Adolescent cannabis use, change in neurocognitive function, and high-school graduation: A longitudinal study from early adolescence to young adulthood / Natalie CASTELLANOS-RYAN in Development and Psychopathology, 29-4 (October 2017)  

Public ISBD [article]  inDevelopment and Psychopathology > 29-4 (October 2017) . - p.1253-1266 Titre : Adolescent cannabis use, change in neurocognitive function, and high-school graduation: A longitudinal study from early adolescence to young adulthood Type de document : texte imprimé Auteurs : Natalie CASTELLANOS-RYAN, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Sophie PARENT, Auteur ; Frank VITARO, Auteur ; Richard E. TREMBLAY, Auteur ; Jean R. SEGUIN, Auteur Article en page(s) : p.1253-1266 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract The main objective of this prospective longitudinal study was to investigate bidirectional associations between adolescent cannabis use (CU) and neurocognitive performance in a community sample of 294 young men from ages 13 to 20 years. The results showed that in early adolescence, and prior to initiation to CU, poor short-term and working memory, but high verbal IQ, were associated with earlier age of onset of CU. In turn, age of CU onset and CU frequency across adolescence were associated with (a) specific neurocognitive decline in verbal IQ and executive function tasks tapping trial and error learning and reward processing by early adulthood and (b) lower rates of high-school graduation. The association between CU onset and change in neurocognitive function, however, was found to be accounted for by CU frequency. Whereas the link between CU frequency across adolescence and change in verbal IQ was explained (mediated) by high school graduation, the link between CU frequency and tasks tapping trial and error learning were independent from high school graduation, concurrent cannabis and other substance use, adolescent alcohol use, and externalizing behaviors. Findings support prevention efforts aimed at delaying onset and reducing frequency of CU. En ligne : http://dx.doi.org/10.1017/s0954579416001280 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=312 [article] Adolescent cannabis use, change in neurocognitive function, and high-school graduation: A longitudinal study from early adolescence to young adulthood [texte imprimé] / Natalie CASTELLANOS-RYAN, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Sophie PARENT, Auteur ; Frank VITARO, Auteur ; Richard E. TREMBLAY, Auteur ; Jean R. SEGUIN, Auteur . - p.1253-1266. Langues : Anglais (eng) in Development and Psychopathology > 29-4 (October 2017) . - p.1253-1266 Index. décimale : PER Périodiques Résumé : Abstract The main objective of this prospective longitudinal study was to investigate bidirectional associations between adolescent cannabis use (CU) and neurocognitive performance in a community sample of 294 young men from ages 13 to 20 years. The results showed that in early adolescence, and prior to initiation to CU, poor short-term and working memory, but high verbal IQ, were associated with earlier age of onset of CU. In turn, age of CU onset and CU frequency across adolescence were associated with (a) specific neurocognitive decline in verbal IQ and executive function tasks tapping trial and error learning and reward processing by early adulthood and (b) lower rates of high-school graduation. The association between CU onset and change in neurocognitive function, however, was found to be accounted for by CU frequency. Whereas the link between CU frequency across adolescence and change in verbal IQ was explained (mediated) by high school graduation, the link between CU frequency and tasks tapping trial and error learning were independent from high school graduation, concurrent cannabis and other substance use, adolescent alcohol use, and externalizing behaviors. Findings support prevention efforts aimed at delaying onset and reducing frequency of CU. En ligne : http://dx.doi.org/10.1017/s0954579416001280 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=312

