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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)
[article]
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
in Journal of Child Psychology and Psychiatry > 57-2 (February 2016) . - p.152-160[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 The interaction between oxytocin receptor gene methylation and maternal behavior on children's early theory of mind abilities / Anna L. MACKINNON in Development and Psychopathology, 32-2 (May 2020)
[article]
Titre : The interaction between oxytocin receptor gene methylation and maternal behavior on children's early theory of mind abilities Type de document : Texte imprimé et/ou numérique Auteurs : Anna L. MACKINNON, Auteur ; Nancy FEELEY, Auteur ; Ian GOLD, Auteur ; Barbara HAYTON, Auteur ; Leonora KING, Auteur ; Corina NAGY, Auteur ; Stephanie ROBINS, Auteur ; Gustavo TURECKI, Auteur ; Phyllis ZELKOWITZ, Auteur Article en page(s) : p.511-519 Langues : Anglais (eng) Mots-clés : OXTR gene maternal behavior methylation oxytocin theory of mind Index. décimale : PER Périodiques Résumé : Theory of mind, the ability to represent the mental states of others, is an important social cognitive process, which contributes to the development of social competence. Recent research suggests that interactions between gene and environmental factors, such as oxytocin receptor gene (OXTR) polymorphisms and maternal parenting behavior, may underlie individual differences in children's theory of mind. However, the potential influence of DNA methylation of OXTR remains unclear. The current study investigated the roles of OXTR methylation, maternal behavior, and their statistical interaction on toddlers' early emerging theory of mind abilities. Participants included a community sample of 189 dyads of mothers and their 2- to 3-year-old children, whose salivary DNA was analyzed. Results indicated that more maternal structuring behavior was associated with better performance, on a battery of three theory of mind tasks, while higher OXTR methylation within exon 3 was associated with poorer performance. A significant interaction also emerged, such that OXTR methylation was related to theory of mind among children whose mothers displayed less structuring, when controlling for children's age, sex, ethnicity, number of child-aged siblings, verbal ability, and maternal education. Maternal structuring behavior may buffer the potential negative impact of hypermethylation on OXTR gene expression and function. En ligne : http://dx.doi.org/10.1017/s0954579419000257 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=426
in Development and Psychopathology > 32-2 (May 2020) . - p.511-519[article] The interaction between oxytocin receptor gene methylation and maternal behavior on children's early theory of mind abilities [Texte imprimé et/ou numérique] / Anna L. MACKINNON, Auteur ; Nancy FEELEY, Auteur ; Ian GOLD, Auteur ; Barbara HAYTON, Auteur ; Leonora KING, Auteur ; Corina NAGY, Auteur ; Stephanie ROBINS, Auteur ; Gustavo TURECKI, Auteur ; Phyllis ZELKOWITZ, Auteur . - p.511-519.
Langues : Anglais (eng)
in Development and Psychopathology > 32-2 (May 2020) . - p.511-519
Mots-clés : OXTR gene maternal behavior methylation oxytocin theory of mind Index. décimale : PER Périodiques Résumé : Theory of mind, the ability to represent the mental states of others, is an important social cognitive process, which contributes to the development of social competence. Recent research suggests that interactions between gene and environmental factors, such as oxytocin receptor gene (OXTR) polymorphisms and maternal parenting behavior, may underlie individual differences in children's theory of mind. However, the potential influence of DNA methylation of OXTR remains unclear. The current study investigated the roles of OXTR methylation, maternal behavior, and their statistical interaction on toddlers' early emerging theory of mind abilities. Participants included a community sample of 189 dyads of mothers and their 2- to 3-year-old children, whose salivary DNA was analyzed. Results indicated that more maternal structuring behavior was associated with better performance, on a battery of three theory of mind tasks, while higher OXTR methylation within exon 3 was associated with poorer performance. A significant interaction also emerged, such that OXTR methylation was related to theory of mind among children whose mothers displayed less structuring, when controlling for children's age, sex, ethnicity, number of child-aged siblings, verbal ability, and maternal education. Maternal structuring behavior may buffer the potential negative impact of hypermethylation on OXTR gene expression and function. En ligne : http://dx.doi.org/10.1017/s0954579419000257 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=426 Accelerated epigenetic aging at birth interacts with parenting hostility to predict child temperament and subsequent psychological symptoms / Erika M. MANCZAK in Development and Psychopathology, 35-1 (February 2023)
[article]
