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Maternal antenatal depression and child mental health: Moderation by genomic risk for attention-deficit/hyperactivity disorder / Lawrence M. CHEN in Development and Psychopathology, 32-5 (December 2020)
[article]
Titre : Maternal antenatal depression and child mental health: Moderation by genomic risk for attention-deficit/hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : Lawrence M. CHEN, Auteur ; Marieke S. TOLLENAAR, Auteur ; Shantala A. HARI DASS, Auteur ; Andrée-Anne BOUVETTE-TURCOT, Auteur ; Irina POKHVISNEVA, Auteur ; Helene GAUDREAU, Auteur ; Carine PARENT, Auteur ; Josie DIORIO, Auteur ; Lisa M. MCEWEN, Auteur ; Julia L. MACISAAC, Auteur ; Michael S. KOBOR, Auteur ; Roseriet BEIJERS, Auteur ; Carolina DE WEERTH, Auteur ; Patricia P. SILVEIRA, Auteur ; Sherif KARAMA, Auteur ; Michael J. MEANEY, Auteur ; Kieran J. O'DONNELL, Auteur Article en page(s) : p.1810-1821 Langues : Anglais (eng) Mots-clés : *Attention Deficit Disorder with Hyperactivity/genetics Child Depression/genetics Female Genomics Humans Mental Health Mothers Pregnancy *adhd *child development *gene by environment (GxE) *perinatal mental health *polygenic risk score Index. décimale : PER Périodiques Résumé : Maternal antenatal depression strongly influences child mental health but with considerable inter-individual variation that is, in part, linked to genotype. The challenge is to effectively capture the genotypic influence. We outline a novel approach to describe genomic susceptibility to maternal antenatal depression focusing on child emotional/behavioral difficulties. Two cohorts provided measures of maternal depression, child genetic variation, and child mental health symptoms. We constructed a conventional polygenic risk score (PRS) for attention-deficit/hyperactivity disorder (ADHD) (PRSADHD) that significantly moderated the association between maternal antenatal depression and internalizing problems at 60 months (p = 2.94 × 10-4, R2 = .18). We then constructed an interaction PRS (xPRS) based on a subset of those single nucleotide polymorphisms from the PRSADHD that most accounted for the moderation of the association between maternal antenatal depression and child outcome. The interaction between maternal antenatal depression and this xPRS accounted for a larger proportion of the variance in child emotional/behavioral problems than models based on any PRSADHD (p = 5.50 × 10-9, R2 = .27), with similar findings in the replication cohort. The xPRS was significantly enriched for genes involved in neuronal development and synaptic function. Our study illustrates a novel approach to the study of genotypic moderation on the impact of maternal antenatal depression on child mental health and highlights the utility of the xPRS approach. These findings advance our understanding of individual differences in the developmental origins of mental health. En ligne : http://dx.doi.org/10.1017/s0954579420001418 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437
in Development and Psychopathology > 32-5 (December 2020) . - p.1810-1821[article] Maternal antenatal depression and child mental health: Moderation by genomic risk for attention-deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / Lawrence M. CHEN, Auteur ; Marieke S. TOLLENAAR, Auteur ; Shantala A. HARI DASS, Auteur ; Andrée-Anne BOUVETTE-TURCOT, Auteur ; Irina POKHVISNEVA, Auteur ; Helene GAUDREAU, Auteur ; Carine PARENT, Auteur ; Josie DIORIO, Auteur ; Lisa M. MCEWEN, Auteur ; Julia L. MACISAAC, Auteur ; Michael S. KOBOR, Auteur ; Roseriet BEIJERS, Auteur ; Carolina DE WEERTH, Auteur ; Patricia P. SILVEIRA, Auteur ; Sherif KARAMA, Auteur ; Michael J. MEANEY, Auteur ; Kieran J. O'DONNELL, Auteur . - p.1810-1821.