Combining multivariate genomic approaches to elucidate the comorbidity between autism spectrum disorder and attention deficit hyperactivity disorder / Hugo PEYRE in Journal of Child Psychology and Psychiatry, 62-11 (November 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-11 (November 2021) . - p.1285-1296 Titre : Combining multivariate genomic approaches to elucidate the comorbidity between autism spectrum disorder and attention deficit hyperactivity disorder Type de document : texte imprimé Auteurs : Hugo PEYRE, Auteur ; Tabea SCHOELER, Auteur ; Chaoyu LIU, Auteur ; Camille Michèle WILLIAMS, Auteur ; Nicolas HOERTEL, Auteur ; Alexandra HAVDAHL, Auteur ; Jean-Baptiste PINGAULT, Auteur Article en page(s) : p.1285-1296 Langues : Anglais (eng) Mots-clés : Attention Deficit Disorder with Hyperactivity/epidemiology/genetics  Autism Spectrum Disorder/epidemiology/genetics  Comorbidity  Genome-Wide Association Study  Genomics  Humans  Paired Box Transcription Factors/genetics  Polymorphism, Single Nucleotide  Repressor Proteins/genetics  Autism spectrum disorder  Gwas  Snp  attention deficit hyperactivity disorder  colocalization  common genetic variants  comorbidity  genomic structural equation modelling Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are two highly heritable neurodevelopmental disorders. Several lines of evidence point towards the presence of shared genetic factors underlying ASD and ADHD. We conducted genomic analyses of common risk variants (i.e. single nucleotide polymorphisms, SNPs) shared by ASD and ADHD, and those specific to each disorder. METHODS: With the summary data from two GWAS, one on ASD (N = 46,350) and another on ADHD (N = 55,374) individuals, we used genomic structural equation modelling and colocalization analysis to identify SNPs shared by ASD and ADHD and SNPs specific to each disorder. Functional genomic analyses were then conducted on shared and specific common genetic variants. Finally, we performed a bidirectional Mendelian randomization analysis to test whether the shared genetic risk between ASD and ADHD was interpretable in terms of reciprocal relationships between ASD and ADHD. RESULTS: We found that 37.5% of the SNPs associated with ASD (at p < 1e-6) colocalized with ADHD SNPs and that 19.6% of the SNPs associated with ADHD colocalized with ASD SNPs. We identified genes mapped to SNPs that are specific to ASD or ADHD and that are shared by ASD and ADHD, including two novel genes INSM1 and PAX1. Our bidirectional Mendelian randomization analyses indicated that the risk of ASD was associated with an increased risk of ADHD and vice versa. CONCLUSIONS: Using multivariate genomic analyses, the present study uncovers shared and specific genetic variants associated with ASD and ADHD. Further functional investigation of genes mapped to those shared variants may help identify pathophysiological pathways and new targets for treatment. En ligne : http://dx.doi.org/10.1111/jcpp.13479 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Combining multivariate genomic approaches to elucidate the comorbidity between autism spectrum disorder and attention deficit hyperactivity disorder [texte imprimé] / Hugo PEYRE, Auteur ; Tabea SCHOELER, Auteur ; Chaoyu LIU, Auteur ; Camille Michèle WILLIAMS, Auteur ; Nicolas HOERTEL, Auteur ; Alexandra HAVDAHL, Auteur ; Jean-Baptiste PINGAULT, Auteur . - p.1285-1296. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-11 (November 2021) . - p.1285-1296 Mots-clés : Attention Deficit Disorder with Hyperactivity/epidemiology/genetics  Autism Spectrum Disorder/epidemiology/genetics  Comorbidity  Genome-Wide Association Study  Genomics  Humans  Paired Box Transcription Factors/genetics  Polymorphism, Single Nucleotide  Repressor Proteins/genetics  Autism spectrum disorder  Gwas  Snp  attention deficit hyperactivity disorder  colocalization  common genetic variants  comorbidity  genomic structural equation modelling Index. décimale : PER Périodiques Résumé : BACKGROUND: Attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are two highly heritable neurodevelopmental disorders. Several lines of evidence point towards the presence of shared genetic factors underlying ASD and ADHD. We conducted genomic analyses of common risk variants (i.e. single nucleotide polymorphisms, SNPs) shared by ASD and ADHD, and those specific to each disorder. METHODS: With the summary data from two GWAS, one on ASD (N = 46,350) and another on ADHD (N = 55,374) individuals, we used genomic structural equation modelling and colocalization analysis to identify SNPs shared by ASD and ADHD and SNPs specific to each disorder. Functional genomic analyses were then conducted on shared and specific common genetic variants. Finally, we performed a bidirectional Mendelian randomization analysis to test whether the shared genetic risk between ASD and ADHD was interpretable in terms of reciprocal relationships between ASD and ADHD. RESULTS: We found that 37.5% of the SNPs associated with ASD (at p < 1e-6) colocalized with ADHD SNPs and that 19.6% of the SNPs associated with ADHD colocalized with ASD SNPs. We identified genes mapped to SNPs that are specific to ASD or ADHD and that are shared by ASD and ADHD, including two novel genes INSM1 and PAX1. Our bidirectional Mendelian randomization analyses indicated that the risk of ASD was associated with an increased risk of ADHD and vice versa. CONCLUSIONS: Using multivariate genomic analyses, the present study uncovers shared and specific genetic variants associated with ASD and ADHD. Further functional investigation of genes mapped to those shared variants may help identify pathophysiological pathways and new targets for treatment. En ligne : http://dx.doi.org/10.1111/jcpp.13479 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

