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Associations between psychiatric polygenic risk scores and general and specific psychopathology symptoms in childhood and adolescence between and within dizygotic twin pairs / Cen CHEN in Journal of Child Psychology and Psychiatry, 63-12 (December 2022)
[article]
Titre : Associations between psychiatric polygenic risk scores and general and specific psychopathology symptoms in childhood and adolescence between and within dizygotic twin pairs Type de document : Texte imprimé et/ou numérique Auteurs : Cen CHEN, Auteur ; Yi LU, Auteur ; Sebastian LUNDSTROM, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Erik PETTERSSON, Auteur Article en page(s) : p.1513-1522 Langues : Anglais (eng) Mots-clés : Adolescent Humans Twins, Dizygotic Longitudinal Studies Psychopathology Mental Disorders/epidemiology/genetics Risk Factors Attention Deficit Disorder with Hyperactivity/epidemiology General factor of psychopathology genetic nurture multi-polygenic score polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Although polygenic risk scores (PRS) predict psychiatric problems, these associations might be attributable to indirect pathways including population stratification, assortative mating, or dynastic effects (mediation via parental environments). The goal of this study was to examine whether PRS-psychiatric symptom associations were attributable to indirect versus direct pathways. METHODS: The sample consisted of 3,907 dizygotic (DZ) twin pairs. In childhood, their parents rated them on 98 symptoms. In adolescence (n=2,393 DZ pairs), both the parents and the twins rated themselves on 20 symptoms. We extracted one general and seven specific factors from the childhood data, and one general and three specific factors from the adolescent data. We then regressed each general factor model onto ten psychiatric PRS simultaneously. We first conducted the regressions between individuals (Î2) and then within DZ twin pairs (Î2(w) ), which controls for indirect pathways. RESULTS: In childhood, the PRS for ADHD predicted general psychopathology (Î2=0.09, 95% CI: [0.06, 0.12]; Î2(w) =0.07 [0.01, 0.12]). Furthermore, the PRS for ADHD predicted specific inattention (Î2=0.04 [0.00, 0.08]; Î2(w) =0.09 [0.01, 0.17]) and specific hyperactivity (Î2=0.07 [0.04, 0.11]; Î2(w) =0.09 [0.01, 0.16]); the PRS for schizophrenia predicted specific learning (Î2=0.08 [0.03, 0.13]; Î2(w) =0.19 [0.08, 0.30]) and specific inattention problems (Î2=0.05 [0.01, 0.09]; Î2(w) =0.10 [0.02, 0.19]); and the PRS for neuroticism predicted specific anxiety (Î2=0.06 [0.02, 0.10]; Î2(w) =0.06 [0.00, 0.12]). Overall, the PRS-general factor associations were similar between individuals and within twin pairs, whereas the PRS-specific factors associations amplified by 84% within pairs. CONCLUSIONS: This implies that PRS-psychiatric symptom associations did not appear attributable to indirect pathways such as population stratification, assortative mating, or mediation via parental environments. Rather, genetics appeared to directly influence symptomatology. En ligne : http://dx.doi.org/10.1111/jcpp.13605 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490
in Journal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1513-1522[article] Associations between psychiatric polygenic risk scores and general and specific psychopathology symptoms in childhood and adolescence between and within dizygotic twin pairs [Texte imprimé et/ou numérique] / Cen CHEN, Auteur ; Yi LU, Auteur ; Sebastian LUNDSTROM, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Erik PETTERSSON, Auteur . - p.1513-1522.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-12 (December 2022) . - p.1513-1522
Mots-clés : Adolescent Humans Twins, Dizygotic Longitudinal Studies Psychopathology Mental Disorders/epidemiology/genetics Risk Factors Attention Deficit Disorder with Hyperactivity/epidemiology General factor of psychopathology genetic nurture multi-polygenic score polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Although polygenic risk scores (PRS) predict psychiatric problems, these associations might be attributable to indirect pathways including population stratification, assortative mating, or dynastic effects (mediation via parental environments). The goal of this study was to examine whether PRS-psychiatric symptom associations were attributable