Cognitive, psychosocial, and behaviour gains at age 31 years from the Jamaica early childhood stimulation trial / Susan P. WALKER in Journal of Child Psychology and Psychiatry, 63-6 (June 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-6 (June 2022) . - p.626-635 Titre : Cognitive, psychosocial, and behaviour gains at age 31 years from the Jamaica early childhood stimulation trial Type de document : texte imprimé Auteurs : Susan P. WALKER, Auteur ; Susan M. CHANG, Auteur ; Amika S. WRIGHT, Auteur ; Rodrigo PINTO, Auteur ; James J. HECKMAN, Auteur ; Sally M. GRANTHAM-MCGREGOR, Auteur Article en page(s) : p.626-635 Langues : Anglais (eng) Mots-clés : Early childhood  cognition  psychosocial skills  stimulation  stunting Index. décimale : PER Périodiques Résumé : BACKGROUND: There is little evidence on adult benefits from early childhood interventions in low and middle-income countries. We assessed adult cognition, psychosocial skills and behaviour from a stimulation trial conducted in Jamaica. METHODS: Children with stunted growth (height-for age <-2SD of references) aged 9-24 months were enrolled in a two-year randomised-controlled trial of nutritional supplementation and/or stimulation. At mean age 31.79 (SD 0.40) years, 95 of 127 participants (74.8%; 53.7% male) were assessed. Children without stunted growth were also followed as a comparison group (64 of 84 participants, 76.2%). Measurements included IQ, executive function, mental health, psychosocial skills, personality traits and risk behaviours. A block permutation test, valid for small sample sizes, was used. Analyses accounted for the randomisation protocol, multiple hypothesis testing and attrition. RESULTS: Treatment group participants (stimulation intervention with or without supplementation, n=48) had significantly greater IQ (Hedges g effect size 0. 57; 95%CI 0.20, 0.95) and cognitive flexibility (0.61; 0.25, 0.98) compared with no-treatment (no-intervention and supplementation only, n=47). They also had reduced depressive symptoms (0.61; 0.28, 1.00), increased grit (0.53; 0.16, 0.92) and conscientiousness (0.66; 0.31, 1.07), lower substance use (rank mean score, 0.45; 0.08, 0.81) and risk taking related to health and work (0.64; 0.27, 1.00). There were 18 significant outcomes of 33 assessed. Comparison participants had higher IQ than no-treatment (1.17; 0.81, 1.54) and treatment groups (0.62; 0.18, 1.07); and better executive function, lower social inhibition and risk taking than the no-treatment group. CONCLUSIONS: The wide-ranging benefits at 31 years from the stimulation intervention supports investment in larger scale programmes to promote early childhood development in disadvantaged children. The lower IQ in the treatment group compared with comparison participants, emphasises the need for continued efforts to prevent early childhood growth retardation. En ligne : http://dx.doi.org/10.1111/jcpp.13499 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=475 [article] Cognitive, psychosocial, and behaviour gains at age 31 years from the Jamaica early childhood stimulation trial [texte imprimé] / Susan P. WALKER, Auteur ; Susan M. CHANG, Auteur ; Amika S. WRIGHT, Auteur ; Rodrigo PINTO, Auteur ; James J. HECKMAN, Auteur ; Sally M. GRANTHAM-MCGREGOR, Auteur . - p.626-635. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-6 (June 2022) . - p.626-635 Mots-clés : Early childhood  cognition  psychosocial skills  stimulation  stunting Index. décimale : PER Périodiques Résumé : BACKGROUND: There is little evidence on adult benefits from early childhood interventions in low and middle-income countries. We assessed adult cognition, psychosocial skills and behaviour from a stimulation trial conducted in Jamaica. METHODS: Children with stunted growth (height-for age <-2SD of references) aged 9-24 months were enrolled in a two-year randomised-controlled trial of nutritional supplementation and/or stimulation. At mean age 31.79 (SD 0.40) years, 