Concurrent and longitudinal associations of developmental language disorder with peer victimization in adolescence: evidence from a co-twin study / Kate NATION ; Kai Xiang LIM ; Jean-Baptiste PINGAULT ; Lucy BOWES in Journal of Child Psychology and Psychiatry, 65-10 (October 2024)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 65-10 (October 2024) . - p.1283-1298 Titre : Concurrent and longitudinal associations of developmental language disorder with peer victimization in adolescence: evidence from a co-twin study Type de document : texte imprimé Auteurs : Kate NATION, Auteur ; Kai Xiang LIM, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Lucy BOWES, Auteur Article en page(s) : p.1283-1298 Langues : Anglais (eng) Mots-clés : Developmental language disorder  bullying victimization  behavioral genetics  pragmatic language  adolescence Index. décimale : PER Périodiques Résumé : Background Children with developmental language disorder (DLD) experience higher levels of peer victimization than their peers. However, it is not known if such associations reflect genetic and environmental confounding. We used a co-twin control design to investigate the association of language difficulties (DLD and separately poor pragmatic language) with peer victimization and compare the developmental trajectories of peer victimization across adolescence for those with and without language difficulties. Methods Participants were 3,400 pairs of twins in the Twins Early Development Study (TEDS), a UK-based population birth cohort. Language abilities were assessed via online tests at age 11 and peer victimization was self-reported at ages 11, 14 and 16. Language difficulties were defined as language abilities at least 1.25 SD below the mean of the TEDS sample. We performed linear regressions and latent growth curve modeling at a population level and within monozygotic and same-sex dizygotic twin pairs. Results At population level, youth with DLD experienced higher levels of peer victimization at ages 11 (? 0.27, 95% Confidence Interval (CI) 0.20 0.35), 14 (? 0.15, 95% CI 0.03 0.27) and 16 (? 0.17, 95% CI 0.03 0.32) and a sharper decline in peer victimization between ages 11 and 16 compared to their peers without DLD. The associations between DLD and peer victimization were reduced in strength and not statistically significant in within-twin models. Moreover, there was no difference in the rate of change in peer victimization between twin pairs discordant for DLD. Results were similar for the association of poor pragmatic language with peer victimization. Conclusions Associations between language difficulties (DLD and separately, poor pragmatic language) and peer victimization were confounded by genetic and shared environmental factors. Identifying specific factors underlying these associations is important for guiding future work to reduce peer victimization among adolescents with language difficulties. En ligne : https://doi.org/10.1111/jcpp.13969 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=535 [article] Concurrent and longitudinal associations of developmental language disorder with peer victimization in adolescence: evidence from a co-twin study [texte imprimé] / Kate NATION, Auteur ; Kai Xiang LIM, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Lucy BOWES, Auteur . - p.1283-1298. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 65-10 (October 2024) . - p.1283-1298 Mots-clés : Developmental language disorder  bullying victimization  behavioral genetics  pragmatic language  adolescence Index. décimale : PER Périodiques Résumé : Background Children with developmental language disorder (DLD) experience higher levels of peer victimization than their peers. However, it is not known if such associations reflect genetic and environmental confounding. We used a co-twin control design to investigate the association of language difficulties (DLD and separately poor pragmatic language) with peer victimization and compare the developmental trajectories of peer victimization across adolescence for those with and without language difficulties. Methods Participants were 3,400 pairs of twins in the Twins Early Development Study (TEDS), a UK-based population birth cohort. Language abilities were assessed via online tests at age 11 and peer victimization was self-reported at ages 11, 14 and 16. Language difficulties were defined as language abilities at least 1.25 SD below the mean of the TEDS sample. We performed linear regressions and latent growth curve modeling at a population level and within monozygotic and same-sex dizygotic twin pairs. Results At population level, youth with DLD experienced higher levels of peer victimization at ages 11 (? 0.27, 95% Confidence Interval (CI) 0.20 0.35), 14 (? 0.15, 95% CI 0.03 0.27) and 16 (? 0.17, 95% CI 0.03 0.32) and a sharper decline in peer victimization between ages 11 and 16 compared to their peers without DLD. The associations between DLD and peer victimization were reduced in strength and not statistically significant in within-twin models. Moreover, there was no difference in the rate of change in peer victimization between twin pairs discordant for DLD. Results were similar for the association of poor pragmatic language with peer victimization. Conclusions Associations between language difficulties (DLD and separately, poor pragmatic language) and peer victimization were confounded by genetic and shared environmental factors. Identifying specific factors underlying these associations is important for guiding future work to reduce peer victimization among adolescents with language difficulties. En ligne : https://doi.org/10.1111/jcpp.13969 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=535

Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader / Edward D. BARKER in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1107-1110 Titre : Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader Type de document : texte imprimé Auteurs : Edward D. BARKER, Auteur ; Barbara MAUGHAN, Auteur ; Andrea G. ALLEGRINI, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Edmund J.S. SONUGA-BARKE, Auteur Année de publication : 2022 Article en page(s) : p.1107-1110 Langues : Anglais (eng) Mots-clés : Child  Humans  Mental Disorders/genetics/psychology  Psychopathology  Receptor for Advanced Glycation End Products  Risk Factors Index. décimale : PER Périodiques Résumé : The primary goal motivating the scientific field of Developmental Psychopathology is to discover why some individuals develop mental health and neuro-developmental difficulties while others do not. This is not simply a 'blue skies' preoccupation: the underlying hope, of course, is to translate such discoveries to the benefit of individuals, families and communities, reducing poor outcomes for those at risk and - in the best case scenario - ensuring that they thrive. A core tenet of the bio-psycho-social framework within which this field of enquiry operates is that children's difficulties are determined by the interplay of predisposing genetic risk and resilience factors and the environments and experiences to which individuals are exposed. From this perspective, understanding gene-environment (GE) interplay is a necessary condition for explaining and, as importantly predicting, why one individual is at risk while another is not. If we believe this, then the risk calculators designed to show who will and will not get a particular disorder - all the rage at the moment - are doomed to fail until they can go beyond modelling the main effects of genes and environments, and reliably estimate GE processes too. Despite significant progress, we remain a considerable way off cracking this problem. En ligne : http://dx.doi.org/10.1111/jcpp.13692 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 [article] Editorial: Does the polygenic revolution herald a watershed in the study of GE interplay in developmental psychopathology? Some considerations for the Special Issue reader [texte imprimé] / Edward D. BARKER, Auteur ; Barbara MAUGHAN, Auteur ; Andrea G. ALLEGRINI, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Edmund J.S. SONUGA-BARKE, Auteur . - 2022 . - p.1107-1110. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-10 (October 2022) . - p.1107-1110 Mots-clés : Child  Humans  Mental Disorders/genetics/psychology  Psychopathology  Receptor for Advanced Glycation End Products  Risk Factors Index. décimale : PER Périodiques Résumé : The primary goal motivating the scientific field of Developmental Psychopathology is to discover why some individuals develop mental health and neuro-developmental difficulties while others do not. This is not simply a 'blue skies' preoccupation: the underlying hope, of course, is to translate such discoveries to the benefit of individuals, families and communities, reducing poor outcomes for those at risk and - in the best case scenario - ensuring that they thrive. A core tenet of the bio-psycho-social framework within which this field of enquiry operates is that children's difficulties are determined by the interplay of predisposing genetic risk and resilience factors and the environments and experiences to which individuals are exposed. From this perspective, understanding gene-environment (GE) interplay is a necessary condition for explaining and, as importantly predicting, why one individual is at risk while another is not. If we believe this, then the risk calculators designed to show who will and will not get a particular disorder - all the rage at the moment - are doomed to fail until they can go beyond modelling the main effects of genes and environments, and reliably estimate GE processes too. Despite significant progress, we remain a considerable way off cracking this problem. En ligne : http://dx.doi.org/10.1111/jcpp.13692 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486