Langues : Anglais (eng)
in Development and Psychopathology > 32-5 (December 2020) . - p.1810-1821
Mots-clés : *Attention Deficit Disorder with Hyperactivity/genetics Child Depression/genetics Female Genomics Humans Mental Health Mothers Pregnancy *adhd *child development *gene by environment (GxE) *perinatal mental health *polygenic risk score Index. décimale : PER Périodiques Résumé : Maternal antenatal depression strongly influences child mental health but with considerable inter-individual variation that is, in part, linked to genotype. The challenge is to effectively capture the genotypic influence. We outline a novel approach to describe genomic susceptibility to maternal antenatal depression focusing on child emotional/behavioral difficulties. Two cohorts provided measures of maternal depression, child genetic variation, and child mental health symptoms. We constructed a conventional polygenic risk score (PRS) for attention-deficit/hyperactivity disorder (ADHD) (PRSADHD) that significantly moderated the association between maternal antenatal depression and internalizing problems at 60 months (p = 2.94 × 10-4, R2 = .18). We then constructed an interaction PRS (xPRS) based on a subset of those single nucleotide polymorphisms from the PRSADHD that most accounted for the moderation of the association between maternal antenatal depression and child outcome. The interaction between maternal antenatal depression and this xPRS accounted for a larger proportion of the variance in child emotional/behavioral problems than models based on any PRSADHD (p = 5.50 × 10-9, R2 = .27), with similar findings in the replication cohort. The xPRS was significantly enriched for genes involved in neuronal development and synaptic function. Our study illustrates a novel approach to the study of genotypic moderation on the impact of maternal antenatal depression on child mental health and highlights the utility of the xPRS approach. These findings advance our understanding of individual differences in the developmental origins of mental health. En ligne : http://dx.doi.org/10.1017/s0954579420001418 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=437 A methylation study implicates the rewiring of brain neural circuits during puberty in the emergence of sex differences in depression symptoms / Robin F. CHAN in Journal of Child Psychology and Psychiatry, 63-7 (July 2022)
[article]
Titre : A methylation study implicates the rewiring of brain neural circuits during puberty in the emergence of sex differences in depression symptoms Type de document : Texte imprimé et/ou numérique Auteurs : Robin F. CHAN, Auteur ; William E. COPELAND, Auteur ; Min ZHAO, Auteur ; Lin Y. XIE, Auteur ; Jane COSTELLO, Auteur ; Karolina A. ABERG, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur Article en page(s) : p.802-809 Langues : Anglais (eng) Mots-clés : Brain DNA Methylation Depression/genetics Female Genome-Wide Association Study Humans Male Puberty Sex Characteristics Affective disorders biomarkers epigenetics sex differences Index. décimale : PER Périodiques Résumé : BACKGROUND: Women are 1.5-3 times more likely to suffer from depression than men. This sex bias first emerges during puberty and then persists across the reproductive years. As the cause remains largely elusive, we performed a methylation-wide association study (MWAS) to generate novel hypotheses. METHODS: We assayed nearly all 28 million possible methylation sites in blood in 595 blood samples from 487 participants aged 9-17. MWASs were performed to identify methylation sites associated with increasing sex differences in depression symptoms as a function of pubertal stage. Epigenetic deconvolution was applied to perform analyses on a cell-type specific level. RESULTS: In monocytes, a substantial number of significant associations were detected after controlling the FDR at 0.05. These results could not be explained by plasma testosterone/estradiol or current/lifetime trauma. Our top results in monocytes were significantly enriched (ratio of 2.48) for genes in the top of a large genome-wide association study (GWAS) meta-analysis of depression and neurodevelopment-related Gene Ontology (GO) terms that remained significant after correcting for multiple testing. Focusing on our most robust findings (70 genes overlapping with the GWAS meta-analysis and the significant GO terms), we find genes coding for members of each of the major classes of axon guidance molecules (netrins, slits, semaphorins, ephrins, and cell adhesion molecules). Many of these genes were previously implicated in rodent studies of brain development and depression-like phenotypes, as well as human methylation, gene expression and GWAS studies. CONCLUSIONS: Our study suggests that the emergence of sex differences in depression may be related to the differential rewiring of brain circuits between boys and girls during puberty. En ligne : http://dx.doi.org/10.1111/jcpp.13522 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=477