95 of 127 participants (74.8%; 53.7% male) were assessed. Children without stunted growth were also followed as a comparison group (64 of 84 participants, 76.2%). Measurements included IQ, executive function, mental health, psychosocial skills, personality traits and risk behaviours. A block permutation test, valid for small sample sizes, was used. Analyses accounted for the randomisation protocol, multiple hypothesis testing and attrition. RESULTS: Treatment group participants (stimulation intervention with or without supplementation, n=48) had significantly greater IQ (Hedges g effect size 0. 57; 95%CI 0.20, 0.95) and cognitive flexibility (0.61; 0.25, 0.98) compared with no-treatment (no-intervention and supplementation only, n=47). They also had reduced depressive symptoms (0.61; 0.28, 1.00), increased grit (0.53; 0.16, 0.92) and conscientiousness (0.66; 0.31, 1.07), lower substance use (rank mean score, 0.45; 0.08, 0.81) and risk taking related to health and work (0.64; 0.27, 1.00). There were 18 significant outcomes of 33 assessed. Comparison participants had higher IQ than no-treatment (1.17; 0.81, 1.54) and treatment groups (0.62; 0.18, 1.07); and better executive function, lower social inhibition and risk taking than the no-treatment group. CONCLUSIONS: The wide-ranging benefits at 31 years from the stimulation intervention supports investment in larger scale programmes to promote early childhood development in disadvantaged children. The lower IQ in the treatment group compared with comparison participants, emphasises the need for continued efforts to prevent early childhood growth retardation. En ligne : http://dx.doi.org/10.1111/jcpp.13499 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=475

Copy number variation in Han Chinese individuals with autism spectrum disorder / MatthewJ GAZZELLONE in Journal of Neurodevelopmental Disorders, 6-1 (December 2014)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 6-1 (December 2014) . - p.34 Titre : Copy number variation in Han Chinese individuals with autism spectrum disorder Type de document : texte imprimé Auteurs : MatthewJ GAZZELLONE, Auteur ; Xue ZHOU, Auteur ; Anath C. LIONEL, Auteur ; Mohammed UDDIN, Auteur ; Bhooma THIRUVAHINDRAPURAM, Auteur ; Shuang LIANG, Auteur ; Caihong SUN, Auteur ; Jing WANG, Auteur ; Mingyang ZOU, Auteur ; Kristiina TAMMIMIES, Auteur ; Susan WALKER, Auteur ; Thanuja SELVANAYAGAM, Auteur ; John WEI, Auteur ; Ziqi WANG, Auteur ; Lijie WU, Auteur ; Stephen SCHERER, Auteur Article en page(s) : p.34 Langues : Anglais (eng) Mots-clés : Autism spectrum disorder (ASD)  Copy number variations (CNVs)  Han Chinese  Microarray diagnostic testing Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASDs) are a group of neurodevelopmental conditions with a demonstrated genetic etiology. Rare (<1% frequency) copy number variations (CNVs) account for a proportion of the genetic events involved, but the contribution of these events in non-European ASD populations has not been well studied. Here, we report on rare CNVs detected in a cohort of individuals with ASD of Han Chinese background. METHODS: DNA samples were obtained from 104 ASD probands and their parents who were recruited from Harbin, China. Samples were genotyped on the Affymetrix CytoScan HD platform. Rare CNVs were identified by comparing data with 873 technology-matched controls from Ontario and 1,235 additional population controls of Han Chinese ethnicity. RESULTS: Of the probands, 8.6% had at least 1 de novo CNV (overlapping the GIGYF2, SPRY1, 16p13.3, 16p11.2, 17p13.3-17p13.2, DMD, and NAP1L6 genes/loci). Rare inherited CNVs affected other plausible neurodevelopmental candidate genes including GRID2, LINGO2, and SLC39A12. A 24-kb duplication was also identified at YWHAE, a gene previously implicated in ASD and other developmental disorders. This duplication is observed at a similar frequency in cases and in population controls and is likely a benign