to indirect versus direct pathways. METHODS: The sample consisted of 3,907 dizygotic (DZ) twin pairs. In childhood, their parents rated them on 98 symptoms. In adolescence (n=2,393 DZ pairs), both the parents and the twins rated themselves on 20 symptoms. We extracted one general and seven specific factors from the childhood data, and one general and three specific factors from the adolescent data. We then regressed each general factor model onto ten psychiatric PRS simultaneously. We first conducted the regressions between individuals (Î2) and then within DZ twin pairs (Î2(w) ), which controls for indirect pathways. RESULTS: In childhood, the PRS for ADHD predicted general psychopathology (Î2=0.09, 95% CI: [0.06, 0.12]; Î2(w) =0.07 [0.01, 0.12]). Furthermore, the PRS for ADHD predicted specific inattention (Î2=0.04 [0.00, 0.08]; Î2(w) =0.09 [0.01, 0.17]) and specific hyperactivity (Î2=0.07 [0.04, 0.11]; Î2(w) =0.09 [0.01, 0.16]); the PRS for schizophrenia predicted specific learning (Î2=0.08 [0.03, 0.13]; Î2(w) =0.19 [0.08, 0.30]) and specific inattention problems (Î2=0.05 [0.01, 0.09]; Î2(w) =0.10 [0.02, 0.19]); and the PRS for neuroticism predicted specific anxiety (Î2=0.06 [0.02, 0.10]; Î2(w) =0.06 [0.00, 0.12]). Overall, the PRS-general factor associations were similar between individuals and within twin pairs, whereas the PRS-specific factors associations amplified by 84% within pairs. CONCLUSIONS: This implies that PRS-psychiatric symptom associations did not appear attributable to indirect pathways such as population stratification, assortative mating, or mediation via parental environments. Rather, genetics appeared to directly influence symptomatology. En ligne : http://dx.doi.org/10.1111/jcpp.13605 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=490 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 Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence / A. A. LUSSIER in Journal of Child Psychology and Psychiatry, 62-7 (July 2021)
[article]
Titre : Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence Type de document : Texte imprimé et/ou numérique Auteurs : A. A. LUSSIER, Auteur ; M. HAWRILENKO, Auteur ; M. J. WANG, Auteur ; Karmel W. CHOI, Auteur ; J. CERUTTI, Auteur ; Y. ZHU, Auteur ; E. C. DUNN, Auteur Article en page(s) : p.895-904 Langues : Anglais (eng) Mots-clés : Adolescent Adult Child Depression Depressive Disorder, Major/epidemiology/genetics Genetic Predisposition to Disease/genetics Genome-Wide Association Study Humans Longitudinal Studies Prospective Studies Alspac Depression trajectories development longitudinal polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Early-onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early-onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence. METHODS: Data came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time-dependent measures of depressive symptoms trajectories spanning 4-16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome-wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene-level associations with these measures. RESULTS: Youth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level. CONCLUSIONS: This study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age-independent patterns. En ligne : http://dx.doi.org/10.1111/jcpp.13342 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456
in Journal of Child Psychology and Psychiatry > 62-7 (July 2021) . - p.895-904[article] Genetic susceptibility for major depressive disorder associates with trajectories of depressive symptoms across childhood and adolescence [Texte imprimé et/ou numérique] / A. A. LUSSIER, Auteur ; M. HAWRILENKO, Auteur ; M. J. WANG, Auteur ; Karmel W. CHOI, Auteur ; J. CERUTTI, Auteur ; Y. ZHU, Auteur ; E. C. DUNN, Auteur . - p.895-904.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 62-7 (July 2021) . - p.895-904