Titre : Accelerated epigenetic aging at birth interacts with parenting hostility to predict child temperament and subsequent psychological symptoms Type de document : Texte imprimé et/ou numérique Auteurs : Erika M. MANCZAK, Auteur ; Samantha R. SCOTT, Auteur ; Summer N. MILLWOOD, Auteur Article en page(s) : p.109-118 Langues : Anglais (eng) Mots-clés : epigenetics methylation parenting psychopathology symptoms temperament Index. décimale : PER Périodiques Résumé : In an effort to elucidate new factors that may contribute to developmental psychopathology, the current study examined whether accelerated epigenetic aging at birth related to children's differential susceptibility to the effects of aversive parenting on early emerging mental health risk. Using data from a multiethnic birth cohort, the interaction between Horvath's methylation age in umbilical cord blood and hostile parenting behaviors was examined in relation to perceptions of infant's temperament at 6 months and to children's psychological symptoms at 3 years in 154 families. Results broadly revealed that children with higher levels of accelerated methylation aging evinced more unpredictable temperaments and more psychological symptoms if their mothers reported more hostile parenting, but showed fewer difficulties if mothers engaged in less hostile parenting; children with lower levels of accelerated methylation age did not show associations between hostility and temperament or psychological symptoms. Effects were not accounted for by gestational age at birth, demographic factors, or the distribution of cell subtypes. These findings suggest that accelerated epigenetic age may function as a form of differential susceptibility, signaling increased risk for psychopathology in more aversive contexts but decreased risk in less aversive early environments. Taken together, they point to a novel biological process to consider within risk for psychopathology. En ligne : https://doi.org/10.1017/S0954579421000614 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=499
in Development and Psychopathology > 35-1 (February 2023) . - p.109-118[article] Accelerated epigenetic aging at birth interacts with parenting hostility to predict child temperament and subsequent psychological symptoms [Texte imprimé et/ou numérique] / Erika M. MANCZAK, Auteur ; Samantha R. SCOTT, Auteur ; Summer N. MILLWOOD, Auteur . - p.109-118.
Langues : Anglais (eng)
in Development and Psychopathology > 35-1 (February 2023) . - p.109-118
Mots-clés : epigenetics methylation parenting psychopathology symptoms temperament Index. décimale : PER Périodiques Résumé : In an effort to elucidate new factors that may contribute to developmental psychopathology, the current study examined whether accelerated epigenetic aging at birth related to children's differential susceptibility to the effects of aversive parenting on early emerging mental health risk. Using data from a multiethnic birth cohort, the interaction between Horvath's methylation age in umbilical cord blood and hostile parenting behaviors was examined in relation to perceptions of infant's temperament at 6 months and to children's psychological symptoms at 3 years in 154 families. Results broadly revealed that children with higher levels of accelerated methylation aging evinced more unpredictable temperaments and more psychological symptoms if their mothers reported more hostile parenting, but showed fewer difficulties if mothers engaged in less hostile parenting; children with lower levels of accelerated methylation age did not show associations between hostility and temperament or psychological symptoms. Effects were not accounted for by gestational age at birth, demographic factors, or the distribution of cell subtypes. These findings suggest that accelerated epigenetic age may function as a form of differential susceptibility, signaling increased risk for psychopathology in more aversive contexts but decreased risk in less aversive early environments. Taken together, they point to a novel biological process to consider within risk for psychopathology. En ligne : https://doi.org/10.1017/S0954579421000614 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=499 Biochemical Effects of Ribose and NADH Therapy in Children with Autism / Stuart H. FREEDENFELD in Autism Insights, 3 ([01/01/2011])
[article]
Titre : Biochemical Effects of Ribose and NADH Therapy in Children with Autism Type de document : Application, site Internet Auteurs : Stuart H. FREEDENFELD, Auteur ; Kim HAMADA, Auteur ; Tapan AUDHYA, Auteur ; James B. ADAMS, Auteur Année de publication : 2011 Article en page(s) : 11 p. Langues : Anglais (eng) Mots-clés : NADH ribose autism mitochondria glutathione methylation adenosine Index. décimale : PER Périodiques Résumé : Objectives: Several studies have previously indicated that children with autism often have abnormalities in methylation, glutathione redox, and mitochondrial function. A common feature of these abnormalities is that they are affected directly or indirectly by levels of ribose, reduced Nicotinamide Adenine Dinucleotide (NADH), reduced Nicotinamide Adenine Dinucleotide Phosphate (NADPH), and Adenosine-5’-triphosphate (ATP). The objective of this study was to investigate the possible biochemical effect of ribose therapy and NADH therapy on children with autism.
