Genome-wide DNA methylation analysis of aggressive behaviour: a longitudinal population-based study / Ehsan PISHVA in Journal of Child Psychology and Psychiatry, 64-7 (July 2023)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 64-7 (July 2023) . - p.998-1006 Titre : Genome-wide DNA methylation analysis of aggressive behaviour: a longitudinal population-based study Type de document : Texte imprimé et/ou numérique Auteurs : Ehsan PISHVA, Auteur ; Daniel L. A. VAN DEN HOVE, Auteur ; Valentin LAROCHE, Auteur ; Aneth LVOVS, Auteur ; Arunima ROY, Auteur ; Gabriela ORTEGA, Auteur ; Joe BURRAGE, Auteur ; Toomas VEIDEBAUM, Auteur ; Margus KANARIK, Auteur ; Jonathan MILL, Auteur ; Klaus-Peter LESCH, Auteur ; Jaanus HARRO, Auteur Article en page(s) : p.998-1006 Langues : Anglais (eng) Mots-clés : Aggression  DNA methylation  epigenetics  genetics Index. décimale : PER Périodiques Résumé : Background Human aggression is influenced by an interplay between genetic predisposition and experience across the life span. This interaction is thought to occur through epigenetic mechanisms, inducing differential gene expression, thereby moderating neuronal cell and circuit function, and thus shaping aggressive behaviour. Methods Genome-wide DNA methylation (DNAm) levels were measured in peripheral blood obtained from 95 individuals participating in the Estonian Children Personality Behaviours and Health Study (ECPBHS) at 15 and 25years of age. We examined the association between aggressive behaviour, as measured by Life History of Aggression (LHA) total score and DNAm levels both assessed at age 25. We further examined the pleiotropic effect of genetic variants regulating LHA-associated differentially methylated positions (DMPs) and multiple traits related to aggressive behaviours. Lastly, we tested whether the DNA methylomic loci identified in association with LHA at age 25 were also present at age 15. Results We found one differentially methylated position (DMP) (cg17815886; p =1.12108) and five differentially methylated regions (DMRs) associated with LHA after multiple testing adjustments. The DMP annotated to the PDLIM5 gene, and DMRs resided in the vicinity of four protein-encoding genes (TRIM10, GTF2H4, SLC45A4, B3GALT4) and a long intergenic non-coding RNA (LINC02068). We observed evidence for the colocalization of genetic variants associated with top DMPs and general cognitive function, educational attainment and cholesterol levels. Notably, a subset of the DMPs associated with LHA at age 25 also displayed altered DNAm patterns at age 15 with high accuracy in predicting aggression. Conclusions Our findings highlight the potential role of DNAm in the development of aggressive behaviours. We observed pleiotropic genetic variants associated with identified DMPs, and various traits previously established to be relevant in shaping aggression in humans. The concordance of DNAm signatures in adolescents and young adults may have predictive value for inappropriate and maladaptive aggression later in life. En ligne : https://doi.org/10.1111/jcpp.13782 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=508 [article] Genome-wide DNA methylation analysis of aggressive behaviour: a longitudinal population-based study [Texte imprimé et/ou numérique] / Ehsan PISHVA, Auteur ; Daniel L. A. VAN DEN HOVE, Auteur ; Valentin LAROCHE, Auteur ; Aneth LVOVS, Auteur ; Arunima ROY, Auteur ; Gabriela ORTEGA, Auteur ; Joe BURRAGE, Auteur ; Toomas VEIDEBAUM, Auteur ; Margus KANARIK, Auteur ; Jonathan MILL, Auteur ; Klaus-Peter LESCH, Auteur ; Jaanus HARRO, Auteur . - p.998-1006. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 64-7 (July 2023) . - p.998-1006 Mots-clés : Aggression  DNA methylation  epigenetics  genetics Index. décimale : PER Périodiques Résumé : Background Human aggression is influenced by an interplay between genetic predisposition and experience across the life span. This interaction is thought to occur through epigenetic mechanisms, inducing differential gene expression, thereby moderating neuronal cell and circuit function, and thus shaping aggressive behaviour. Methods Genome-wide DNA methylation (DNAm) levels were measured in peripheral blood obtained from 95 individuals participating in the Estonian Children Personality Behaviours and Health Study (ECPBHS) at 15 and 25years of age. We examined the association between aggressive behaviour, as measured by Life History of Aggression (LHA) total score and DNAm levels both assessed at age 25. We further examined the pleiotropic effect of genetic variants regulating LHA-associated differentially methylated positions (DMPs) and multiple traits related to aggressive behaviours. Lastly, we tested whether the DNA methylomic loci identified in association with LHA at age 25 were also present at age 15. Results We found one differentially methylated position (DMP) (cg17815886; p =1.12108) and five differentially methylated regions (DMRs) associated with LHA after multiple testing adjustments. The DMP annotated to the PDLIM5 gene, and DMRs resided in the vicinity of four protein-encoding genes (TRIM10, GTF2H4, SLC45A4, B3GALT4) and a long intergenic non-coding RNA (LINC02068). We observed evidence for the colocalization of genetic variants associated with top DMPs and general cognitive function, educational attainment and cholesterol levels. Notably, a subset of the DMPs associated with LHA at age 25 also displayed altered DNAm patterns at age 15 with high accuracy in predicting aggression. Conclusions Our findings highlight the potential role of DNAm in the development of aggressive behaviours. We observed pleiotropic genetic variants associated with identified DMPs, and various traits previously established to be relevant in shaping aggression in humans. The concordance of DNAm signatures in adolescents and young adults may have predictive value for inappropriate and maladaptive aggression later in life. En ligne : https://doi.org/10.1111/jcpp.13782 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=508

Measuring adolescents' exposure to victimization: The Environmental Risk (E-Risk) Longitudinal Twin Study / Helen L. FISHER in Development and Psychopathology, 27-4 (Part 2) (November 2015)  

Public ISBD [article]  inDevelopment and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1399-1416 Titre : Measuring adolescents' exposure to victimization: The Environmental Risk (E-Risk) Longitudinal Twin Study Type de document : Texte imprimé et/ou numérique Auteurs : Helen L. FISHER, Auteur ; Avshalom CASPI, Auteur ; Terrie E. MOFFITT, Auteur ; Jasmin WERTZ, Auteur ; Rebecca GRAY, Auteur ; Joanne NEWBURY, Auteur ; Antony AMBLER, Auteur ; Helena ZAVOS, Auteur ; Andrea DANESE, Auteur ; Jonathan MILL, Auteur ; Candice L. ODGERS, Auteur ; Carmine PARIANTE, Auteur ; Chloe C. Y. WONG, Auteur ; Louise ARSENEAULT, Auteur Article en page(s) : p.1399-1416 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : This paper presents multilevel findings on adolescents' victimization exposure from a large longitudinal cohort of twins. Data were obtained from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) followed to 18 years of age (with 93% retention). To assess adolescent victimization, we combined best practices in survey research on victimization with optimal approaches to measuring life stress and traumatic experiences, and introduce a reliable system for coding severity of victimization. One in three children experienced at least one type of severe victimization during adolescence (crime victimization, peer/sibling victimization, Internet/mobile phone victimization, sexual victimization, family violence, maltreatment, or neglect), and most types of victimization were more prevalent among children from low socioeconomic backgrounds. Exposure to multiple victimization types was common, as was revictimization; over half of those physically maltreated in childhood were also exposed to severe physical violence in adolescence. Biometric twin analyses revealed that environmental factors had the greatest influence on most types of victimization, while severe physical maltreatment from caregivers during adolescence was predominantly influenced by heritable factors. The findings from this study showcase how distinct levels of victimization measurement can be harmonized in large-scale studies of health and development. En ligne : http://dx.doi.org/10.1017/S0954579415000838 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273 [article] Measuring adolescents' exposure to victimization: The Environmental Risk (E-Risk) Longitudinal Twin Study [Texte imprimé et/ou numérique] / Helen L. FISHER, Auteur ; Avshalom CASPI, Auteur ; Terrie E. MOFFITT, Auteur ; Jasmin WERTZ, Auteur ; Rebecca GRAY, Auteur ; Joanne NEWBURY, Auteur ; Antony AMBLER, Auteur ; Helena ZAVOS, Auteur ; Andrea DANESE, Auteur ; Jonathan MILL, Auteur ; Candice L. ODGERS, Auteur ; Carmine PARIANTE, Auteur ; Chloe C. Y. WONG, Auteur ; Louise ARSENEAULT, Auteur . - p.1399-1416. Langues : Anglais (eng) in Development and Psychopathology > 27-4 (Part 2) (November 2015) . - p.1399-1416 Index. décimale : PER Périodiques Résumé : This paper presents multilevel findings on adolescents' victimization exposure from a large longitudinal cohort of twins. Data were obtained from the Environmental Risk (E-Risk) Longitudinal Twin Study, an epidemiological study of 2,232 children (1,116 twin pairs) followed to 18 years of age (with 93% retention). To assess adolescent victimization, we combined best practices in survey research on victimization with optimal approaches to measuring life stress and traumatic experiences, and introduce a reliable system for coding severity of victimization. One in three children experienced at least one type of severe victimization during adolescence (crime victimization, peer/sibling victimization, Internet/mobile phone