Asian-specific copy number polymorphism. CONCLUSIONS: Our findings help define genomic features relevant to ASD in the Han Chinese and emphasize the importance of using ancestry-matched controls in medical genetic interpretations. En ligne : http://dx.doi.org/10.1186/1866-1955-6-34 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=346 [article] Copy number variation in Han Chinese individuals with autism spectrum disorder [texte imprimé] / MatthewJ GAZZELLONE, Auteur ; Xue ZHOU, Auteur ; Anath C. LIONEL, Auteur ; Mohammed UDDIN, Auteur ; Bhooma THIRUVAHINDRAPURAM, Auteur ; Shuang LIANG, Auteur ; Caihong SUN, Auteur ; Jing WANG, Auteur ; Mingyang ZOU, Auteur ; Kristiina TAMMIMIES, Auteur ; Susan WALKER, Auteur ; Thanuja SELVANAYAGAM, Auteur ; John WEI, Auteur ; Ziqi WANG, Auteur ; Lijie WU, Auteur ; Stephen SCHERER, Auteur . - p.34. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 6-1 (December 2014) . - p.34 Mots-clés : Autism spectrum disorder (ASD)  Copy number variations (CNVs)  Han Chinese  Microarray diagnostic testing Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorders (ASDs) are a group of neurodevelopmental conditions with a demonstrated genetic etiology. Rare (<1% frequency) copy number variations (CNVs) account for a proportion of the genetic events involved, but the contribution of these events in non-European ASD populations has not been well studied. Here, we report on rare CNVs detected in a cohort of individuals with ASD of Han Chinese background. METHODS: DNA samples were obtained from 104 ASD probands and their parents who were recruited from Harbin, China. Samples were genotyped on the Affymetrix CytoScan HD platform. Rare CNVs were identified by comparing data with 873 technology-matched controls from Ontario and 1,235 additional population controls of Han Chinese ethnicity. RESULTS: Of the probands, 8.6% had at least 1 de novo CNV (overlapping the GIGYF2, SPRY1, 16p13.3, 16p11.2, 17p13.3-17p13.2, DMD, and NAP1L6 genes/loci). Rare inherited CNVs affected other plausible neurodevelopmental candidate genes including GRID2, LINGO2, and SLC39A12. A 24-kb duplication was also identified at YWHAE, a gene previously implicated in ASD and other developmental disorders. This duplication is observed at a similar frequency in cases and in population controls and is likely a benign Asian-specific copy number polymorphism. CONCLUSIONS: Our findings help define genomic features relevant to ASD in the Han Chinese and emphasize the importance of using ancestry-matched controls in medical genetic interpretations. En ligne : http://dx.doi.org/10.1186/1866-1955-6-34 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=346

Mutations in RAB39B in individuals with intellectual disability, autism spectrum disorder, and macrocephaly / Marc WOODBURY-SMITH in Molecular Autism, 8 (2017)  

Public ISBD [article]  inMolecular Autism > 8 (2017) . - 59p. Titre : Mutations in RAB39B in individuals with intellectual disability, autism spectrum disorder, and macrocephaly Type de document : texte imprimé Auteurs : Marc WOODBURY-SMITH, Auteur ; Eric DENEAULT, Auteur ; Ryan K.C. YUEN, Auteur ; Susan WALKER, Auteur ; Mehdi ZARREI, Auteur ; Giovanna PELLECCHIA, Auteur ; Jennifer L. HOWE, Auteur ; Ny HOANG, Auteur ; Mohammed UDDIN, Auteur ; Christian R. MARSHALL, Auteur ; Christina CHRYSLER, Auteur ; Aleda THOMPSON, Auteur ; Peter SZATMARI, Auteur ; Stephen SCHERER, Auteur Article en page(s) : 59p. Langues : Anglais (eng) Mots-clés : Intellectual disability (ID)  Rab39b  RNAseq  Whole genome sequencing (WGS) Index. décimale : PER Périodiques Résumé : Background: Autism spectrum disorder (ASD), a developmental disorder of early childhood onset, affects males four times more frequently than females, suggesting a role for the sex chromosomes. In this study, we describe a family with ASD in which a predicted pathogenic nonsense mutation in the X-chromosome gene RAB39B segregates with ASD phenotype. Methods: Clinical