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Auteur E. STERGIAKOULI |
Documents disponibles écrits par cet auteur (3)



Childhood neurodevelopmental difficulties and risk of adolescent depression: the role of irritability / O. EYRE in Journal of Child Psychology and Psychiatry, 60-8 (August 2019)
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Titre : Childhood neurodevelopmental difficulties and risk of adolescent depression: the role of irritability Type de document : Texte imprimé et/ou numérique Auteurs : O. EYRE, Auteur ; R. A. HUGHES, Auteur ; Ajay K. THAPAR, Auteur ; E. LEIBENLUFT, Auteur ; A. STRINGARIS, Auteur ; George DAVEY SMITH, Auteur ; E. STERGIAKOULI, Auteur ; S. COLLISHAW, Auteur ; A. THAPAR, Auteur Article en page(s) : p.866-874 Langues : Anglais (eng) Mots-clés : Alspac attention-deficit/hyperactivity disorder autism depression irritability neurodevelopmental Index. décimale : PER Périodiques Résumé : BACKGROUND: Children with neurodevelopmental disorders are at increased risk of developing depression. Irritability predicts depression in the general population and is common in children with neurodevelopmental disorders. Thus, it is possible that irritability in children with neurodevelopmental disorders contributes to the link with later depression. This study aimed to (a) examine the association between childhood neurodevelopmental difficulties and adolescent depression and (b) test whether irritability explains this association. METHODS: Children with any neurodevelopmental difficulty at the age of 7-9 (n = 1,697) and a selected, comparison group without any neurodevelopmental difficulty (n = 3,177) were identified from a prospective, UK population-based cohort, the Avon Longitudinal Study of Parents and Children. Neurodevelopmental difficulties were defined as a score in the bottom 5% of the sample on at least one measure of cognitive ability, communication, autism spectrum symptoms, attention-deficit/hyperactivity symptoms, reading or motor coordination. The Development and Well-Being Assessment measured parent-reported child irritability at the age of 7, parent-reported adolescent depression at the age of 10 and 13, and self-reported depression at the age of 15. Depression measures were combined, deriving an outcome of major depressive disorder (MDD) in adolescence. Logistic regression examined the association between childhood neurodevelopmental difficulties and adolescent MDD, controlling for gender. Path analysis estimated the proportion of this association explained by irritability. Analyses were repeated for individual neurodevelopmental problems. RESULTS: Childhood neurodevelopmental difficulties were associated with adolescent MDD (OR = 2.11, 95% CI = 1.24, 3.60, p = .006). Childhood irritability statistically accounted for 42% of this association. On examining each neurodevelopmental difficulty separately, autistic, communication and ADHD problems were each associated with depression, with irritability explaining 29%-51% of these links. CONCLUSIONS: Childhood irritability appears to be a key contributor to the link between childhood neurodevelopmental difficulties and adolescent MDD. High rates of irritability in children with autistic and ADHD difficulties may explain elevated rates of depression in the neurodevelopmental group. En ligne : http://dx.doi.org/10.1111/jcpp.13053 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=404
in Journal of Child Psychology and Psychiatry > 60-8 (August 2019) . - p.866-874[article] Childhood neurodevelopmental difficulties and risk of adolescent depression: the role of irritability [Texte imprimé et/ou numérique] / O. EYRE, Auteur ; R. A. HUGHES, Auteur ; Ajay K. THAPAR, Auteur ; E. LEIBENLUFT, Auteur ; A. STRINGARIS, Auteur ; George DAVEY SMITH, Auteur ; E. STERGIAKOULI, Auteur ; S. COLLISHAW, Auteur ; A. THAPAR, Auteur . - p.866-874.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 60-8 (August 2019) . - p.866-874
Mots-clés : Alspac attention-deficit/hyperactivity disorder autism depression irritability neurodevelopmental Index. décimale : PER Périodiques Résumé : BACKGROUND: Children with neurodevelopmental disorders are at increased risk of developing depression. Irritability predicts depression in the general population and is common in children with neurodevelopmental disorders. Thus, it is possible that irritability in children with neurodevelopmental disorders contributes to the link with later depression. This study aimed to (a) examine the association between childhood neurodevelopmental difficulties and adolescent depression and (b) test whether irritability explains this association. METHODS: Children with any neurodevelopmental difficulty at the age of 7-9 (n = 1,697) and a selected, comparison group without any neurodevelopmental difficulty (n = 3,177) were identified from a prospective, UK population-based cohort, the Avon Longitudinal Study of Parents and Children. Neurodevelopmental difficulties were defined as a score in the bottom 5% of the sample on at least one measure of cognitive ability, communication, autism spectrum symptoms, attention-deficit/hyperactivity symptoms, reading or motor coordination. The Development and Well-Being Assessment measured parent-reported child irritability at the age of 7, parent-reported adolescent depression at the age of 10 and 13, and self-reported depression at the age of 15. Depression measures were combined, deriving an outcome of major depressive disorder (MDD) in adolescence. Logistic regression examined the association between childhood neurodevelopmental difficulties and adolescent MDD, controlling for gender. Path analysis estimated the proportion of this association explained by irritability. Analyses were repeated for individual neurodevelopmental problems. RESULTS: Childhood neurodevelopmental difficulties were associated with adolescent MDD (OR = 2.11, 95% CI = 1.24, 3.60, p = .006). Childhood irritability statistically accounted for 42% of this association. On examining each neurodevelopmental difficulty separately, autistic, communication and ADHD problems were each associated with depression, with irritability explaining 29%-51% of these links. CONCLUSIONS: Childhood irritability appears to be a key contributor to the link between childhood neurodevelopmental difficulties and adolescent MDD. High rates of irritability in children with autistic and ADHD difficulties may explain elevated rates of depression in the neurodevelopmental group. En ligne : http://dx.doi.org/10.1111/jcpp.13053 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=404 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)
