Mots-clés : ADHD  parenting  gene-environment correlation  adoption Index. décimale : PER Périodiques Résumé : Background Families of children with attention deficit hyperactivity disorder (ADHD) report more negative family relationships than families of children without ADHD. Questions remain as to the role of genetic factors underlying associations between family relationships and children's ADHD symptoms, and the role of children's ADHD symptoms as an evocative influence on the quality of relationships experienced within such families. Utilizing the attributes of two genetically sensitive research designs, the present study examined associations between biologically related and nonbiologically related maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. The combined attributes of the study designs permit assessment of associations while controlling for passive genotype-environment correlation and directly examining evocative genotype-environment correlation (rGE); two relatively under examined confounds of past research in this area. Methods A cross-sectional adoption-at-conception design (Cardiff IVF Study; C-IVF) and a longitudinal adoption-at-birth design (Early Growth and Development Study; EGDS) were used. The C-IVF sample included 160 mothers and children (age 5–8 years). The EGDS sample included 320 linked sets of adopted children (age 6 years), adoptive-, and biologically related mothers. Questionnaires were used to assess maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. A cross-rater approach was used across measures of maternal behavior (mother reports) and child ADHD symptoms (father reports). Results Significant associations were revealed between rearing mother ADHD symptoms, hostile parenting behavior, and child ADHD symptoms in both samples. Because both samples consisted of genetically unrelated mothers and children, passive rGE was removed as a possible explanatory factor underlying these associations. Further, path analysis revealed evidence for evocative rGE processes in the longitudinal adoption-at-birth study (EGDS) from biologically related maternal ADHD symptoms to biologically unrelated maternal hostile parenting through early disrupted child behavior (impulsivity/activation), with maternal hostile parenting and disrupted child behavior associated with later child ADHD symptoms, controlling for concurrent adoptive mother ADHD symptoms. Conclusions Results highlight the importance of genetically influenced child ADHD-related temperamental attributes on genetically unrelated maternal hostility that in turn links to later child ADHD symptoms. Implications for intervention programs focusing on early family processes and the precursors of child ADHD symptoms are discussed. En ligne : http://dx.doi.org/10.1111/jcpp.12100 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Biological and rearing mother influences on child ADHD symptoms: revisiting the developmental interface between nature and nurture [texte imprimé] / Gordon T. HAROLD, Auteur ; Leslie D. LEVE, Auteur ; Douglas BARRETT, Auteur ; Kit K. ELAM, Auteur ; Jenae M. NEIDERHISER, Auteur ; Misaki N. NATSUAKI, Auteur ; Daniel S. SHAW, Auteur ; David REISS, Auteur ; Anita THAPAR, Auteur . - p.1038-1046. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1038-1046 Mots-clés : ADHD  parenting  gene-environment correlation  adoption Index. décimale : PER Périodiques Résumé : Background Families of children with attention deficit hyperactivity disorder (ADHD) report more negative family relationships than families of children without ADHD. Questions remain as to the role of genetic factors underlying associations between family relationships and children's ADHD symptoms, and the role of children's ADHD symptoms as an evocative influence on the quality of relationships experienced within such families. Utilizing the attributes of two genetically sensitive research designs, the present study examined associations between biologically related and nonbiologically related maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. The combined attributes of the study designs permit assessment of associations while controlling for passive genotype-environment correlation and directly examining evocative genotype-environment correlation (rGE); two relatively under examined confounds of past research in this area. Methods A cross-sectional adoption-at-conception design (Cardiff IVF Study; C-IVF) and a longitudinal adoption-at-birth design (Early Growth and Development Study; EGDS) were used. The C-IVF sample included 160 mothers and children (age 5–8 years). The EGDS sample included 320 linked sets of adopted children (age 6 years), adoptive-, and biologically related mothers. Questionnaires were used to assess maternal ADHD symptoms, parenting practices, child impulsivity/activation, and child ADHD symptoms. A cross-rater approach was used across measures of maternal behavior (mother reports) and child ADHD symptoms (father reports). Results Significant associations were revealed between rearing mother ADHD symptoms, hostile parenting behavior, and child ADHD symptoms in both samples. Because both samples consisted of genetically unrelated mothers and children, passive rGE was removed as a possible explanatory factor underlying these associations. Further, path analysis revealed evidence for evocative rGE processes in the longitudinal adoption-at-birth study (EGDS) from biologically related maternal ADHD symptoms to biologically unrelated maternal hostile parenting through early disrupted child behavior (impulsivity/activation), with maternal hostile parenting and disrupted child behavior associated with later child ADHD symptoms, controlling for concurrent adoptive mother ADHD symptoms. Conclusions Results highlight the importance of genetically influenced child ADHD-related temperamental attributes on genetically unrelated maternal hostility that in turn links to later child ADHD symptoms. Implications for intervention programs focusing on early family processes and the precursors of child ADHD symptoms are discussed. En ligne : http://dx.doi.org/10.1111/jcpp.12100 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Brief Report: Analysis of the Relationship Between Turn Taking and Joint Attention for Toddlers with Autism / Kwangwon LEE in Journal of Autism and Developmental Disorders, 50-7 (July 2020)  

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Brief Report: The Training and Assessment of Relational Precursors and Abilities (TARPA): A Preliminary Analysis / Laura MORAN in Journal of Autism and Developmental Disorders, 40-9 (September 2010)  

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Chaotic homes and school achievement: a twin study / Ken B. HANSCOMBE in Journal of Child Psychology and Psychiatry, 52-11 (November 2011)  

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Commentary: Will genomics revolutionise research on gene-environment interplay? / Robert PLOMIN in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

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Content, diagnostic, correlational, and genetic similarities between common measures of childhood aggressive behaviors and related psychiatric traits / Anne M. HENDRIKS in Journal of Child Psychology and Psychiatry, 61-12 (December 2020)  

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