Design: In a pilot study, ribose was administered orally to eight children with autism for two weeks, and NADH was administered orally to another group of eight children with autism for two weeks. Children were ages 3–9 years with clinical symptoms of low energy and/or low muscle tone. Eighteen biomarkers related to methylation (including S-adenosylmethionine (SAM)), glutathione (including the reduced form, GSH, and the oxidized form GSSG), adenosine triphosphate (ATP), and folic acid and were measured at the beginning and end of the therapy.
Results: The NADH group had significant improvements in levels of ribose-5-phosphate, GSH, NADH, NADPH, and SAM. The Ribose group had significant improvements in ribose-5-phosphate, NADH, ATP, and folic acid. There was no significant change in GSSG in either group after two weeks.
Conclusions: This small study suggests that both NADH and Ribose therapy results in some improvements in biochemistry, and may be beneficial for treating children with those abnormalities. Larger studies are recommended.En ligne : http://dx.doi.org/10.4137/AUI.S6947 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131
in Autism Insights > 3 [01/01/2011] . - 11 p.[article] Biochemical Effects of Ribose and NADH Therapy in Children with Autism [Application, site Internet] / Stuart H. FREEDENFELD, Auteur ; Kim HAMADA, Auteur ; Tapan AUDHYA, Auteur ; James B. ADAMS, Auteur . - 2011 . - 11 p.
Langues : Anglais (eng)
in Autism Insights > 3 [01/01/2011] . - 11 p.
Mots-clés : NADH ribose autism mitochondria glutathione methylation adenosine Index. décimale : PER Périodiques Résumé : Objectives: Several studies have previously indicated that children with autism often have abnormalities in methylation, glutathione redox, and mitochondrial function. A common feature of these abnormalities is that they are affected directly or indirectly by levels of ribose, reduced Nicotinamide Adenine Dinucleotide (NADH), reduced Nicotinamide Adenine Dinucleotide Phosphate (NADPH), and Adenosine-5’-triphosphate (ATP). The objective of this study was to investigate the possible biochemical effect of ribose therapy and NADH therapy on children with autism.
Design: In a pilot study, ribose was administered orally to eight children with autism for two weeks, and NADH was administered orally to another group of eight children with autism for two weeks. Children were ages 3–9 years with clinical symptoms of low energy and/or low muscle tone. Eighteen biomarkers related to methylation (including S-adenosylmethionine (SAM)), glutathione (including the reduced form, GSH, and the oxidized form GSSG), adenosine triphosphate (ATP), and folic acid and were measured at the beginning and end of the therapy.
Results: The NADH group had significant improvements in levels of ribose-5-phosphate, GSH, NADH, NADPH, and SAM. The Ribose group had significant improvements in ribose-5-phosphate, NADH, ATP, and folic acid. There was no significant change in GSSG in either group after two weeks.
Conclusions: This small study suggests that both NADH and Ribose therapy results in some improvements in biochemistry, and may be beneficial for treating children with those abnormalities. Larger studies are recommended.En ligne : http://dx.doi.org/10.4137/AUI.S6947 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131 Developmental vitamin D deficiency increases foetal exposure to testosterone / Asad Amanat ALI in Molecular Autism, 11 (2020)
[article]
Titre : Developmental vitamin D deficiency increases foetal exposure to testosterone Type de document : Texte imprimé et/ou numérique Auteurs : Asad Amanat ALI, Auteur ; Xiaoying CUI, Auteur ; Renata Aparecida Nedel PERTILE, Auteur ; Xiang LI, Auteur ; Gregory MEDLEY, Auteur ; Suzanne Adele ALEXANDER, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; John Joseph MCGRATH, Auteur ; Darryl Walter EYLES, Auteur Langues : Anglais (eng) Mots-clés : Animal model Aromatase Autism Developmental vitamin D deficiency Methylation Testosterone Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders which are more common in males. The 'prenatal sex steroid' hypothesis links excessive sex-steroid exposure during foetal life with the behavioural differences observed in ASD. However, the reason why sex steroid exposure may be excessive remains unclear. Epidemiological studies have identified several environmental risk factors associated with ASD, including developmental vitamin D (DVD) deficiency. We have demonstrated in an animal model that DVD-deficiency is associated with a hyper-inflammatory response in placentas from male but not female foetuses. Vitamin D also regulates the expression of several steroidogenic enzymes in vitro. Therefore using this animal model, we have examined whether DVD-deficiency leads to increased sex-steroid levels in both the maternal and foetal compartments. METHODS: Female rats are fed a vitamin D