in Journal of Child Psychology and Psychiatry > 63-7 (July 2022) . - p.802-809[article] A methylation study implicates the rewiring of brain neural circuits during puberty in the emergence of sex differences in depression symptoms [Texte imprimé et/ou numérique] / Robin F. CHAN, Auteur ; William E. COPELAND, Auteur ; Min ZHAO, Auteur ; Lin Y. XIE, Auteur ; Jane COSTELLO, Auteur ; Karolina A. ABERG, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur . - p.802-809.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-7 (July 2022) . - p.802-809
Mots-clés : Brain DNA Methylation Depression/genetics Female Genome-Wide Association Study Humans Male Puberty Sex Characteristics Affective disorders biomarkers epigenetics sex differences Index. décimale : PER Périodiques Résumé : BACKGROUND: Women are 1.5-3 times more likely to suffer from depression than men. This sex bias first emerges during puberty and then persists across the reproductive years. As the cause remains largely elusive, we performed a methylation-wide association study (MWAS) to generate novel hypotheses. METHODS: We assayed nearly all 28 million possible methylation sites in blood in 595 blood samples from 487 participants aged 9-17. MWASs were performed to identify methylation sites associated with increasing sex differences in depression symptoms as a function of pubertal stage. Epigenetic deconvolution was applied to perform analyses on a cell-type specific level. RESULTS: In monocytes, a substantial number of significant associations were detected after controlling the FDR at 0.05. These results could not be explained by plasma testosterone/estradiol or current/lifetime trauma. Our top results in monocytes were significantly enriched (ratio of 2.48) for genes in the top of a large genome-wide association study (GWAS) meta-analysis of depression and neurodevelopment-related Gene Ontology (GO) terms that remained significant after correcting for multiple testing. Focusing on our most robust findings (70 genes overlapping with the GWAS meta-analysis and the significant GO terms), we find genes coding for members of each of the major classes of axon guidance molecules (netrins, slits, semaphorins, ephrins, and cell adhesion molecules). Many of these genes were previously implicated in rodent studies of brain development and depression-like phenotypes, as well as human methylation, gene expression and GWAS studies. CONCLUSIONS: Our study suggests that the emergence of sex differences in depression may be related to the differential rewiring of brain circuits between boys and girls during puberty. En ligne : http://dx.doi.org/10.1111/jcpp.13522 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=477 Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence / A. S. F. KWONG in Journal of Child Psychology and Psychiatry, 62-12 (December 2021)
[article]
Titre : Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence Type de document : Texte imprimé et/ou numérique Auteurs : A. S. F. KWONG, Auteur ; T. T. MORRIS, Auteur ; R. M. PEARSON, Auteur ; N. J. TIMPSON, Auteur ; F. RICE, Auteur ; E. STERGIAKOULI, Auteur ; K. TILLING, Auteur Article en page(s) : p.1462-1474 Langues : Anglais (eng) Mots-clés : Adolescent Adult Anxiety Child Cross-Sectional Studies Depression/genetics Depressive Disorder, Major/epidemiology/genetics Genetic Predisposition to Disease/genetics Genome-Wide Association Study Humans Longitudinal Studies Multifactorial Inheritance/genetics Neuroticism Young Adult Alspac Polygenic risk scores adolescence depressive symptoms development longitudinal trajectories Index. décimale : PER Périodiques Résumé : BACKGROUND: Adolescence marks a period where depression will commonly onset. Twin studies show that genetic influences play a role in how depression develops and changes across adolescence. Recent genome-wide association studies highlight that common genetic variants - which can be combined into polygenic risk scores (PRS) - are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine associations between PRS for five psychiatric traits and depressive symptoms measured across adolescence using cross-sectional and growth-curve models. The five PRS were as follows: depression (DEP), major depressive disorder (MDD), anxiety (ANX), neuroticism (NEU) and schizophrenia (SCZ). METHODS: We used data from over 6,000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine associations between the five PRS and self-reported depressive symptoms (Short Mood and Feelings Questionnaire) over 9 occasions from 10 to 24?years. The PRS were created from well-powered genome-wide association studies conducted in adult populations. We examined cross-sectional associations between the PRS at each age and then again with longitudinal trajectories of depressive symptoms in a repeated measures framework using multilevel growth-curve analysis to examine the severity and the rate of change. RESULTS: There was strong evidence