Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders / Sarah J. LEWIS in Journal of Child Psychology and Psychiatry, 54-10 (October 2013)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1095-1108 Titre : Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders Type de document : texte imprimé Auteurs : Sarah J. LEWIS, Auteur ; Caroline L. RELTON, Auteur ; Stanley ZAMMIT, Auteur ; George DAVEY SMITH, Auteur Article en page(s) : p.1095-1108 Langues : Anglais (eng) Mots-clés : Mendelian randomisation  causal inference  childhood behaviour  psychiatric disorders  instrumental variable analysis Index. décimale : PER Périodiques Résumé : Background The risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful. Scope In this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived using in vitro fertilisation and not least Mendelian randomisation. We have illustrated these approaches using examples of behavioural and psychiatric disorders. Conclusion By having these approaches outlined together in one review, researchers can consider which of these methods would be most suitable for their study question. We have particularly focussed on Mendelian randomisation, as this is a relatively novel concept, in doing so, we have illustrated the concept and discused the implementation and the limitations of this approach. En ligne : http://dx.doi.org/10.1111/jcpp.12127 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212 [article] Approaches for strengthening causal inference regarding prenatal risk factors for childhood behavioural and psychiatric disorders [texte imprimé] / Sarah J. LEWIS, Auteur ; Caroline L. RELTON, Auteur ; Stanley ZAMMIT, Auteur ; George DAVEY SMITH, Auteur . - p.1095-1108. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 54-10 (October 2013) . - p.1095-1108 Mots-clés : Mendelian randomisation  causal inference  childhood behaviour  psychiatric disorders  instrumental variable analysis Index. décimale : PER Périodiques Résumé : Background The risk of childhood behavioural and psychiatric diseases could be substantially reduced if modifiable risk factors for these disorders were identified. The critical period for many of these exposures is likely to be in utero as this is the time when brain development is most rapid. However, due to confounding and other limitations of traditional epidemiological studies, identification of causal risk factors has proved challenging and on the whole research in this area has not been fruitful. Scope In this review, we highlight several alternative approaches including; comparisons across settings, the use of negative controls and natural experiments, which includes migration studies, studies of individuals conceived using in vitro fertilisation and not least Mendelian randomisation. We have illustrated these approaches using examples of behavioural and psychiatric disorders. Conclusion By having these approaches outlined together in one review, researchers can consider which of these methods would be most suitable for their study question. We have particularly focussed on Mendelian randomisation, as this is a relatively novel concept, in doing so, we have illustrated the concept and discused the implementation and the limitations of this approach. En ligne : http://dx.doi.org/10.1111/jcpp.12127 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=212

Epigenetic profiling of social communication trajectories and co-occurring mental health problems: a prospective, methylome-wide association study / Jolien RIJLAARSDAM in Development and Psychopathology, 34-3 (August 2022)  

Public ISBD [article]  inDevelopment and Psychopathology > 34-3 (August 2022) . - p.854-863 Titre : Epigenetic profiling of social communication trajectories and co-occurring mental health problems: a prospective, methylome-wide association study Type de document : texte imprimé Auteurs : Jolien RIJLAARSDAM, Auteur ; Charlotte A.M. CECIL, Auteur ; Caroline L. RELTON, Auteur ; Edward D. BARKER, Auteur Article en page(s) : p.854-863 Langues : Anglais (eng) Mots-clés : ALSPAC  autistic traits  DNA methylation  longitudinal  methylome-wide Index. décimale : PER Périodiques Résumé : While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8 “17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated. En ligne : http://dx.doi.org/10.1017/S0954579420001662 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=484 [article] Epigenetic profiling of social communication trajectories and co-occurring mental health problems: a prospective, methylome-wide association study [texte imprimé] / Jolien RIJLAARSDAM, Auteur ; Charlotte A.M. CECIL, Auteur ; Caroline L. RELTON, Auteur ; Edward D. BARKER, Auteur . - p.854-863. Langues : Anglais (eng) in Development and Psychopathology > 34-3 (August 2022) . - p.854-863 Mots-clés : ALSPAC  autistic traits  DNA methylation  longitudinal  methylome-wide Index. décimale : PER Périodiques Résumé : While previous studies suggest that both genetic and environmental factors play an important role in the development of autism-related traits, little is known about potential biological mechanisms underlying these associations. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we examined prospective associations between DNA methylation (DNAm: nbirth = 804, nage 7 = 877) and trajectories of social communication deficits at age 8 “17 years. Methylomic variation at three loci across the genome (false discovery rate = 0.048) differentiated children following high (n = 80) versus low (n = 724) trajectories of social communication deficits. This differential DNAm was specific to the neonatal period and not observed at 7 years of age. Associations between DNAm and trajectory membership remained robust after controlling for co-occurring mental health problems (i.e., hyperactivity/inattention, conduct problems). The three loci identified at birth were not replicated in the Generation R Study. However, to the best of our knowledge, ALSPAC is the only study to date that is prospective enough to examine DNAm in relation to longitudinal trajectories of social communication deficits from childhood to adolescence. Although the present findings might point to potentially novel sites that differentiate between a high versus low trajectory of social communication deficits, the results should be considered tentative until further replicated. En ligne : http://dx.doi.org/10.1017/S0954579420001662 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=484

Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence / Edward D. BARKER in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.1145-1156 Titre : Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence Type de document : texte imprimé Auteurs : Edward D. BARKER, Auteur ; Charlotte A.M. CECIL, Auteur ; Esther WALTON, Auteur ; Lotte C. HOUTEPEN, Auteur ; Thomas G. O'CONNOR, Auteur ; Andrea DANESE, Auteur ; Sara R. JAFFEE, Auteur ; Sarah K.G. JENSEN, Auteur ; Carmine M. PARIANTE, Auteur ; Wendy MCARDLE, Auteur ; Tom R. GAUNT, Auteur ; Caroline L. RELTON, Auteur ; S. Wendy ROBERTS, Auteur Article en page(s) : p.1145-1156 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : In 785 mother-child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7-15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7-15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health. En ligne : http://dx.doi.org/10.1017/s0954579418000330 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367 [article] Inflammation-related epigenetic risk and child and adolescent mental health: A prospective study from pregnancy to middle adolescence [texte imprimé] / Edward D. BARKER, Auteur ; Charlotte A.M. CECIL, Auteur ; Esther WALTON, Auteur ; Lotte C. HOUTEPEN, Auteur ; Thomas G. O'CONNOR, Auteur ; Andrea DANESE, Auteur ; Sara R. JAFFEE, Auteur ; Sarah K.G. JENSEN, Auteur ; Carmine M. PARIANTE, Auteur ; Wendy MCARDLE, Auteur ; Tom R. GAUNT, Auteur ; Caroline L. RELTON, Auteur ; S. Wendy ROBERTS, Auteur . - p.1145-1156. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.1145-1156 Index. décimale : PER Périodiques Résumé : In 785 mother-child (50% male) pairs from a longitudinal epidemiological birth cohort, we investigated associations between inflammation-related epigenetic polygenic risk scores (i-ePGS), environmental exposures, cognitive function, and child and adolescent internalizing and externalizing problems. We examined prenatal and postnatal effects. For externalizing problems, one prenatal effect was found: i-ePGS at birth associated with higher externalizing problems (ages 7-15) indirectly through lower cognitive function (age 7). For internalizing problems, we identified two effects. For a prenatal effect, i-ePGS at birth associated with higher internalizing symptoms via continuity in i-ePGS at age 7. For a postnatal effect, higher postnatal adversity exposure (birth through age 7) associated with higher internalizing problems (ages 7-15) via higher i-ePGS (age 7). Hence, externalizing problems were related mainly to prenatal effects involving lower cognitive function, whereas internalizing problems appeared related to both prenatal and postnatal effects. The present study supports a link between i-ePGS and child and adolescent mental health. En ligne : http://dx.doi.org/10.1017/s0954579418000330 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=367