deficient diet from 6 weeks before mating until tissue collection at embryonic day 18. We examined the levels of testosterone, androstenedione and corticosterone in maternal plasma, foetal brains and amniotic fluid. We further examined gene expressions of steroidogenic enzymes and DNA methylation of aromatase promoters in foetal brains as a potential molecular mechanism regulating testosterone expression. RESULTS: We show that DVD-deficiency increases testosterone levels in maternal blood. We also show elevated levels of testosterone and androstenedione in the amniotic fluid of female but not male DVD-deficient foetuses. Testosterone levels were also elevated in DVD-deficient male brains. Vitamin D, like other steroid-related hormones, regulates gene expression via methylation. Therefore we examined whether the significant elevation in testosterone in male brains was due to such a potential gene-silencing mechanism. We show that the promoter of aromatase was hyper-methylated compared to male controls. LIMITATIONS: A reduction in aromatase, in addition to causing excessive testosterone, could also lead to a reduction in estradiol which was not examined here. CONCLUSIONS: This study is the first to show how an epidemiologically established environmental risk factor for ASD may selectively elevate testosterone in male embryonic brains. These findings provide further mechanistic support for the prenatal sex steroid theory of ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00399-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438
in Molecular Autism > 11 (2020)[article] Developmental vitamin D deficiency increases foetal exposure to testosterone [Texte imprimé et/ou numérique] / Asad Amanat ALI, Auteur ; Xiaoying CUI, Auteur ; Renata Aparecida Nedel PERTILE, Auteur ; Xiang LI, Auteur ; Gregory MEDLEY, Auteur ; Suzanne Adele ALEXANDER, Auteur ; Andrew J. O. WHITEHOUSE, Auteur ; John Joseph MCGRATH, Auteur ; Darryl Walter EYLES, Auteur.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020)
Mots-clés : Animal model Aromatase Autism Developmental vitamin D deficiency Methylation Testosterone Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders which are more common in males. The 'prenatal sex steroid' hypothesis links excessive sex-steroid exposure during foetal life with the behavioural differences observed in ASD. However, the reason why sex steroid exposure may be excessive remains unclear. Epidemiological studies have identified several environmental risk factors associated with ASD, including developmental vitamin D (DVD) deficiency. We have demonstrated in an animal model that DVD-deficiency is associated with a hyper-inflammatory response in placentas from male but not female foetuses. Vitamin D also regulates the expression of several steroidogenic enzymes in vitro. Therefore using this animal model, we have examined whether DVD-deficiency leads to increased sex-steroid levels in both the maternal and foetal compartments. METHODS: Female rats are fed a vitamin D deficient diet from 6 weeks before mating until tissue collection at embryonic day 18. We examined the levels of testosterone, androstenedione and corticosterone in maternal plasma, foetal brains and amniotic fluid. We further examined gene expressions of steroidogenic enzymes and DNA methylation of aromatase promoters in foetal brains as a potential molecular mechanism regulating testosterone expression. RESULTS: We show that DVD-deficiency increases testosterone levels in maternal blood. We also show elevated levels of testosterone and androstenedione in the amniotic fluid of female but not male DVD-deficient foetuses. Testosterone levels were also elevated in DVD-deficient male brains. Vitamin D, like other steroid-related hormones, regulates gene expression via methylation. Therefore we examined whether the significant elevation in testosterone in male brains was due to such a potential gene-silencing mechanism. We show that the promoter of aromatase was hyper-methylated compared to male controls. LIMITATIONS: A reduction in aromatase, in addition to causing excessive testosterone, could also lead to a reduction in estradiol which was not examined here. CONCLUSIONS: This study is the first to show how an epidemiologically established environmental risk factor for ASD may selectively elevate testosterone in male embryonic brains. These findings provide further mechanistic support for the prenatal sex steroid theory of ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00399-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 Neurobehavioral Testing of Mouse Models of Rett Syndrome / Jean-Christophe ROUX
PermalinkPopulation- and Family-Based Studies Associate the MTHFR Gene with Idiopathic Autism in Simplex Families / Xudong LIU in Journal of Autism and Developmental Disorders, 41-7 (July 2011)
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