Mots-clés : Adolescent Adult Child Depression Depressive Disorder, Major/epidemiology/genetics Genetic Predisposition to Disease/genetics Genome-Wide Association Study Humans Longitudinal Studies Prospective Studies Alspac Depression trajectories development longitudinal polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Early-onset depression during childhood and adolescence is associated with a worse course of illness and outcome than adult onset. However, the genetic factors that influence risk for early-onset depression remain mostly unknown. Using data collected over 13 years, we examined whether polygenic risk scores (PRS) that capture genetic risk for depression were associated with depressive symptom trajectories assessed from childhood to adolescence. METHODS: Data came from the Avon Longitudinal Study of Parents and Children, a prospective, longitudinal birth cohort (analytic sample = 7,308 youth). We analyzed the relationship between genetic susceptibility to depression and three time-dependent measures of depressive symptoms trajectories spanning 4-16.5 years of age (class, onset, and cumulative burden). Trajectories were constructed using a growth mixture model with structured residuals. PRS were generated from the summary statistics of a genome-wide association study of depression risk using data from the Psychiatric Genomics Consortium, UK Biobank, and 23andMe, Inc. We used MAGMA to identify gene-level associations with these measures. RESULTS: Youth were classified into six classes of depressive symptom trajectories: high/renitent (27.9% of youth), high/reversing (9.1%), childhood decrease (7.3%), late childhood peak (3.3%), adolescent spike (2.5%), and minimal symptoms (49.9%). PRS discriminated between youth in the late childhood peak, high/reversing, and high/renitent classes compared to the minimal symptoms and childhood decrease classes. No significant associations were detected at the gene level. CONCLUSIONS: This study highlights differences in polygenic loading for depressive symptoms across childhood and adolescence, particularly among youths with high symptoms in early adolescence, regardless of age-independent patterns. En ligne : http://dx.doi.org/10.1111/jcpp.13342 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 Pupil size and pupillary light reflex in early infancy: heritability and link to genetic liability to schizophrenia / Ana Maria PORTUGAL in Journal of Child Psychology and Psychiatry, 63-9 (September 2022)
[article]
Titre : Pupil size and pupillary light reflex in early infancy: heritability and link to genetic liability to schizophrenia Type de document : Texte imprimé et/ou numérique Auteurs : Ana Maria PORTUGAL, Auteur ; Mark J. TAYLOR, Auteur ; Charlotte VIKTORSSON, Auteur ; Pär NYSTROM, Auteur ; Danyang LI, Auteur ; Kristiina TAMMIMIES, Auteur ; Angelica RONALD, Auteur ; Terje FALCK-YTTER, Auteur Article en page(s) : p.1068-1077 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder Depressive Disorder, Major Humans Infant Pupil/physiology Reflex, Pupillary/physiology Schizophrenia/genetics Pupillometry infancy polygenic risk scores pupillary light reflex schizophrenia twin design Index. décimale : PER Périodiques Résumé : BACKGROUND: Measures based on pupillometry, such as the pupillary light reflex (PLR) and baseline pupil size, reflect physiological responses linked to specific neural circuits that have been implicated as atypical in some psychiatric and neurodevelopmental conditions. METHODS: We investigated the contribution of genetic and environmental factors to the baseline pupil size and the PLR in 510 infant twins assessed at 5months of age (281 monozygotic and 229 dizygotic pairs), and its associations with common genetic variants associated with neurodevelopmental (autism spectrum disorder and attention deficit hyperactivity disorder) and mental health (bipolar disorder, major depressive disorder and schizophrenia) conditions using genome-wide polygenic scores (GPSs). RESULTS: Univariate twin modelling showed high heritability at 5months for both pupil size (h(2) =.64) and constriction in response to light (h(2) =.62), and bivariate twin modeling indicated substantial independence between the genetic factors influencing each (r(G) =.38). A statistically significant positive association between infant tonic pupil size and the GPS for schizophrenia was found (Î2=.15, p=.024), while there was no significant association with the GPS for autism or any other GPSs. CONCLUSIONS: This study shows that some pupil measures are highly heritable in early infancy, although substantially independent in their genetic etiologies, and associated with common genetic variants linked to schizophrenia. It illustrates how genetically informed studies of infants may help us understand early physiological responses associated with psychiatric disorders which emerge much later in life. En ligne : http://dx.doi.org/10.1111/jcpp.13564 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486
