An epigenetic pathway approach to investigating associations between prenatal exposure to maternal mood disorder and newborn neurobehavior / E. CONRADT in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.881-890 Titre : An epigenetic pathway approach to investigating associations between prenatal exposure to maternal mood disorder and newborn neurobehavior Type de document : Texte imprimé et/ou numérique Auteurs : E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; C. MONK, Auteur ; M. S. KOBOR, Auteur Article en page(s) : p.881-890 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Following recent advances in behavioral and psychiatric epigenetics, researchers are increasingly using epigenetic methods to study prenatal exposure to maternal mood disorder and its effects on fetal and newborn neurobehavior. Despite notable progress, various methodological limitations continue to obscure our understanding of the epigenetic mechanisms underpinning prenatal exposure to maternal mood disorder on newborn neurobehavioral development. Here we detail this problem, discussing limitations of the currently dominant analytical approaches (i.e., candidate epigenetic and epigenome-wide association studies), then present a solution that retains many benefits of existing methods while minimizing their shortcomings: epigenetic pathway analysis. We argue that the application of pathway-based epigenetic approaches that target DNA methylation at transcription factor binding sites could substantially deepen our mechanistic understanding of how prenatal exposures influence newborn neurobehavior. En ligne : http://dx.doi.org/10.1017/s0954579418000688 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] An epigenetic pathway approach to investigating associations between prenatal exposure to maternal mood disorder and newborn neurobehavior [Texte imprimé et/ou numérique] / E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; C. MONK, Auteur ; M. S. KOBOR, Auteur . - p.881-890. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.881-890 Index. décimale : PER Périodiques Résumé : Following recent advances in behavioral and psychiatric epigenetics, researchers are increasingly using epigenetic methods to study prenatal exposure to maternal mood disorder and its effects on fetal and newborn neurobehavior. Despite notable progress, various methodological limitations continue to obscure our understanding of the epigenetic mechanisms underpinning prenatal exposure to maternal mood disorder on newborn neurobehavioral development. Here we detail this problem, discussing limitations of the currently dominant analytical approaches (i.e., candidate epigenetic and epigenome-wide association studies), then present a solution that retains many benefits of existing methods while minimizing their shortcomings: epigenetic pathway analysis. We argue that the application of pathway-based epigenetic approaches that target DNA methylation at transcription factor binding sites could substantially deepen our mechanistic understanding of how prenatal exposures influence newborn neurobehavior. En ligne : http://dx.doi.org/10.1017/s0954579418000688 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

Incorporating epigenetic mechanisms to advance fetal programming theories / E. CONRADT in Development and Psychopathology, 30-3 (August 2018)  

Public ISBD [article]  inDevelopment and Psychopathology > 30-3 (August 2018) . - p.807-824 Titre : Incorporating epigenetic mechanisms to advance fetal programming theories Type de document : Texte imprimé et/ou numérique Auteurs : E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; K. L. RABY, Auteur ; L. M. DIAMOND, Auteur ; B. ELLIS, Auteur Article en page(s) : p.807-824 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match-mismatch model (an evolutionary-developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field. En ligne : http://dx.doi.org/10.1017/s0954579418000469 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366 [article] Incorporating epigenetic mechanisms to advance fetal programming theories [Texte imprimé et/ou numérique] / E. CONRADT, Auteur ; Daniel E. ADKINS, Auteur ; S. E. CROWELL, Auteur ; K. L. RABY, Auteur ; L. M. DIAMOND, Auteur ; B. ELLIS, Auteur . - p.807-824. Langues : Anglais (eng) in Development and Psychopathology > 30-3 (August 2018) . - p.807-824 Index. décimale : PER Périodiques Résumé : Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match-mismatch model (an evolutionary-developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field. En ligne : http://dx.doi.org/10.1017/s0954579418000469 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=366

The influence of five monoamine genes on trajectories of depressive symptoms across adolescence and young adulthood / Daniel E. ADKINS in Development and Psychopathology, 24-1 (January 2012)  

Public ISBD [article]  inDevelopment and Psychopathology > 24-1 (January 2012) . - p.267-285 Titre : The influence of five monoamine genes on trajectories of depressive symptoms across adolescence and young adulthood Type de document : Texte imprimé et/ou numérique Auteurs : Daniel E. ADKINS, Auteur ; Jonathan K. DAW, Auteur ; Joseph L. MCCLAY, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur Année de publication : 2012 Article en page(s) : p.267-285 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course. En ligne : http://dx.doi.org/10.1017/S0954579411000824 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152 [article] The influence of five monoamine genes on trajectories of depressive symptoms across adolescence and young adulthood [Texte imprimé et/ou numérique] / Daniel E. ADKINS, Auteur ; Jonathan K. DAW, Auteur ; Joseph L. MCCLAY, Auteur ; Edwin J. C. G. VAN DEN OORD, Auteur . - 2012 . - p.267-285. Langues : Anglais (eng) in Development and Psychopathology > 24-1 (January 2012) . - p.267-285 Index. décimale : PER Périodiques Résumé : The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course. En ligne : http://dx.doi.org/10.1017/S0954579411000824 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=152

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