Genetic and environmental influences on the developmental trajectory of callous-unemotional traits from childhood to adolescence / Yusuke TAKAHASHI in Journal of Child Psychology and Psychiatry, 62-4 (April 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-4 (April 2021) . - p.414-423 Titre : Genetic and environmental influences on the developmental trajectory of callous-unemotional traits from childhood to adolescence Type de document : texte imprimé Auteurs : Yusuke TAKAHASHI, Auteur ; Christopher R. PEASE, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Essi VIDING, Auteur Article en page(s) : p.414-423 Langues : Anglais (eng) Mots-clés : Callous-unemotional traits  genetic and environmental aetiology  latent growth model  trajectory  twin study Index. décimale : PER Périodiques Résumé : BACKGROUND: This study examined the genetic and environmental influences underlying baseline level and developmental course of callous-unemotional (CU) traits across childhood and adolescence. METHODS: The data on 8,958 twin pairs (3,108 MZ twin pairs and 5,850 DZ twin pairs) from the Twins Early Development Study were analysed. CU traits were assessed at ages 7, 9, 12 and 16 by mothers and analysed using a biometric latent growth model. RESULTS: Individual differences in the baseline level of CU traits were highly heritable (76.5%), while the heritability of the developmental course of CU traits was moderate (43.6%). The genetic influences on baseline level and developmental course of CU traits were mostly nonoverlapping. Nonshared environment made a modest contribution to the baseline level of CU traits (21.7%). Nonshared environmental influences on the developmental course of CU traits were moderate (43.2%), with nearly half of them being the same as those influencing the baseline level and just over half being specific. Shared environmental effects did not contribute to systematic change across childhood and adolescence but were rather age-specific. CONCLUSIONS: Our findings demonstrate that rather than only being conceptualized as factors of stability, genes also play a dynamic role in explaining systematic change in CU traits. Genetic effects for the initial risk and subsequent development of CU traits are not the same. In addition to genetic factors, nonshared environmental influences play an important role in explaining why some children will increase or maintain their CU traits over time, whereas other will desist. New genetic and environmental influences with age suggest that repeated, age-tailored interventions may be required throughout development to make a lasting difference in the presentation of CU traits and associated outcomes. En ligne : http://dx.doi.org/10.1111/jcpp.13259 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=445 [article] Genetic and environmental influences on the developmental trajectory of callous-unemotional traits from childhood to adolescence [texte imprimé] / Yusuke TAKAHASHI, Auteur ; Christopher R. PEASE, Auteur ; Jean-Baptiste PINGAULT, Auteur ; Essi VIDING, Auteur . - p.414-423. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-4 (April 2021) . - p.414-423 Mots-clés : Callous-unemotional traits  genetic and environmental aetiology  latent growth model  trajectory  twin study Index. décimale : PER Périodiques Résumé : BACKGROUND: This study examined the genetic and environmental influences underlying baseline level and developmental course of callous-unemotional (CU) traits across childhood and adolescence. METHODS: The data on 8,958 twin pairs (3,108 MZ twin pairs and 5,850 DZ twin pairs) from the Twins Early Development Study were analysed. CU traits were assessed at ages 7, 9, 12 and 16 by mothers and analysed using a biometric latent growth model. RESULTS: Individual differences in the baseline level of CU traits were highly heritable (76.5%), while the heritability of the developmental course of CU traits was moderate (43.6%). The genetic influences on baseline level and developmental course of CU traits were mostly nonoverlapping. Nonshared environment made a modest contribution to the baseline level of CU traits (21.7%). Nonshared environmental influences on the developmental course of CU traits were moderate (43.2%), with nearly half of them being the same as those influencing the baseline level and just over half being specific. Shared environmental effects did not contribute to systematic change across childhood and adolescence but were rather age-specific. CONCLUSIONS: Our findings demonstrate that rather than only being conceptualized as factors of stability, genes also play a dynamic role in explaining systematic change in CU traits. Genetic effects for the initial risk and subsequent development of CU traits are not the same. In addition to genetic factors, nonshared environmental influences play an important role in explaining why some children will increase or maintain their CU traits over time, whereas other will desist. New genetic and environmental influences with age suggest that repeated, age-tailored interventions may be required throughout development to make a lasting difference in the presentation of CU traits and associated outcomes. En ligne : http://dx.doi.org/10.1111/jcpp.13259 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=445