phenotyping, microarray, and whole genome sequencing (WGS) were performed on the five members of this family. Maternal and female sibling X inactivation ratio was calculated, and phase was investigated. Mutant-induced pluripotent stem cells engineered for an exon 2 nonsense mutation were generated and differentiated into cortical neurons for expression and pathway analyses. Results: Two males with an inherited RAB39B mutation both presented with macrocephaly, intellectual disability (ID), and ASD. Their female sibling with the same mutation presented with ID and a broad autism phenotype. In contrast, their transmitting mother has no neurodevelopmental diagnosis. Our investigation of phase indicated maternal preferential inactivation of the mutated allele, with no such bias observed in the female sibling. We offer the explanation that this bias in X inactivation may explain the absence of a neurocognitive phenotype in the mother. Our cellular knockout model of RAB39B revealed an impact on expression in differentiated neurons for several genes implicated in brain development and function, supported by our pathway enrichment analysis. Conclusions: Penetrance for ASD is high among males but more variable among females with RAB39B mutations. A critical role for this gene in brain development and function is demonstrated. En ligne : http://dx.doi.org/10.1186/s13229-017-0175-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331 [article] Mutations in RAB39B in individuals with intellectual disability, autism spectrum disorder, and macrocephaly [texte imprimé] / Marc WOODBURY-SMITH, Auteur ; Eric DENEAULT, Auteur ; Ryan K.C. YUEN, Auteur ; Susan WALKER, Auteur ; Mehdi ZARREI, Auteur ; Giovanna PELLECCHIA, Auteur ; Jennifer L. HOWE, Auteur ; Ny HOANG, Auteur ; Mohammed UDDIN, Auteur ; Christian R. MARSHALL, Auteur ; Christina CHRYSLER, Auteur ; Aleda THOMPSON, Auteur ; Peter SZATMARI, Auteur ; Stephen SCHERER, Auteur . - 59p. Langues : Anglais (eng) in Molecular Autism > 8 (2017) . - 59p. Mots-clés : Intellectual disability (ID)  Rab39b  RNAseq  Whole genome sequencing (WGS) Index. décimale : PER Périodiques Résumé : Background: Autism spectrum disorder (ASD), a developmental disorder of early childhood onset, affects males four times more frequently than females, suggesting a role for the sex chromosomes. In this study, we describe a family with ASD in which a predicted pathogenic nonsense mutation in the X-chromosome gene RAB39B segregates with ASD phenotype. Methods: Clinical phenotyping, microarray, and whole genome sequencing (WGS) were performed on the five members of this family. Maternal and female sibling X inactivation ratio was calculated, and phase was investigated. Mutant-induced pluripotent stem cells engineered for an exon 2 nonsense mutation were generated and differentiated into cortical neurons for expression and pathway analyses. Results: Two males with an inherited RAB39B mutation both presented with macrocephaly, intellectual disability (ID), and ASD. Their female sibling with the same mutation presented with ID and a broad autism phenotype. In contrast, their transmitting mother has no neurodevelopmental diagnosis. Our investigation of phase indicated maternal preferential inactivation of the mutated allele, with no such bias observed in the female sibling. We offer the explanation that this bias in X inactivation may explain the absence of a neurocognitive phenotype in the mother. Our cellular knockout model of RAB39B revealed an impact on expression in differentiated neurons for several genes implicated in brain development and function, supported by our pathway enrichment analysis. Conclusions: Penetrance for ASD is high among males but more variable among females with RAB39B mutations. A critical role for this gene in brain development and function is demonstrated. En ligne : http://dx.doi.org/10.1186/s13229-017-0175-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=331