in Journal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1068-1077[article] Pupil size and pupillary light reflex in early infancy: heritability and link to genetic liability to schizophrenia [Texte imprimé et/ou numérique] / Ana Maria PORTUGAL, Auteur ; Mark J. TAYLOR, Auteur ; Charlotte VIKTORSSON, Auteur ; Pär NYSTROM, Auteur ; Danyang LI, Auteur ; Kristiina TAMMIMIES, Auteur ; Angelica RONALD, Auteur ; Terje FALCK-YTTER, Auteur . - p.1068-1077.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1068-1077
Mots-clés : Autism Spectrum Disorder Depressive Disorder, Major Humans Infant Pupil/physiology Reflex, Pupillary/physiology Schizophrenia/genetics Pupillometry infancy polygenic risk scores pupillary light reflex schizophrenia twin design Index. décimale : PER Périodiques Résumé : BACKGROUND: Measures based on pupillometry, such as the pupillary light reflex (PLR) and baseline pupil size, reflect physiological responses linked to specific neural circuits that have been implicated as atypical in some psychiatric and neurodevelopmental conditions. METHODS: We investigated the contribution of genetic and environmental factors to the baseline pupil size and the PLR in 510 infant twins assessed at 5months of age (281 monozygotic and 229 dizygotic pairs), and its associations with common genetic variants associated with neurodevelopmental (autism spectrum disorder and attention deficit hyperactivity disorder) and mental health (bipolar disorder, major depressive disorder and schizophrenia) conditions using genome-wide polygenic scores (GPSs). RESULTS: Univariate twin modelling showed high heritability at 5months for both pupil size (h(2) =.64) and constriction in response to light (h(2) =.62), and bivariate twin modeling indicated substantial independence between the genetic factors influencing each (r(G) =.38). A statistically significant positive association between infant tonic pupil size and the GPS for schizophrenia was found (Î2=.15, p=.024), while there was no significant association with the GPS for autism or any other GPSs. CONCLUSIONS: This study shows that some pupil measures are highly heritable in early infancy, although substantially independent in their genetic etiologies, and associated with common genetic variants linked to schizophrenia. It illustrates how genetically informed studies of infants may help us understand early physiological responses associated with psychiatric disorders which emerge much later in life. En ligne : http://dx.doi.org/10.1111/jcpp.13564 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 Heterotypic trajectories of dimensional psychopathology across the lifespan: the case of youth-onset attention deficit/hyperactivity disorder / A. G. MANFRO in Journal of Child Psychology and Psychiatry, 60-5 (May 2019)
[article]
Titre : Heterotypic trajectories of dimensional psychopathology across the lifespan: the case of youth-onset attention deficit/hyperactivity disorder Type de document : Texte imprimé et/ou numérique Auteurs : A. G. MANFRO, Auteur ; M. SANTORO, Auteur ; Guilherme V. POLANCZYK, Auteur ; A. GADELHA, Auteur ; Pedro M. PAN, Auteur ; Rodrigo Affonseca BRESSAN, Auteur ; E. BRIETZKE, Auteur ; F. TALARICO, Auteur ; S. BELANGERO, Auteur ; L. A. ROHDE, Auteur ; Giovanni A. SALUM, Auteur Article en page(s) : p.533-544 Langues : Anglais (eng) Mots-clés : Youth-onset cognition executive function p-factor polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Recent studies have demonstrated the existence of a distinct late-onset attention deficit/hyperactivity disorder (ADHD) trajectory. Our objective is to test if there are distinct ADHD trajectories regarding age of onset from childhood to adolescence and to compare clinical manifestations, cognitive functions and genetic risk for ADHD among distinct longitudinal groups. METHOD: Nine hundred and twenty four children and adolescents from the community participated in the study. We compared clinical, cognitive features and genetic risk among four groups of participants: (a) childhood-limited, (b) youth-onset, (c) childhood-onset with youth persistence, and (d) community comparisons without ADHD. Symptomatic and diagnostic assessments were performed using the Development and Well-Being Behavior Assessment, the Strengths and