3 recherche sur le mot-clé 'biological pathways'

Developmental epigenomic effects of maternal financial problems / Cyrielle HOLUKA in Development and Psychopathology, 37-2 (May 2025)  

Public ISBD [article]  inDevelopment and Psychopathology > 37-2 (May 2025) . - p.1004-1017 Titre : Developmental epigenomic effects of maternal financial problems Type de document : texte imprimé Auteurs : Cyrielle HOLUKA, Auteur ; Giorgia MENTA, Auteur ; Juan Carlos CARO, Auteur ; Claus VÖGELE, Auteur ; Conchita D'AMBROSIO, Auteur ; Jonathan D. TURNER, Auteur Article en page(s) : p.1004-1017 Langues : Anglais (eng) Mots-clés : ALSPAC  Aging  DNA methylation  Pace of Ageing  biological pathways  epigenome-wide association studies  financial issues Index. décimale : PER Périodiques Résumé : Early-life adversity as neglect or low socioeconomic status is associated with negative physical/mental health outcomes and plays an important role in health trajectories through life. The early-life environment has been shown to be encoded as changes in epigenetic markers that are retained for many years.We investigated the effect of maternal major financial problems (MFP) and material deprivation (MD) on their children s epigenome in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Epigenetic aging, measured with epigenetic clocks, was weakly accelerated with increased MFP. In subsequent EWAS, MFP, and MD showed strong, independent programing effects on children s genomes. MFP in the period from birth to age seven was associated with genome-wide epigenetic modifications on children s genome visible at age 7 and partially remaining at age 15.These results support the hypothesis that physiological processes at least partially explain associations between early-life adversity and health problems later in life. Both maternal stressors (MFP/MD) had similar effects on biological pathways, providing preliminary evidence for the mechanisms underlying the effects of low socioeconomic status in early life and disease outcomes later in life. Understanding these associations is essential to explain disease susceptibility, overall life trajectories and the transition from health to disease. En ligne : https://dx.doi.org/10.1017/S095457942400083X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=552 [article] Developmental epigenomic effects of maternal financial problems [texte imprimé] / Cyrielle HOLUKA, Auteur ; Giorgia MENTA, Auteur ; Juan Carlos CARO, Auteur ; Claus VÖGELE, Auteur ; Conchita D'AMBROSIO, Auteur ; Jonathan D. TURNER, Auteur . - p.1004-1017. Langues : Anglais (eng) in Development and Psychopathology > 37-2 (May 2025) . - p.1004-1017 Mots-clés : ALSPAC  Aging  DNA methylation  Pace of Ageing  biological pathways  epigenome-wide association studies  financial issues Index. décimale : PER Périodiques Résumé : Early-life adversity as neglect or low socioeconomic status is associated with negative physical/mental health outcomes and plays an important role in health trajectories through life. The early-life environment has been shown to be encoded as changes in epigenetic markers that are retained for many years.We investigated the effect of maternal major financial problems (MFP) and material deprivation (MD) on their children s epigenome in the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Epigenetic aging, measured with epigenetic clocks, was weakly accelerated with increased MFP. In subsequent EWAS, MFP, and MD showed strong, independent programing effects on children s genomes. MFP in the period from birth to age seven was associated with genome-wide epigenetic modifications on children s genome visible at age 7 and partially remaining at age 15.These results support the hypothesis that physiological processes at least partially explain associations between early-life adversity and health problems later in life. Both maternal stressors (MFP/MD) had similar effects on biological pathways, providing preliminary evidence for the mechanisms underlying the effects of low socioeconomic status in early life and disease outcomes later in life. Understanding these associations is essential to explain disease susceptibility, overall life trajectories and the transition from health to disease. En ligne : https://dx.doi.org/10.1017/S095457942400083X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=552

Genome-wide association study and identification of chromosomal enhancer maps in multiple brain regions related to autism spectrum disorder / Liang ZHANG in Autism Research, 12-1 (January 2019)  