Rare copy number variations affecting the synaptic gene DMXL2 in neurodevelopmental disorders / Gregory COSTAIN in Journal of Neurodevelopmental Disorders, 11-1 (December 2019)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 11-1 (December 2019) . - 3 p. Titre : Rare copy number variations affecting the synaptic gene DMXL2 in neurodevelopmental disorders Type de document : texte imprimé Auteurs : Gregory COSTAIN, Auteur ; Susan WALKER, Auteur ; Bob ARGIROPOULOS, Auteur ; Danielle A. BARIBEAU, Auteur ; Anne S. BASSETT, Auteur ; Erik BOOT, Auteur ; Koenraad DEVRIENDT, Auteur ; Barbara KELLAM, Auteur ; Christian R. MARSHALL, Auteur ; Aparna PRASAD, Auteur ; Moises A. SERRANO, Auteur ; Dimitri J. STAVROPOULOS, Auteur ; Hope TWEDE, Auteur ; Joris R. VERMEESCH, Auteur ; Jacob A.S. VORSTMAN, Auteur ; Stephen SCHERER, Auteur Article en page(s) : 3 p. Langues : Anglais (eng) Mots-clés : Adhd  Autism  Copy number variation  Dmxl2  Grik5  Genome sequencing Index. décimale : PER Périodiques Résumé : BACKGROUND: Ultra-rare genetic variants, including non-recurrent copy number variations (CNVs) affecting important dosage-sensitive genes, are important contributors to the etiology of neurodevelopmental disorders (NDDs). Pairing family-based whole-genome sequencing (WGS) with detailed phenotype data can enable novel gene associations in NDDs. METHODS: We performed WGS of six members from a three-generation family, where three individuals each had a spectrum of features suggestive of a NDD. CNVs and sequence-level variants were identified and further investigated in disease and control databases. RESULTS: We identified a novel 252-kb deletion at 15q21 that overlaps the synaptic gene DMXL2 and the gene GLDN. The microdeletion segregated in NDD-affected individuals. Additional rare inherited and de novo sequence-level variants were found that may also be involved, including a missense change in GRIK5. Multiple CNVs and loss-of-function sequence variants affecting DMXL2 were discovered in additional unrelated individuals with a range of NDDs. CONCLUSIONS: Disruption of DMXL2 may predispose to NDDs including autism spectrum disorder. The robust interpretation of private variants requires a multifaceted approach that incorporates multigenerational pedigrees and genome-wide and population-scale data. En ligne : http://dx.doi.org/10.1186/s11689-019-9263-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386 [article] Rare copy number variations affecting the synaptic gene DMXL2 in neurodevelopmental disorders [texte imprimé] / Gregory COSTAIN, Auteur ; Susan WALKER, Auteur ; Bob ARGIROPOULOS, Auteur ; Danielle A. BARIBEAU, Auteur ; Anne S. BASSETT, Auteur ; Erik BOOT, Auteur ; Koenraad DEVRIENDT, Auteur ; Barbara KELLAM, Auteur ; Christian R. MARSHALL, Auteur ; Aparna PRASAD, Auteur ; Moises A. SERRANO, Auteur ; Dimitri J. STAVROPOULOS, Auteur ; Hope TWEDE, Auteur ; Joris R. VERMEESCH, Auteur ; Jacob A.S. VORSTMAN, Auteur ; Stephen SCHERER, Auteur . - 3 p. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 11-1 (December 2019) . - 3 p. Mots-clés : Adhd  Autism  Copy number variation  Dmxl2  Grik5  Genome sequencing Index. décimale : PER Périodiques Résumé : BACKGROUND: Ultra-rare genetic variants, including non-recurrent copy number variations (CNVs) affecting important dosage-sensitive genes, are important contributors to the etiology of neurodevelopmental disorders (NDDs). Pairing family-based whole-genome sequencing (WGS) with detailed phenotype data can enable novel gene associations in NDDs. METHODS: We performed WGS of six members from a three-generation family, where three individuals each had a spectrum of features suggestive of a NDD. CNVs and sequence-level variants were identified and further investigated in disease and control databases. RESULTS: We identified a novel 252-kb deletion at 15q21 that overlaps the synaptic gene DMXL2 and the gene GLDN. The microdeletion segregated in NDD-affected individuals. Additional