Common variation contributes to the genetic architecture of social communication traits / Beate ST POURCAIN in Molecular Autism, (September 2013)  

Public ISBD [article]  inMolecular Autism > (September 2013) Titre : Common variation contributes to the genetic architecture of social communication traits Type de document : texte imprimé Auteurs : Beate ST POURCAIN, Auteur ; Andrew J.O. WHITEHOUSE, Auteur ; Wei ANG, Auteur ; Nicole WARRINGTON, Auteur ; Joseph GLESSNER, Auteur ; Kai WANG, Auteur ; Nicholas TIMPSON, Auteur ; David EVANS, Auteur ; John KEMP, Auteur ; Susan RING, Auteur ; Wendy MCARDLE, Auteur ; Jean GOLDING, Auteur ; Hakon HAKONARSON, Auteur ; Craig E. PENNELL, Auteur ; George SMITH, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Social communication difficulties represent an autistic trait that is highly heritable and persistent during the course of development. However, little is known about the underlying genetic architecture of this phenotype. We performed a genome-wide association study on parent-reported social communication problems using items of the children's communication checklist (age 10 to 11 years) studying single and/or joint marker effects. Analyses were conducted in a large UK population-based birth cohort (Avon Longitudinal Study of Parents and their Children, ALSPAC, N = 5,584) and followed-up within a sample of children with comparable measures from Western Australia (RAINE, N = 1364). Two of our seven independent top signals (P-discovery 1.0E-05) were replicated (0.009 P-replication [less than or equal to]0.02) within RAINE and suggested evidence for association at 6p22.1 (rs9257616, meta-P = 2.5E-07) and 14q22.1 (rs2352908, meta-P = 1.1E-06). The signal at 6p22.1 was identified within the olfactory receptor gene cluster within the broader major histocompatibility complex (MHC) region. The strongest candidate locus within this genomic area was TRIM27. This gene encodes an ubiquitin E3 ligase, which is an interaction partner of methyl-CpG-binding domain (MBD) proteins, such as MBD3 and MBD4, and rare protein-coding mutations within MBD3 and MBD4 have been linked to autism. The signal at 14q22.1 was found within a gene-poor region.Single-variant findings were complemented by estimations of the narrow-sense heritability in ALSPAC suggesting that approximately a fifth of the phenotypic variance in social communication traits is accounted for by joint additive effects of genotyped single nucleotide polymorphisms throughout the genome (h2(SE) = 0.18(0.066), P = 0.0027). Overall, our study provides both joint and single-SNP-based evidence for the contribution of common polymorphisms to variation in social communication phenotypes. En ligne : http://dx.doi.org/10.1186/2040-2392-4-34 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227 [article] Common variation contributes to the genetic architecture of social communication traits [texte imprimé] / Beate ST POURCAIN, Auteur ; Andrew J.O. WHITEHOUSE, Auteur ; Wei ANG, Auteur ; Nicole WARRINGTON, Auteur ; Joseph GLESSNER, Auteur ; Kai WANG, Auteur ; Nicholas TIMPSON, Auteur ; David EVANS, Auteur ; John KEMP, Auteur ; Susan RING, Auteur ; Wendy MCARDLE, Auteur ; Jean GOLDING, Auteur ; Hakon HAKONARSON, Auteur ; Craig E. PENNELL, Auteur ; George SMITH, Auteur. Langues : Anglais (eng) in Molecular Autism > (September 2013) Index. décimale : PER Périodiques Résumé : Social communication difficulties represent an autistic trait that is highly heritable and persistent during the course of development. However, little is known about the underlying genetic architecture of this phenotype. We performed a genome-wide association study on parent-reported social communication problems using items of the children's communication checklist (age 10 to 11 years) studying single and/or joint marker effects. Analyses were conducted in a large UK population-based birth cohort (Avon Longitudinal Study of Parents and their Children, ALSPAC, N = 5,584) and followed-up within a sample of children with comparable measures from Western Australia (RAINE, N = 1364). Two of our seven independent top signals (P-discovery 1.0E-05) were replicated (0.009 P-replication [less than or equal to]0.02) within RAINE and suggested evidence for association at 6p22.1 (rs9257616, meta-P = 2.5E-07) and 14q22.1 (rs2352908, meta-P = 1.1E-06). The signal at 6p22.1 was identified within the olfactory receptor gene cluster within the broader major histocompatibility complex (MHC) region. The strongest candidate locus within this genomic area was TRIM27. This gene encodes an ubiquitin E3 ligase, which is an interaction partner of methyl-CpG-binding domain (MBD) proteins, such as MBD3 and MBD4, and rare protein-coding mutations within MBD3 and MBD4 have been linked to autism. The signal at 14q22.1 was found within a gene-poor region.Single-variant findings were complemented by estimations of the narrow-sense heritability in ALSPAC suggesting that approximately a fifth of the phenotypic variance in social communication traits is accounted for by joint additive effects of genotyped single nucleotide polymorphisms throughout the genome (h2(SE) = 0.18(0.066), P = 0.0027). Overall, our study provides both joint and single-SNP-based evidence for the contribution of common polymorphisms to variation in social communication phenotypes. En ligne : http://dx.doi.org/10.1186/2040-2392-4-34 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227

Direct and indirect genetic effects on early neurodevelopmental traits / Laura HEGEMANN in Journal of Child Psychology and Psychiatry, 66-7 (July 2025)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 66-7 (July 2025) . - p.1053-1064 Titre : Direct and indirect genetic effects on early neurodevelopmental traits Type de document : texte imprimé Auteurs : Laura HEGEMANN, Auteur ; Espen M. EILERTSEN, Auteur ; Johanne HAGEN PETTERSEN, Auteur ; Elizabeth C. CORFIELD, Auteur ; Rosa CHEESMAN, Auteur ; Leonard FRACH, Auteur ; Ludvig DAAE BJØRNDAL, Auteur ; Helga ASK, Auteur ; Beate ST POURCAIN, Auteur ; Alexandra HAVDAHL, Auteur ; Laurie J. HANNIGAN, Auteur Article en page(s) : p.1053-1064 Langues : Anglais (eng) Mots-clés : Autism  ADHD  MoBa  indirect genetic effects  genetic nurture  neurodevelopmental traits Index. décimale : PER Périodiques Résumé : Background Neurodevelopmental conditions are highly heritable. Recent studies have shown that genomic heritability estimates can be confounded by genetic effects mediated via the environment (indirect genetic effects). However, the relative importance of direct versus indirect genetic effects on early variability in traits related to neurodevelopmental conditions is unknown. Methods The sample included up to 24,692 parent-offspring trios from the Norwegian MoBa cohort. We use Trio-GCTA to estimate latent direct and indirect genetic effects on mother-reported neurodevelopmental traits at age of 3 years (restricted and repetitive behaviors and interests, inattention, hyperactivity, language, social, and motor development). Further, we investigate to what extent direct and indirect effects are attributable to common genetic variants associated with autism, ADHD, developmental dyslexia, educational attainment, and cognitive ability using polygenic scores (PGS) in regression modeling. Results We find evidence for contributions of direct and indirect latent common genetic effects to inattention (direct: explaining 4.8% of variance, indirect: 6.7%) hyperactivity (direct: 1.3%, indirect: 9.6%), and restricted and repetitive behaviors (direct: 0.8%, indirect: 7.3%). Direct effects best explained variation in social and communication, language, and motor development (5.1% 5.7%). Direct genetic effects on inattention were captured by PGS for ADHD, educational attainment, and cognitive ability, whereas direct genetic effects on language development were captured by cognitive ability, educational attainment, and autism PGS. Indirect genetic effects on neurodevelopmental traits were primarily captured by educational attainment and/or cognitive ability PGS. Conclusions Results were consistent with differential contributions to neurodevelopmental traits in early childhood from direct and indirect genetic effects. Indirect effects were particularly important for hyperactivity and restricted and repetitive behaviors and interests and may be linked to genetic variation associated with cognition and educational attainment. Our findings illustrate the importance of within-family methods for disentangling genetic processes that influence early neurodevelopmental traits, even when identifiable associations are small. En ligne : https://doi.org/10.1111/jcpp.14122 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=562 [article] Direct and indirect genetic effects on early neurodevelopmental traits [texte imprimé] / Laura HEGEMANN, Auteur ; Espen M. EILERTSEN, Auteur ; Johanne HAGEN PETTERSEN, Auteur ; Elizabeth C. CORFIELD, Auteur ; Rosa CHEESMAN, Auteur ; Leonard FRACH, Auteur ; Ludvig DAAE BJØRNDAL, Auteur ; Helga ASK, Auteur ; Beate ST POURCAIN, Auteur ; Alexandra HAVDAHL, Auteur ; Laurie J. HANNIGAN, Auteur . - p.1053-1064. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 66-7 (July 2025) . - p.1053-1064 Mots-clés : Autism  ADHD  MoBa  indirect genetic effects  genetic nurture  neurodevelopmental traits Index. décimale : PER Périodiques Résumé : Background Neurodevelopmental conditions are highly heritable. Recent studies have shown that genomic heritability estimates can be confounded by genetic effects mediated via the environment (indirect genetic effects). However, the relative importance of direct versus indirect genetic effects on early variability in traits related to neurodevelopmental conditions is unknown. Methods The sample included up to 24,692 parent-offspring trios from the Norwegian MoBa cohort. We use Trio-GCTA to estimate latent direct and indirect genetic effects on mother-reported neurodevelopmental traits at age of 3 years (restricted and repetitive behaviors and interests, inattention, hyperactivity, language, social, and motor development). Further, we investigate to what extent direct and indirect effects are attributable to common genetic variants associated with autism, ADHD, developmental dyslexia, educational attainment, and cognitive ability using polygenic scores (PGS) in regression modeling. Results We find evidence for contributions of direct and indirect latent common genetic effects to inattention (direct: explaining 4.8% of variance, indirect: 6.7%) hyperactivity (direct: 1.3%, indirect: 9.6%), and restricted and repetitive behaviors (direct: 0.8%, indirect: 7.3%). Direct effects best explained variation in social and communication, language, and motor development (5.1% 5.7%). Direct genetic effects on inattention were captured by PGS for ADHD, educational attainment, and cognitive ability, whereas direct genetic effects on language development were captured by cognitive ability, educational attainment, and autism PGS. Indirect genetic effects on neurodevelopmental traits were primarily captured by educational attainment and/or cognitive ability PGS. Conclusions Results were consistent with differential contributions to neurodevelopmental traits in early childhood from direct and indirect genetic effects. Indirect effects were particularly important for hyperactivity and restricted and repetitive behaviors and interests and may be linked to genetic variation associated with cognition and educational attainment. Our findings illustrate the importance of within-family methods for disentangling genetic processes that influence early neurodevelopmental traits, even when identifiable associations are small. En ligne : https://doi.org/10.1111/jcpp.14122 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=562

Genetic and phenotypic heterogeneity in early neurodevelopmental traits in the Norwegian Mother, Father and Child Cohort Study / Laura HEGEMANN in Molecular Autism, 15 (2024)  

Public ISBD [article]  inMolecular Autism > 15 (2024) . - 25p. Titre : Genetic and phenotypic heterogeneity in early neurodevelopmental traits in the Norwegian Mother, Father and Child Cohort Study Type de document : texte imprimé Auteurs : Laura HEGEMANN, Auteur ; Elizabeth C. CORFIELD, Auteur ; Adrian Dahl ASKELUND, Auteur ; Andrea G. ALLEGRINI, Auteur ; Ragna Bugge ASKELAND, Auteur ; Angelica RONALD, Auteur ; Helga ASK, Auteur ; Beate ST POURCAIN, Auteur ; Ole A. ANDREASSEN, Auteur ; Laurie J. HANNIGAN, Auteur ; Alexandra HAVDAHL, Auteur Article en page(s) : 25p. Langues : Anglais (eng) Mots-clés : Humans  Norway  Female  Male  Phenotype  Child, Preschool  Cohort Studies  Neurodevelopmental Disorders/genetics/diagnosis  Mothers  Autistic Disorder/genetics  Genetic Predisposition to Disease  Adult  Fathers  Genome-Wide Association Study  Attention Deficit Disorder with Hyperactivity/genetics/diagnosis  Schizophrenia/genetics  Genetic