Difficulties Questionnaire, and the Child Behavior Checklist. Cognitive functions were measured using a battery of standardized tests. Genetic risk for ADHD was calculating using summary statistics from the Psychiatric Genomics Consortium. RESULTS: Half of the adolescents (52%) with ADHD had their symptom onset in adolescence. The impairment level of this group in adolescence is similar to the persistent group. Despite not having ADHD, the youth-onset group already presented in childhood more symptoms from other domains of psychopathology, higher shared variance in psychiatric symptomatology (p-factor), school impairment, and executive dysfunctions than community comparisons. Furthermore, the youth-onset group presented lower levels of genetic risk for ADHD compared to other cases. CONCLUSIONS: A significant proportion of adolescents with ADHD were youth-onset cases and presented similar impairment levels as those cases with early-onset ADHD. The presence of cognitive impairments and higher levels of clinical symptoms in the youth-onset group already at childhood speaks in favor of a heterotypic trajectory of psychopathology suggesting that youth-onset ADHD might be an artificial consequence of categorizing dimensional psychopathology into discrete diagnostic groups. En ligne : http://dx.doi.org/10.1111/jcpp.12987 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=392
in Journal of Child Psychology and Psychiatry > 60-5 (May 2019) . - p.533-544[article] Heterotypic trajectories of dimensional psychopathology across the lifespan: the case of youth-onset attention deficit/hyperactivity disorder [Texte imprimé et/ou numérique] / A. G. MANFRO, Auteur ; M. SANTORO, Auteur ; Guilherme V. POLANCZYK, Auteur ; A. GADELHA, Auteur ; Pedro M. PAN, Auteur ; Rodrigo Affonseca BRESSAN, Auteur ; E. BRIETZKE, Auteur ; F. TALARICO, Auteur ; S. BELANGERO, Auteur ; L. A. ROHDE, Auteur ; Giovanni A. SALUM, Auteur . - p.533-544.
Langues : Anglais (eng)
in Journal of Child Psychology and Psychiatry > 60-5 (May 2019) . - p.533-544
Mots-clés : Youth-onset cognition executive function p-factor polygenic risk scores Index. décimale : PER Périodiques Résumé : BACKGROUND: Recent studies have demonstrated the existence of a distinct late-onset attention deficit/hyperactivity disorder (ADHD) trajectory. Our objective is to test if there are distinct ADHD trajectories regarding age of onset from childhood to adolescence and to compare clinical manifestations, cognitive functions and genetic risk for ADHD among distinct longitudinal groups. METHOD: Nine hundred and twenty four children and adolescents from the community participated in the study. We compared clinical, cognitive features and genetic risk among four groups of participants: (a) childhood-limited, (b) youth-onset, (c) childhood-onset with youth persistence, and (d) community comparisons without ADHD. Symptomatic and diagnostic assessments were performed using the Development and Well-Being Behavior Assessment, the Strengths and Difficulties Questionnaire, and the Child Behavior Checklist. Cognitive functions were measured using a battery of standardized tests. Genetic risk for ADHD was calculating using summary statistics from the Psychiatric Genomics Consortium. RESULTS: Half of the adolescents (52%) with ADHD had their symptom onset in adolescence. The impairment level of this group in adolescence is similar to the persistent group. Despite not having ADHD, the youth-onset group already presented in childhood more symptoms from other domains of psychopathology, higher shared variance in psychiatric symptomatology (p-factor), school impairment, and executive dysfunctions than community comparisons. Furthermore, the youth-onset group presented lower levels of genetic risk for ADHD compared to other cases. CONCLUSIONS: A significant proportion of adolescents with ADHD were youth-onset cases and presented similar impairment levels as those cases with early-onset ADHD. The presence of cognitive impairments and higher levels of clinical symptoms in the youth-onset group already at childhood speaks in favor of a heterotypic trajectory of psychopathology suggesting that youth-onset ADHD might be an artificial consequence of categorizing dimensional psychopathology into discrete diagnostic groups. En ligne : http://dx.doi.org/10.1111/jcpp.12987 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=392