rare inherited and de novo sequence-level variants were found that may also be involved, including a missense change in GRIK5. Multiple CNVs and loss-of-function sequence variants affecting DMXL2 were discovered in additional unrelated individuals with a range of NDDs. CONCLUSIONS: Disruption of DMXL2 may predispose to NDDs including autism spectrum disorder. The robust interpretation of private variants requires a multifaceted approach that incorporates multigenerational pedigrees and genome-wide and population-scale data. En ligne : http://dx.doi.org/10.1186/s11689-019-9263-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386

Recurrent duplications of the annexin A1 gene (ANXA1) in autism spectrum disorders / Catarina T. CORREIA in Molecular Autism, (April 2014)  

Public ISBD [article]  inMolecular Autism > (April 2014) . - p.1-14 Titre : Recurrent duplications of the annexin A1 gene (ANXA1) in autism spectrum disorders Type de document : texte imprimé Auteurs : Catarina T. CORREIA, Auteur ; Inês C. CONCEIÇÃO, Auteur ; Bárbara OLIVEIRA, Auteur ; Joana COELHO, Auteur ; Inês SOUSA, Auteur ; Ana F. SEQUEIRA, Auteur ; Joana ALMEIDA, Auteur ; Cátia CAFÉ, Auteur ; Frederico DUQUE, Auteur ; Susana MOUGA, Auteur ; Wendy ROBERTS, Auteur ; Kun GAO, Auteur ; Jennifer K. LOWE, Auteur ; Bhooma THIRUVAHINDRAPURAM, Auteur ; Susan WALKER, Auteur ; Christian R. MARSHALL, Auteur ; Dalila PINTO, Auteur ; John NURNBERGER, Auteur ; Stephen SCHERER, Auteur ; Daniel H. GESCHWIND, Auteur ; Guiomar OLIVEIRA, Auteur ; Astrid M. VICENTE, Auteur Article en page(s) : p.1-14 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Validating the potential pathogenicity of copy number variants (CNVs) identified in genome-wide studies of autism spectrum disorders (ASD) requires detailed assessment of case/control frequencies, inheritance patterns, clinical correlations, and functional impact. Here, we characterize a small recurrent duplication in the annexin A1 (ANXA1) gene, identified by the Autism Genome Project (AGP) study. En ligne : http://dx.doi.org/10.1186/2040-2392-5-28 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=276 [article] Recurrent duplications of the annexin A1 gene (ANXA1) in autism spectrum disorders [texte imprimé] / Catarina T. CORREIA, Auteur ; Inês C. CONCEIÇÃO, Auteur ; Bárbara OLIVEIRA, Auteur ; Joana COELHO, Auteur ; Inês SOUSA, Auteur ; Ana F. SEQUEIRA, Auteur ; Joana ALMEIDA, Auteur ; Cátia CAFÉ, Auteur ; Frederico DUQUE, Auteur ; Susana MOUGA, Auteur ; Wendy ROBERTS, Auteur ; Kun GAO, Auteur ; Jennifer K. LOWE, Auteur ; Bhooma THIRUVAHINDRAPURAM, Auteur ; Susan WALKER, Auteur ; Christian R. MARSHALL, Auteur ; Dalila PINTO, Auteur ; John NURNBERGER, Auteur ; Stephen SCHERER, Auteur ; Daniel H. GESCHWIND, Auteur ; Guiomar OLIVEIRA, Auteur ; Astrid M. VICENTE, Auteur . - p.1-14. Langues : Anglais (eng) in Molecular Autism > (April 2014) . - p.1-14 Index. décimale : PER Périodiques Résumé : Validating the potential pathogenicity of copy number variants (CNVs) identified in genome-wide studies of autism spectrum disorders (ASD) requires detailed assessment of case/control frequencies, inheritance patterns, clinical correlations, and functional impact. Here, we characterize a small recurrent duplication in the annexin A1 (ANXA1) gene, identified by the Autism Genome Project (AGP) study. En ligne : http://dx.doi.org/10.1186/2040-2392-5-28 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=276

Stronger Associations Between Sleep and Mental Health in Adults with Autism: A UK Biobank Study / Lisa M. HENDERSON in Journal of Autism and Developmental Disorders, 53-4 (April 2023)  

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Uncovering obsessive-compulsive disorder risk genes in a pediatric cohort by high-resolution analysis of copy number variation / MatthewJ GAZZELLONE in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)  

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