Longitudinal epigenetic predictors of amygdala:hippocampus volume ratio / Esther WALTON in Journal of Child Psychology and Psychiatry, 58-12 (December 2017)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 58-12 (December 2017) . - p.1341-1350 Titre : Longitudinal epigenetic predictors of amygdala:hippocampus volume ratio Type de document : texte imprimé Auteurs : Esther WALTON, Auteur ; Charlotte A.M. CECIL, Auteur ; Matthew SUDERMAN, Auteur ; Jingyu LIU, Auteur ; Jessica A. TURNER, Auteur ; Vince D. CALHOUN, Auteur ; Stefan EHRLICH, Auteur ; Caroline L. RELTON, Auteur ; Edward D. BARKER, Auteur Article en page(s) : p.1341-1350 Langues : Anglais (eng) Mots-clés : DNA methylation  methylome-wide  amygdala  hippocampus  longitudinal  Avon Longitudinal Study of Parents and Children Index. décimale : PER Périodiques Résumé : Background The ratio between amygdala:hippocampal (AH) volume has been associated with multiple psychiatric problems, including anxiety and aggression. Yet, little is known about its biological underpinnings. Here, we used a methylome-wide approach to test (a) whether DNA methylation in early life (birth, age 7) prospectively associates with total AH volume ratio in early adulthood, and (b) whether significant DNA methylation markers are influenced by prenatal risk factors. Methods Analyses were based on a subsample (n = 109 males) from the Avon Longitudinal Study of Parents and Children, which included measures of prenatal risk, DNA methylation (Infinium Illumina 450k), T1-weighted brain scans and psychopathology in early adulthood (age 18–21). Amygdala and hippocampus measures were derived using Freesurfer 5.3.0. Methylation markers related to AH volume ratio across time were identified using longitudinal multilevel modeling. Results Amygdala:hippocampal volume ratio correlated positively with age 18 psychosis-like symptoms (p = .007). Methylation of a probe in the gene SP6 associated longitudinally with (a) higher AH volume ratio (FDR q-value = .01) and (b) higher stressful life events during pregnancy (p = .046). SP6 is expressed in the hippocampus and amygdala and has been implicated in cognitive decline in Alzheimer's disease. The association between SP6 DNA methylation, AH volume ratio and psychopathology was replicated in an independent dataset of 101 patients with schizophrenia and 111 healthy controls. Conclusions Our findings suggest that epigenetic alterations in genes implicated in neurodevelopment may contribute to a brain-based biomarker of psychopathology. En ligne : http://dx.doi.org/10.1111/jcpp.12740 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=326 [article] Longitudinal epigenetic predictors of amygdala:hippocampus volume ratio [texte imprimé] / Esther WALTON, Auteur ; Charlotte A.M. CECIL, Auteur ; Matthew SUDERMAN, Auteur ; Jingyu LIU, Auteur ; Jessica A. TURNER, Auteur ; Vince D. CALHOUN, Auteur ; Stefan EHRLICH, Auteur ; Caroline L. RELTON, Auteur ; Edward D. BARKER, Auteur . - p.1341-1350. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 58-12 (December 2017) . - p.1341-1350 Mots-clés : DNA methylation  methylome-wide  amygdala  hippocampus  longitudinal  Avon Longitudinal Study of Parents and Children Index. décimale : PER Périodiques Résumé : Background The ratio between amygdala:hippocampal (AH) volume has been associated with multiple psychiatric problems, including anxiety and aggression. Yet, little is known about its biological underpinnings. Here, we used a methylome-wide approach to test (a) whether DNA methylation in early life (birth, age 7) prospectively associates with total AH volume ratio in early adulthood, and (b) whether significant DNA methylation markers are influenced by prenatal risk factors. Methods Analyses were based on a subsample (n = 109 males) from the Avon Longitudinal Study of Parents and Children, which included measures of prenatal risk, DNA methylation (Infinium Illumina 450k), T1-weighted brain scans and psychopathology in early adulthood (age 18–21). Amygdala and hippocampus measures were derived using Freesurfer 5.3.0. Methylation markers related to AH volume ratio across time were identified using longitudinal multilevel modeling. Results Amygdala:hippocampal volume ratio correlated positively with age 18 psychosis-like symptoms (p = .007). Methylation of a probe in the gene SP6 associated longitudinally with (a) higher AH volume ratio (FDR q-value = .01) and (b) higher stressful life events during pregnancy (p = .046). SP6 is expressed in the hippocampus and amygdala and has been implicated in cognitive decline in Alzheimer's disease. The association between SP6 DNA methylation, AH volume ratio and psychopathology was replicated in an independent dataset of 101 patients with schizophrenia and 111 healthy controls. Conclusions Our findings suggest that epigenetic alterations in genes implicated in neurodevelopment may contribute to a brain-based biomarker of psychopathology. En ligne : http://dx.doi.org/10.1111/jcpp.12740 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=326

Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study / Charlotte A.M. CECIL in Development and Psychopathology, 30-2 (May 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-2 (May 2018) . - p.383-397 Titre : Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study Type de document : texte imprimé Auteurs : Charlotte A.M. CECIL, Auteur ; Esther WALTON, Auteur ; Sara R. JAFFEE, Auteur ; Tom O'CONNOR, Auteur ; Barbara MAUGHAN, Auteur ; Caroline L. RELTON, Auteur ; Rebecca G. SMITH, Auteur ; Wendy MCARDLE, Auteur ; Tom R. GAUNT, Auteur ; Isabelle OUELLET-MORIN, Auteur ; Edward D. BARKER, Auteur Article en page(s) : p.383-397 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Early-onset conduct problems (CP) are a key predictor of adult criminality and poor mental health. While previous studies suggest that both genetic and environmental risks play an important role in the development of early-onset CP, little is known about potential biological processes underlying these associations. In this study, we examined prospective associations between DNA methylation (cord blood at birth) and trajectories of CP (4–13 years), using data drawn from the Avon Longitudinal Study of Parents and Children. Methylomic variation at seven loci across the genome (false discovery rate < 0.05) differentiated children who go on to develop early-onset (n = 174) versus low (n = 86) CP, including sites in the vicinity of the monoglyceride lipase (MGLL) gene (involved in endocannabinoid signaling and pain perception). Subthreshold associations in the vicinity of three candidate genes for CP (monoamine oxidase A [MAOA], brain-derived neurotrophic factor [BDNF], and FK506 binding protein 5 [FKBP5]) were also identified. Within the early-onset CP group, methylation levels of the identified sites did not distinguish children who will go on to persist versus desist in CP behavior over time. Overall, we found that several of the identified sites correlated with prenatal exposures, and none were linked to known genetic methylation quantitative trait loci. Findings contribute to a better understanding of epigenetic patterns associated with early-onset CP. En ligne : http://dx.doi.org/10.1017/S095457941700092X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358 [article] Neonatal DNA methylation and early-onset conduct problems: A genome-wide, prospective study [texte imprimé] / Charlotte A.M. CECIL, Auteur ; Esther WALTON, Auteur ; Sara R. JAFFEE, Auteur ; Tom O'CONNOR, Auteur ; Barbara MAUGHAN, Auteur ; Caroline L. RELTON, Auteur ; Rebecca G. SMITH, Auteur ; Wendy MCARDLE, Auteur ; Tom R. GAUNT, Auteur ; Isabelle OUELLET-MORIN, Auteur ; Edward D. BARKER, Auteur . - p.383-397. Langues : Anglais (eng) in Development and Psychopathology > 30-2 (May 2018) . - p.383-397 Index. décimale : PER Périodiques Résumé : Early-onset conduct problems (CP) are a key predictor of adult criminality and poor mental health. While previous studies suggest that both genetic and environmental risks play an important role in the development of early-onset CP, little is known about potential biological processes underlying these associations. In this study, we examined prospective associations between DNA methylation (cord blood at birth) and trajectories of CP (4–13 years), using data drawn from the Avon Longitudinal Study of Parents and Children. Methylomic variation at seven loci across the genome (false discovery rate < 0.05) differentiated children who go on to develop early-onset (n = 174) versus low (n = 86) CP, including sites in the vicinity of the monoglyceride lipase (MGLL) gene (involved in endocannabinoid signaling and pain perception). Subthreshold associations in the vicinity of three candidate genes for CP (monoamine oxidase A [MAOA], brain-derived neurotrophic factor [BDNF], and FK506 binding protein 5 [FKBP5]) were also identified. Within the early-onset CP group, methylation levels of the identified sites did not distinguish children who will go on to persist versus desist in CP behavior over time. Overall, we found that several of the identified sites correlated with prenatal exposures, and none were linked to known genetic methylation quantitative trait loci. Findings contribute to a better understanding of epigenetic patterns associated with early-onset CP. En ligne : http://dx.doi.org/10.1017/S095457941700092X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=358

Pathways between early-life adversity and adolescent self-harm: the mediating role of inflammation in the Avon Longitudinal Study of Parents and Children / Abigail E. RUSSELL in Journal of Child Psychology and Psychiatry, 60-10 (October 2019)  

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Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems / Jolien RIJLAARSDAM in Journal of Child Psychology and Psychiatry, 58-1 (January 2017)  

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Variation in DNA methylation of the oxytocin receptor gene predicts children's resilience to prenatal stress / Izabela MILANIAK in Development and Psychopathology, 29-5 (December 2017)  

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