Public ISBD [article]  inAutism Research > 12-1 (January 2019) . - p.26-32 Titre : Genome-wide association study and identification of chromosomal enhancer maps in multiple brain regions related to autism spectrum disorder Type de document : texte imprimé Auteurs : Liang ZHANG, Auteur ; Li LIU, Auteur ; Yan WEN, Auteur ; Mei MA, Auteur ; Shiqiang CHENG, Auteur ; Junhua YANG, Auteur ; Pengli LI, Auteur ; Bastian CHENG, Auteur ; Yanan DU, Auteur ; Xingmei LIANG, Auteur ; Yan ZHAO, Auteur ; Miao DING, Auteur ; Xiaonan GUO, Auteur ; Feng ZHANG, Auteur Année de publication : 2019 Article en page(s) : p.26-32 Langues : Anglais (eng) Mots-clés : autism  biological pathways  brain regions  enhancer Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a complex developmental disorder with strong genetic components involved. Recent studies have demonstrated the importance of non-coding regulatory variants for complex diseases. To explore the roles of chromosomal enhancer regions in the pathogenesis of ASD, we conducted an integrative analysis of genome-wide association study (GWAS) and brain region related enhancer-gene networks for ASD. The GWAS data of ASD were driven from a published study, involving 7,387 ASD cases and 8,567 controls. The enhancer-gene networks of eight brain regions were used here. The GWAS of ASD was first merged respectively with the enhancer datasets of eight brain regions. Pathway enrichment analysis was then performed to detect ASD associated pathways based on the enhancer-related single nucleotide polymorphism (SNPs) of each brain region. We detected multiple genes with brain region specific or common association signals, such as PGM3 (P value = 1.93 x 10(-5) ) and RWDD2A (P value = 1.93 x 10(-5) ) for hippocampus middle, and ENPP4 (all P values <0.05), and ENPP5 (all P values <0.05) for seven brain regions. By comparing the pathway enrichment analysis results of various brain regions, several cross brain regions pathways were detected for ASD, such as REACTOME_POTASSIUM_CHANNELS (all P values <0.05) for six brain regions and KEGG_CELL_ADHESION_MOLECULES_CAMS (all P values <0.05) for seven brain regions. In addition, several pathways were also identified for specific brain regions, such as REACTOME_CD28_DEPENDENT_PI3K_AKT_SIGNALING (P value = 4.00 x 10(-3) ) for angular gyrus, REACTOME_SIGNALING_BY_CONSTITUTIVELY_ACTIVE_EGFR (P value = 2.22 x 10(-3) ) for anterior caudate, and KEGG_PRION_DISEASES (P value = 1.00 x 10(-4) ) for germinal matrix. Our results provide novel clues for understanding the genetic basis of ASD. Autism Research 2019, 12: 26-32. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: ASD is a complex developmental disorder with strong genetic components, but the pathogenesis of ASD is still unclear. Using the latest GWAS data and enhancer map, we explored the brain region related biological pathways associated with ASD. Our results provide novel clues for revealing the functional relevance of enhancer variants with ASD and understanding the genetic basis of ASD. En ligne : http://dx.doi.org/10.1002/aur.2001 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=376 [article] Genome-wide association study and identification of chromosomal enhancer maps in multiple brain regions related to autism spectrum disorder [texte imprimé] / Liang ZHANG, Auteur ; Li LIU, Auteur ; Yan WEN, Auteur ; Mei MA, Auteur ; Shiqiang CHENG, Auteur ; Junhua YANG, Auteur ; Pengli LI, Auteur ; Bastian CHENG, Auteur ; Yanan DU, Auteur ; Xingmei LIANG, Auteur ; Yan ZHAO, Auteur ; Miao DING, Auteur ; Xiaonan GUO, Auteur ; Feng ZHANG, Auteur . - 2019 . - p.26-32. Langues : Anglais (eng) in Autism Research > 12-1 (January 2019) . - p.26-32 Mots-clés : autism  biological pathways  brain regions  enhancer Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a complex developmental disorder with strong genetic components involved. Recent studies have demonstrated the importance of non-coding regulatory variants for complex diseases. To explore the roles of chromosomal enhancer regions in the pathogenesis of ASD, we conducted an integrative analysis of genome-wide association study (GWAS) and brain region related enhancer-gene networks for ASD. The GWAS data of ASD were driven from a published study, involving 7,387 ASD cases and 8,567 controls. The enhancer-gene networks of eight brain regions were used here. The GWAS of ASD was first merged respectively with the enhancer datasets of eight brain regions. Pathway enrichment analysis was then performed to detect ASD associated pathways based on the enhancer-related single nucleotide polymorphism (SNPs) of each brain region. We detected multiple genes with brain region specific or common association signals, such as PGM3 (P value = 1.93 x 10(-5) ) and RWDD2A (P value = 1.93 x 10(-5) ) for hippocampus middle, and ENPP4 (all P values <0.05), and ENPP5 (all P values <0.05) for seven brain regions. By comparing the pathway enrichment analysis results of various brain regions, several cross brain regions pathways were detected for ASD, such as REACTOME_POTASSIUM_CHANNELS (all P values <0.05) for six brain regions and KEGG_CELL_ADHESION_MOLECULES_CAMS (all P values <0.05) for seven brain regions. In addition, several pathways were also identified for specific brain regions, such as REACTOME_CD28_DEPENDENT_PI3K_AKT_SIGNALING (P value = 4.00 x 10(-3) ) for angular gyrus, REACTOME_SIGNALING_BY_CONSTITUTIVELY_ACTIVE_EGFR (P value = 2.22 x 10(-3) ) for anterior caudate, and KEGG_PRION_DISEASES (P value = 1.00 x 10(-4) ) for germinal matrix. Our results provide novel clues for understanding the genetic basis of ASD. Autism Research 2019, 12: 26-32. (c) 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: ASD is a complex developmental disorder with strong genetic components, but the pathogenesis of ASD is still unclear. Using the latest GWAS data and enhancer map, we explored the brain region related biological pathways associated with ASD. Our results provide novel clues for revealing the functional relevance of enhancer variants with ASD and understanding the genetic basis of ASD. En ligne : http://dx.doi.org/10.1002/aur.2001 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=376