Heterogeneity Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism and different neurodevelopmental conditions frequently co-occur, as do their symptoms at sub-diagnostic threshold levels. Overlapping traits and shared genetic liability are potential explanations. METHODS: In the population-based Norwegian Mother, Father, and Child Cohort study (MoBa), we leverage item-level data to explore the phenotypic factor structure and genetic architecture underlying neurodevelopmental traits at age 3 years (N = 41,708-58,630) using maternal reports on 76 items assessing children's motor and language development, social functioning, communication, attention, activity regulation, and flexibility of behaviors and interests. RESULTS: We identified 11 latent factors at the phenotypic level. These factors showed associations with diagnoses of autism and other neurodevelopmental conditions. Most shared genetic liabilities with autism, ADHD, and/or schizophrenia. Item-level GWAS revealed trait-specific genetic correlations with autism (items r(g) range = - 0.27-0.78), ADHD (items r(g) range = - 0.40-1), and schizophrenia (items r(g) range = - 0.24-0.34). We find little evidence of common genetic liability across all neurodevelopmental traits but more so for several genetic factors across more specific areas of neurodevelopment, particularly social and communication traits. Some of these factors, such as one capturing prosocial behavior, overlap with factors found in the phenotypic analyses. Other areas, such as motor development, seemed to have more heterogenous etiology, with specific traits showing a less consistent pattern of genetic correlations with each other. CONCLUSIONS: These exploratory findings emphasize the etiological complexity of neurodevelopmental traits at this early age. In particular, diverse associations with neurodevelopmental conditions and genetic heterogeneity could inform follow-up work to identify shared and differentiating factors in the early manifestations of neurodevelopmental traits and their relation to autism and other neurodevelopmental conditions. This in turn could have implications for clinical screening tools and programs. En ligne : https://dx.doi.org/10.1186/s13229-024-00599-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538 [article] Genetic and phenotypic heterogeneity in early neurodevelopmental traits in the Norwegian Mother, Father and Child Cohort Study [texte imprimé] / Laura HEGEMANN, Auteur ; Elizabeth C. CORFIELD, Auteur ; Adrian Dahl ASKELUND, Auteur ; Andrea G. ALLEGRINI, Auteur ; Ragna Bugge ASKELAND, Auteur ; Angelica RONALD, Auteur ; Helga ASK, Auteur ; Beate ST POURCAIN, Auteur ; Ole A. ANDREASSEN, Auteur ; Laurie J. HANNIGAN, Auteur ; Alexandra HAVDAHL, Auteur . - 25p. Langues : Anglais (eng) in Molecular Autism > 15 (2024) . - 25p. Mots-clés : Humans  Norway  Female  Male  Phenotype  Child, Preschool  Cohort Studies  Neurodevelopmental Disorders/genetics/diagnosis  Mothers  Autistic Disorder/genetics  Genetic Predisposition to Disease  Adult  Fathers  Genome-Wide Association Study  Attention Deficit Disorder with Hyperactivity/genetics/diagnosis  Schizophrenia/genetics  Genetic Heterogeneity Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism and different neurodevelopmental conditions frequently co-occur, as do their symptoms at sub-diagnostic threshold levels. Overlapping traits and shared genetic liability are potential explanations. METHODS: In the population-based Norwegian Mother, Father, and Child Cohort study (MoBa), we leverage item-level data to explore the phenotypic factor structure and genetic architecture underlying neurodevelopmental traits at age 3 years (N = 41,708-58,630) using maternal reports on 76 items assessing children's motor and language development, social functioning, communication, attention, activity regulation, and flexibility of behaviors and interests. RESULTS: We identified 11 latent factors at the phenotypic level. These factors showed associations with diagnoses of autism and other neurodevelopmental conditions. Most shared genetic liabilities with autism, ADHD, and/or schizophrenia. Item-level GWAS revealed trait-specific genetic correlations with autism (items r(g) range = - 0.27-0.78), ADHD (items r(g) range = - 0.40-1), and schizophrenia (items r(g) range = - 0.24-0.34). We find little evidence of common genetic liability across all neurodevelopmental traits but more so for several genetic factors across more specific areas of neurodevelopment, particularly social and communication traits. Some of these factors, such as one capturing prosocial behavior, overlap with factors found in the phenotypic analyses. Other areas, such as motor development, seemed to have more heterogenous etiology, with specific traits showing a less consistent pattern of genetic correlations with each other. CONCLUSIONS: These exploratory findings emphasize the etiological complexity of neurodevelopmental traits at this early age. In particular, diverse associations with neurodevelopmental conditions and genetic heterogeneity could inform follow-up work to identify shared and differentiating factors in the early manifestations of neurodevelopmental traits and their relation to autism and other neurodevelopmental conditions. This in turn could have implications for clinical screening tools and programs. En ligne : https://dx.doi.org/10.1186/s13229-024-00599-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538

Joint developmental trajectories of internalizing and externalizing disorders between childhood and adolescence / Michel G. NIVARD in Development and Psychopathology, 29-3 (August 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-3 (August 2017) . - p.919-928 Titre : Joint developmental trajectories of internalizing and externalizing disorders between childhood and adolescence Type de document : texte imprimé Auteurs : Michel G. NIVARD, Auteur ; Gitta H. LUBKE, Auteur ; Conor V. DOLAN, Auteur ; David M. EVANS, Auteur ; Beate ST POURCAIN, Auteur ; Marcus R. MUNAFO, Auteur ; Christel M. MIDDELDORP, Auteur Article en page(s) : p.919-928 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract This study sought to identify trajectories of DSM-IV based internalizing (INT) and externalizing (EXT) problem scores across childhood and adolescence and to provide insight into the comorbidity by modeling the co-occurrence of INT and EXT trajectories. INT and EXT were measured repeatedly between age 7 and age 15 years in over 7,000 children and analyzed using growth mixture models. Five trajectories were identified for both INT and EXT, including very low, low, decreasing, and increasing trajectories. In addition, an adolescent onset trajectory was identified for INT and a stable high trajectory was identified for EXT. Multinomial regression showed that similar EXT and INT trajectories were associated. However, the adolescent onset INT trajectory was independent of high EXT trajectories, and persisting EXT was mainly associated with decreasing INT. Sex and early life environmental risk factors predicted EXT and, to a lesser extent, INT trajectories. The association between trajectories indicates the need to consider comorbidity when a child presents with INT or EXT disorders, particularly when symptoms start early. This is less necessary when INT symptoms start at adolescence. Future studies should investigate the etiology of co-occurring INT and EXT and the specific treatment needs of these severely affected children. En ligne : http://dx.doi.org/10.1017/s0954579416000572 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=312 [article] Joint developmental trajectories of internalizing and externalizing disorders between childhood and adolescence [texte imprimé] / Michel G. NIVARD, Auteur ; Gitta H. LUBKE, Auteur ; Conor V. DOLAN, Auteur ; David M. EVANS, Auteur ; Beate ST POURCAIN, Auteur ; Marcus R. MUNAFO, Auteur ; Christel M. MIDDELDORP, Auteur . - p.919-928. Langues : Anglais (eng) in Development and Psychopathology > 29-3 (August 2017) . - p.919-928 Index. décimale : PER Périodiques Résumé : Abstract This study sought to identify trajectories of DSM-IV based internalizing (INT) and externalizing (EXT) problem scores across childhood and adolescence and to provide insight into the comorbidity by modeling the co-occurrence of INT and EXT trajectories. INT and EXT were measured repeatedly between age 7 and age 15 years in over 7,000 children and analyzed using growth mixture models. Five trajectories were identified for both INT and EXT, including very low, low, decreasing, and increasing trajectories. In addition, an