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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 Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development / E. STERGIAKOULI in Molecular Autism, 8 (2017)
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Titre : Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development Type de document : Texte imprimé et/ou numérique Auteurs : E. STERGIAKOULI, Auteur ; George DAVEY SMITH, Auteur ; J. MARTIN, Auteur ; D. H. SKUSE, Auteur ; W. VIECHTBAUER, Auteur ; S. M. RING, Auteur ; A. RONALD, Auteur ; D. E. EVANS, Auteur ; S. E. FISHER, Auteur ; A. THAPAR, Auteur ; B. 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 = 5551, Social and Communication Disorders Checklist, SCDC) and combined hyperactive-impulsive/inattentive ADHD symptoms (N = 5678, Strengths and Difficulties Questionnaire, SDQ-ADHD) were repeatedly measured in a UK birth cohort (ALSPAC, age 7 to 17 years). Genome-wide summary statistics on clinical ASD (5305 cases; 5305 pseudo-controls) and ADHD (4163 cases; 12,040 controls/pseudo-controls) were available from the Psychiatric Genomics Consortium. Genetic trait variances and genetic overlap between phenotypes were estimated using genome-wide data. RESULTS: In the general population, genetic influences for SCDC and SDQ-ADHD scores were shared throughout development. Genetic correlations across traits reached a similar strength and magnitude (cross-trait rg = 1, pmin = 3 x 10(-4)) as those between repeated measures of the same trait (within-trait rg = 0.94, pmin = 7 x 10(-4)). Shared genetic influences between traits, especially during later adolescence, may implicate variants in K-RAS signalling upregulated genes (p-meta = 6.4 x 10(-4)). Uni-dimensionally, each population-based trait mapped to the expected behavioural continuum: risk-increasing alleles for clinical ADHD were persistently associated with SDQ-ADHD scores throughout development (marginal regression R(2) = 0.084%). An age-specific genetic overlap between clinical ASD and social-communication difficulties during childhood was also shown, as per previous reports. Cross-dimensionally, however, neither SCDC nor SDQ-ADHD scores were linked to genetic risk for disorder. CONCLUSIONS: In the general population, genetic aetiologies between social-communication difficulties and ADHD symptoms are shared throughout child and adolescent development and may implicate similar biological pathways that co-vary during development. Within both the ASD and the ADHD dimension, population-based traits are also linked to clinical disorder, although much larger clinical discovery samples are required to reliably detect cross-dimensional trait-disorder relationships. 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
in Molecular Autism > 8 (2017) . - 18p.[article] Shared genetic influences between dimensional ASD and ADHD symptoms during child and adolescent development [Texte imprimé et/ou numérique] / E. STERGIAKOULI, Auteur ; George DAVEY SMITH, Auteur ; J. MARTIN, Auteur ; D. H. SKUSE, Auteur ; W. VIECHTBAUER, Auteur ; S. M. RING, Auteur ; A. RONALD, Auteur ; D. E. EVANS, Auteur ; S. E. FISHER, Auteur ; A. THAPAR, Auteur ; B. 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 = 5551, Social and Communication Disorders Checklist, SCDC) and combined hyperactive-impulsive/inattentive ADHD symptoms (N = 5678, Strengths and Difficulties Questionnaire, SDQ-ADHD) were repeatedly measured in a UK birth cohort (ALSPAC, age 7 to 17 years). Genome-wide summary statistics on clinical ASD (5305 cases; 5305 pseudo-controls) and ADHD (4163 cases; 12,040 controls/pseudo-controls) were available from the Psychiatric Genomics Consortium. Genetic trait variances and genetic overlap between phenotypes were estimated using genome-wide data. RESULTS: In the general population, genetic influences for SCDC and SDQ-ADHD scores were shared throughout development. Genetic correlations across traits reached a similar strength and magnitude (cross-trait rg = 1, pmin = 3 x 10(-4)) as those between repeated measures of the same trait (within-trait rg = 0.94, pmin = 7 x 10(-4)). Shared genetic influences between traits, especially during later adolescence, may implicate variants in K-RAS signalling upregulated genes (p-meta = 6.4 x 10(-4)). Uni-dimensionally, each population-based trait mapped to the expected behavioural continuum: risk-increasing alleles for clinical ADHD were persistently associated with SDQ-ADHD scores throughout development (marginal regression R(2) = 0.084%). An age-specific genetic overlap between clinical ASD and social-communication difficulties during childhood was also shown, as per previous reports. Cross-dimensionally, however, neither SCDC nor SDQ-ADHD scores were linked to genetic risk for disorder. CONCLUSIONS: In the general population, genetic aetiologies between social-communication difficulties and ADHD symptoms are shared throughout child and adolescent development and may implicate similar biological pathways that co-vary during development. Within both the ASD and the ADHD dimension, population-based traits are also linked to clinical disorder, although much larger clinical discovery samples are required to reliably detect cross-dimensional trait-disorder relationships. 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