victimization, sexual victimization, family violence, maltreatment, or neglect), and most types of victimization were more prevalent among children from low socioeconomic backgrounds. Exposure to multiple victimization types was common, as was revictimization; over half of those physically maltreated in childhood were also exposed to severe physical violence in adolescence. Biometric twin analyses revealed that environmental factors had the greatest influence on most types of victimization, while severe physical maltreatment from caregivers during adolescence was predominantly influenced by heritable factors. The findings from this study showcase how distinct levels of victimization measurement can be harmonized in large-scale studies of health and development. En ligne : http://dx.doi.org/10.1017/S0954579415000838 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=273

Methylomic analysis of salivary DNA in childhood ADHD identifies altered DNA methylation in VIPR2 / Beth WILMOT in Journal of Child Psychology and Psychiatry, 57-2 (February 2016)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 57-2 (February 2016) . - p.152-160 Titre : Methylomic analysis of salivary DNA in childhood ADHD identifies altered DNA methylation in VIPR2 Type de document : Texte imprimé et/ou numérique Auteurs : Beth WILMOT, Auteur ; Rebecca FRY, Auteur ; Lisa SMEESTER, Auteur ; Erica D. MUSSER, Auteur ; Jonathan MILL, Auteur ; Joel T. NIGG, Auteur Article en page(s) : p.152-160 Langues : Anglais (eng) Mots-clés : ADHD  methylation  epigenetic Index. décimale : PER Périodiques Résumé : Background Peripheral epigenetic marks hold promise for understanding psychiatric illness and may represent fingerprints of gene–environment interactions. We conducted an initial examination of CpG methylation variation in children with or without attention-deficit/hyperactivity disorder (ADHD). Methods Children age 7–12 were recruited, screened, evaluated and assigned to ADHD or non-ADHD groups by defined research criteria. Two independent age-matched samples were examined, a discovery set (n = 92, all boys, half control, half ADHD) and a confirmation set (n = 20, half ADHD, all boys). 5-methylcytosine levels were quantified in salivary DNA using the Illumina 450 K HumanMethylation array. Genes for which multiple probes were nominally significant and had a beta difference of at least 2% were evaluated for biological relevance and prioritized for confirmation and sequence validation. Gene pathways were explored and described. Results Two genes met the criteria for confirmation testing, VIPR2 and MYT1L; both had multiple probes meeting cutoffs and strong biological relevance. Probes on VIPR2 passed FDR correction in the confirmation set and were confirmed through bisulfite sequencing. Enrichment analysis suggested involvement of gene sets or pathways related to inflammatory processes and modulation of monoamine and cholinergic neurotransmission. Conclusions Although it is unknown to what extent CpG methylation seen in peripheral tissue reflect transcriptomic changes in the brain, these initial results indicate that peripheral DNA methylation markers in ADHD may be promising and suggest targeted hypotheses for future study in larger samples. En ligne : http://dx.doi.org/10.1111/jcpp.12457 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=280 [article] Methylomic analysis of salivary DNA in childhood ADHD identifies altered DNA methylation in VIPR2 [Texte imprimé et/ou numérique] / Beth WILMOT, Auteur ; Rebecca FRY, Auteur ; Lisa SMEESTER, Auteur ; Erica D. MUSSER, Auteur ; Jonathan MILL, Auteur ; Joel T. NIGG, Auteur . - p.152-160. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 57-2 (February 2016) . - p.152-160 Mots-clés : ADHD  methylation  epigenetic Index. décimale : PER Périodiques Résumé : Background Peripheral epigenetic marks hold promise for understanding psychiatric illness and may represent fingerprints of gene–environment interactions. We conducted an initial examination of CpG methylation variation in children with or without attention-deficit/hyperactivity disorder (ADHD). Methods Children age 7–12 were recruited, screened, evaluated and assigned to ADHD or non-ADHD groups by defined research criteria. Two independent age-matched samples were examined, a discovery set (n = 92, all boys, half control, half ADHD) and a confirmation set (n = 20, half ADHD, all boys). 5-methylcytosine levels were quantified in salivary DNA using the Illumina 450 K HumanMethylation array. Genes for which multiple probes were nominally significant and had a beta difference of at least 2% were evaluated for biological relevance and prioritized for confirmation and sequence validation. Gene pathways were explored and described. Results Two genes met the criteria for confirmation testing, VIPR2 and MYT1L; both had multiple probes meeting cutoffs and strong biological relevance. Probes on VIPR2 passed FDR correction in the confirmation set and were confirmed through bisulfite sequencing. Enrichment analysis suggested involvement of gene sets or pathways related to inflammatory processes and modulation of monoamine and cholinergic neurotransmission. Conclusions Although it is unknown to what extent CpG methylation seen in peripheral tissue reflect transcriptomic changes in the brain, these initial results indicate that peripheral DNA methylation markers in ADHD may be promising and suggest targeted hypotheses for future study in larger samples. En ligne : http://dx.doi.org/10.1111/jcpp.12457 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=280

Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibility / Jonathan MILL in Journal of Child Psychology and Psychiatry, 49-10 (October 2008)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 49-10 (October 2008) . - p.1020-1030 Titre : Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibility Type de document : Texte imprimé et/ou numérique Auteurs : Jonathan MILL, Auteur ; Arturas PETRONIS, Auteur Année de publication : 2008 Article en page(s) : p.1020-1030 Langues : Anglais (eng) Mots-clés : Epigenetics DNA-methylation environment prenatal attention-deficit-hyperactivity-disorder-(ADHD) genetics psychiatry DOHaD fetal-programming Index. décimale : PER Périodiques Résumé : Attention-deficit hyperactivity disorder (ADHD) is a common childhood neurobehavioural disorder defined by symptoms of developmentally inappropriate inattention, impulsivity and hyperactivity. As is the norm for most psychiatric phenotypes, traditional aetiological studies have focused primarily on the interplay between genetic and environmental factors. It is likely that epigenetic factors, i.e., heritable, but reversible changes to genomic function that are independent of DNA sequence, are also important. It is known that epigenetic processes can be induced following exposure to a range of external factors, and thus provide a mechanism by which the environment can lead to long-term alterations in phenotype. In this article we hypothesise that epigenetic dysregulation may mediate the association observed between early-development environmental insults and ADHD. We propose that understanding the epigenetic processes involved in linking specific environmental pathogens to an increased risk for ADHD may offer new possibilities for preventative and therapeutic intervention. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2008.01909.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=606 [article] Pre- and peri-natal environmental risks for attention-deficit hyperactivity disorder (ADHD): the potential role of epigenetic processes in mediating susceptibility [Texte imprimé et/ou numérique] / Jonathan MILL, Auteur ; Arturas PETRONIS, Auteur . - 2008 . - p.1020-1030. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 49-10 (October 2008) . - p.1020-1030 Mots-clés : Epigenetics DNA-methylation environment prenatal attention-deficit-hyperactivity-disorder-(ADHD) genetics psychiatry DOHaD fetal-programming Index. décimale : PER Périodiques Résumé : Attention-deficit hyperactivity disorder (ADHD) is a common childhood neurobehavioural disorder defined by symptoms of developmentally inappropriate inattention, impulsivity and hyperactivity. As is the norm for most psychiatric phenotypes, traditional aetiological studies have focused primarily on the interplay between genetic and environmental factors. It is likely that epigenetic factors, i.e., heritable, but reversible changes to genomic function that are independent of DNA sequence, are also important. It is known that epigenetic processes can be induced following exposure to a range of external factors, and thus provide a mechanism by which the environment can lead to long-term alterations in phenotype. In this article we hypothesise that epigenetic dysregulation may mediate the association observed between early-development environmental insults and ADHD. We propose that understanding the epigenetic processes involved in linking specific environmental pathogens to an increased risk for ADHD may offer new possibilities for preventative and therapeutic intervention. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2008.01909.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=606