adolescent onset trajectory was identified for INT and a stable high trajectory was identified for EXT. Multinomial regression showed that similar EXT and INT trajectories were associated. However, the adolescent onset INT trajectory was independent of high EXT trajectories, and persisting EXT was mainly associated with decreasing INT. Sex and early life environmental risk factors predicted EXT and, to a lesser extent, INT trajectories. The association between trajectories indicates the need to consider comorbidity when a child presents with INT or EXT disorders, particularly when symptoms start early. This is less necessary when INT symptoms start at adolescence. Future studies should investigate the etiology of co-occurring INT and EXT and the specific treatment needs of these severely affected children. En ligne : http://dx.doi.org/10.1017/s0954579416000572 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=312

Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development / Evangelia STERGIAKOULI in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 18p. Titre : Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development Type de document : texte imprimé Auteurs : Evangelia STERGIAKOULI, Auteur ; George DAVEY SMITH, Auteur ; Joanna MARTIN, Auteur ; David H. SKUSE, Auteur ; Wolfgang VIECHTBAUER, Auteur ; Susan M. RING, Auteur ; Angelica RONALD, Auteur ; David E. EVANS, Auteur ; Simon E. FISHER, Auteur ; Anita THAPAR, Auteur ; Beate ST POURCAIN, Auteur Article en page(s) : 18p. Langues : Anglais (eng) Mots-clés : ADHD symptoms  Alspac  Clinical ADHD  Genetic overlap  Social communication Index. décimale : PER Périodiques Résumé : BACKGROUND: Shared genetic influences between attention-deficit/hyperactivity disorder (ADHD) symptoms and autism spectrum disorder (ASD) symptoms have been reported. Cross-trait genetic relationships are, however, subject to dynamic changes during development. We investigated the continuity of genetic overlap between ASD and ADHD symptoms in a general population sample during childhood and adolescence. We also studied uni- and cross-dimensional trait-disorder links with respect to genetic ADHD and ASD risk. METHODS: Social-communication difficulties (N En ligne : http://dx.doi.org/10.1186/s13229-017-0131-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331 [article] Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development [texte imprimé] / Evangelia STERGIAKOULI, Auteur ; George DAVEY SMITH, Auteur ; Joanna MARTIN, Auteur ; David H. SKUSE, Auteur ; Wolfgang VIECHTBAUER, Auteur ; Susan M. RING, Auteur ; Angelica RONALD, Auteur ; David E. EVANS, Auteur ; Simon E. FISHER, Auteur ; Anita THAPAR, Auteur ; Beate ST POURCAIN, Auteur . - 18p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 18p. Mots-clés : ADHD symptoms  Alspac  Clinical ADHD  Genetic overlap  Social communication Index. décimale : PER Périodiques Résumé : BACKGROUND: Shared genetic influences between attention-deficit/hyperactivity disorder (ADHD) symptoms and autism spectrum disorder (ASD) symptoms have been reported. Cross-trait genetic relationships are, however, subject to dynamic changes during development. We investigated the continuity of genetic overlap between ASD and ADHD symptoms in a general population sample during childhood and adolescence. We also studied uni- and cross-dimensional trait-disorder links with respect to genetic ADHD and ASD risk. METHODS: Social-communication difficulties (N En ligne : http://dx.doi.org/10.1186/s13229-017-0131-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331

The development of autistic social traits across childhood and adolescence in males and females / William MANDY in Journal of Child Psychology and Psychiatry, 59-11 (November 2018)  

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The developmental origins of genetic factors influencing language and literacy: Associations with early-childhood vocabulary / Ellen VERHOEF in Journal of Child Psychology and Psychiatry, 62-6 (June 2021)  

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Variability in the common genetic architecture of social-communication spectrum phenotypes during childhood and adolescence / Beate ST POURCAIN in Molecular Autism, (February 2014)  

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