Commentary: G × E in child psychiatry and psychology: a broadening of the scope of enquiry as prompted by Munafò et al. (2014) / Michael RUTTER in Journal of Child Psychology and Psychiatry, 55-10 (October 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-10 (October 2014) . - p.1102-1104 Titre : Commentary: G × E in child psychiatry and psychology: a broadening of the scope of enquiry as prompted by Munafò et al. (2014) Type de document : texte imprimé Auteurs : Michael RUTTER, Auteur Article en page(s) : p.1102-1104 Langues : Anglais (eng) Mots-clés : Gene–environment interactions  G × E correlations  biological pathways  child mental health disorders Index. décimale : PER Périodiques Résumé : The accompanying Practitioner Review by Munafò et al. (2014) presents two main arguments: (1) that there are few (if any) examples of G × E in psychiatry so it cannot aid gene discovery, and (2) that genome-wide association studies (GWAS) are already yielding important findings. With respect to the supposed weakness of G × E research, they fail to mention any of the substantial body of evidence in support of G × E – see various chapters in Dodge and Rutter (2011). En ligne : http://dx.doi.org/10.1111/jcpp.12309 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=238 [article] Commentary: G × E in child psychiatry and psychology: a broadening of the scope of enquiry as prompted by Munafò et al. (2014) [texte imprimé] / Michael RUTTER, Auteur . - p.1102-1104. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 55-10 (October 2014) . - p.1102-1104 Mots-clés : Gene–environment interactions  G × E correlations  biological pathways  child mental health disorders Index. décimale : PER Périodiques Résumé : The accompanying Practitioner Review by Munafò et al. (2014) presents two main arguments: (1) that there are few (if any) examples of G × E in psychiatry so it cannot aid gene discovery, and (2) that genome-wide association studies (GWAS) are already yielding important findings. With respect to the supposed weakness of G × E research, they fail to mention any of the substantial body of evidence in support of G × E – see various chapters in Dodge and Rutter (2011). En ligne : http://dx.doi.org/10.1111/jcpp.12309 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=238