Trajectories leading to autism spectrum disorders are affected by paternal age: findings from two nationally representative twin studies / Sebastian LUNDSTROM in Journal of Child Psychology and Psychiatry, 51-7 (July 2010)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 51-7 (July 2010) . - p.850-856 Titre : Trajectories leading to autism spectrum disorders are affected by paternal age: findings from two nationally representative twin studies Type de document : Texte imprimé et/ou numérique Auteurs : Sebastian LUNDSTROM, Auteur ; Christopher GILLBERG, Auteur ; Henrik ANCKARSATER, Auteur ; Christina M. HULTMAN, Auteur ; Eva CARLSTROM, Auteur ; Abraham REICHENBERG, Auteur ; Jonathan MILL, Auteur ; Angelica RONALD, Auteur ; Robert PLOMIN, Auteur ; Maria RASTAM, Auteur ; Paul LICHTENSTEIN, Auteur ; Claire Margaret Alison HAWORTH, Auteur Année de publication : 2010 Article en page(s) : p.850-856 Langues : Anglais (eng) Mots-clés : Autism-spectrum-disorders paternal-age autistic-traits behavioral-genetics Index. décimale : PER Périodiques Résumé : Background: Despite extensive efforts, the causes of autism remain unknown. Advancing paternal age has been associated with various neurodevelopmental disorders. We aim to investigate three unresolved questions: (a) What is the association between paternal age and autism spectrum disorders (ASD)?; (b) Does paternal age moderate the genetic and environmental etiological factors for ASD? (c) Does paternal age affect normal variation in autistic-like traits? Methods: Two nationally representative twin studies from Sweden (n = 11, 122, assessed at age 9 or 12) and the UK (n = 13, 524, assessed at age 9) were used. Categorical and continuous measures of ASD, autistic-like traits and autistic similarity were calculated and compared over paternal age categories. Results: Both cohorts showed a strong association between paternal age and the risk for ASD. A U-shaped risk association could be discerned since the offspring of both the youngest and oldest fathers showed an elevation in the risk for ASD. Autistic similarity increased with advancing paternal age in both monozygotic and dizygotic twins. Both cohorts showed significantly higher autistic-like traits in the offspring of the youngest and oldest fathers. Conclusions: Phenomena associated with paternal age are clearly involved in the trajectories leading to autistic-like traits and ASD. Mechanisms influencing the trajectories might differ between older and younger fathers. Molecular genetic studies are now needed in order to further understand the association between paternal age and ASD, as well as normal variation in social, language, and repetitive behaviors in the general population. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02223.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=102 [article] Trajectories leading to autism spectrum disorders are affected by paternal age: findings from two nationally representative twin studies [Texte imprimé et/ou numérique] / Sebastian LUNDSTROM, Auteur ; Christopher GILLBERG, Auteur ; Henrik ANCKARSATER, Auteur ; Christina M. HULTMAN, Auteur ; Eva CARLSTROM, Auteur ; Abraham REICHENBERG, Auteur ; Jonathan MILL, Auteur ; Angelica RONALD, Auteur ; Robert PLOMIN, Auteur ; Maria RASTAM, Auteur ; Paul LICHTENSTEIN, Auteur ; Claire Margaret Alison HAWORTH, Auteur . - 2010 . - p.850-856. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 51-7 (July 2010) . - p.850-856 Mots-clés : Autism-spectrum-disorders paternal-age autistic-traits behavioral-genetics Index. décimale : PER Périodiques Résumé : Background: Despite extensive efforts, the causes of autism remain unknown. Advancing paternal age has been associated with various neurodevelopmental disorders. We aim to investigate three unresolved questions: (a) What is the association between paternal age and autism spectrum disorders (ASD)?; (b) Does paternal age moderate the genetic and environmental etiological factors for ASD? (c) Does paternal age affect normal variation in autistic-like traits? Methods: Two nationally representative twin studies from Sweden (n = 11, 122, assessed at age 9 or 12) and the UK (n = 13, 524, assessed at age 9) were used. Categorical and continuous measures of ASD, autistic-like traits and autistic similarity were calculated and compared over paternal age categories. Results: Both cohorts showed a strong association between paternal age and the risk for ASD. A U-shaped risk association could be discerned since the offspring of both the youngest and oldest fathers showed an elevation in the risk for ASD. Autistic similarity increased with advancing paternal age in both monozygotic and dizygotic twins. Both cohorts showed significantly higher autistic-like traits in the offspring of the youngest and oldest fathers. Conclusions: Phenomena associated with paternal age are clearly involved in the trajectories leading to autistic-like traits and ASD. Mechanisms influencing the trajectories might differ between older and younger fathers. Molecular genetic studies are now needed in order to further understand the association between paternal age and ASD, as well as normal variation in social, language, and repetitive behaviors in the general population. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02223.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=102

Transcriptomic changes in the frontal cortex associated with paternal age / Rebecca G. SMITH in Molecular Autism, (March 2014)  

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