that higher PRS for DEP, MDD and NEU were associated with worse depressive symptoms throughout adolescence and into young adulthood in our cross-sectional analysis, with consistent associations observed across all nine occasions. Growth-curve analyses provided stronger associations (as measured by effect sizes) and additional insights, demonstrating that individuals with higher PRS for DEP, MDD and NEU had steeper trajectories of depressive symptoms across development, all with a greater increasing rate of change during adolescence. Evidence was less consistent for the ANX and SCZ PRS in the cross-sectional analysis, yet there was some evidence for an increasing rate of change in adolescence in the growth-curve analyses with the ANX PRS. CONCLUSIONS: These results show that common genetic variants as indexed by varying psychiatric PRS show patterns of specificity that influence both the severity and rate of change in depressive symptoms throughout adolescence and then into young adulthood. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights how genetic factors influence the onset and persistence of adolescent depression. En ligne : http://dx.doi.org/10.1111/jcpp.13422 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456
in Journal of Child Psychology and Psychiatry > 62-12 (December 2021) . - p.1462-1474[article] Polygenic risk for depression, anxiety and neuroticism are associated with the severity and rate of change in depressive symptoms across adolescence [Texte imprimé et/ou numérique] / A. S. F. KWONG, Auteur ; T. T. MORRIS, Auteur ; R. M. PEARSON, Auteur ; N. J. TIMPSON, Auteur ; F. RICE, Auteur ; E. STERGIAKOULI, Auteur ; K. TILLING, Auteur . - p.1462-1474.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 62-12 (December 2021) . - p.1462-1474
Mots-clés : Adolescent Adult Anxiety Child Cross-Sectional Studies Depression/genetics Depressive Disorder, Major/epidemiology/genetics Genetic Predisposition to Disease/genetics Genome-Wide Association Study Humans Longitudinal Studies Multifactorial Inheritance/genetics Neuroticism Young Adult Alspac Polygenic risk scores adolescence depressive symptoms development longitudinal trajectories Index. décimale : PER Périodiques Résumé : BACKGROUND: Adolescence marks a period where depression will commonly onset. Twin studies show that genetic influences play a role in how depression develops and changes across adolescence. Recent genome-wide association studies highlight that common genetic variants - which can be combined into polygenic risk scores (PRS) - are also implicated in depression. However, the role of PRS in adolescent depression and changes in adolescent depression is not yet understood. We aimed to examine associations between PRS for five psychiatric traits and depressive symptoms measured across adolescence using cross-sectional and growth-curve models. The five PRS were as follows: depression (DEP), major depressive disorder (MDD), anxiety (ANX), neuroticism (NEU) and schizophrenia (SCZ). METHODS: We used data from over 6,000 participants of the Avon Longitudinal Study of Parents and Children (ALSPAC) to examine associations between the five PRS and self-reported depressive symptoms (Short Mood and Feelings Questionnaire) over 9 occasions from 10 to 24?years. The PRS were created from well-powered genome-wide association studies conducted in adult populations. We examined cross-sectional associations between the PRS at each age and then again with longitudinal trajectories of depressive symptoms in a repeated measures framework using multilevel growth-curve analysis to examine the severity and the rate of change. RESULTS: There was strong evidence that higher PRS for DEP, MDD and NEU were associated with worse depressive symptoms throughout adolescence and into young adulthood in our cross-sectional analysis, with consistent associations observed across all nine occasions. Growth-curve analyses provided stronger associations (as measured by effect sizes) and additional insights, demonstrating that individuals with higher PRS for DEP, MDD and NEU had steeper trajectories of depressive symptoms across development, all with a greater increasing rate of change during adolescence. Evidence was less consistent for the ANX and SCZ PRS in the cross-sectional analysis, yet there was some evidence for an increasing rate of change in adolescence in the growth-curve analyses with the ANX PRS. CONCLUSIONS: These results show that common genetic variants as indexed by varying psychiatric PRS show patterns of specificity that influence both the severity and rate of change in depressive symptoms throughout adolescence and then into young adulthood. Longitudinal data that make use of repeated measures designs have the potential to provide greater insights how genetic factors influence the onset and persistence of adolescent depression. En ligne : http://dx.doi.org/10.1111/jcpp.13422 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456