Heightened amygdala reactivity and increased stress generation predict internalizing symptoms in adults following childhood maltreatment / Mattia I. GERIN in Journal of Child Psychology and Psychiatry, 60-7 (July 2019)  

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Initiation and stability of self-harm in adolescence and early adulthood: investigating social and aetiological factors in twins / Yasmin I. AHMADZADEH ; Olakunle OGINNI ; Jean-Baptiste PINGAULT ; Thomas A. MCADAMS ; Helena M.S. ZAVOS in Journal of Child Psychology and Psychiatry, 66-6 (June 2025)  

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Mother's and children's ADHD genetic risk, household chaos and children's ADHD symptoms: A gene-environment correlation study / Jessica AGNEW-BLAIS in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

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On the importance of parenting in externalizing disorders: an evaluation of indirect genetic effects in families / Espen M. EILERTSEN in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

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Research Review: A guide to computing and implementing polygenic scores in developmental research / Andrea G. ALLEGRINI in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

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Research Review: How to interpret associations between polygenic scores, environmental risks, and phenotypes / Jean-Baptiste PINGAULT in Journal of Child Psychology and Psychiatry, 63-10 (October 2022)  

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School quality ratings are weak predictors of students' achievement and well-being / Sophie VON STUMM in Journal of Child Psychology and Psychiatry, 62-3 (March 2021)  

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Sex differences in socioemotional functioning, attentional bias, and gray matter volume in maltreated children: A multilevel investigation / Philip A. KELLY in Development and Psychopathology, 27-4 (Part 2) (November 2015)  

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Subjective and objective experiences of childhood adversity: a meta-analysis of their agreement and relationships with psychopathology / Emma R. FRANCIS in Journal of Child Psychology and Psychiatry, 64-8 (August 2023)  

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The p factor: genetic analyses support a general dimension of psychopathology in childhood and adolescence / Andrea G. ALLEGRINI in Journal of Child Psychology and Psychiatry, 61-1 (January 2020)  

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