Glucocorticoid receptor variants in childhood attention-deficit/hyperactivity disorder and comorbid psychiatric disorders.
Identifieur interne : 000031 ( PubMed/Corpus ); précédent : 000030; suivant : 000032Glucocorticoid receptor variants in childhood attention-deficit/hyperactivity disorder and comorbid psychiatric disorders.
Auteurs : Andrea B. Schote ; Martina Bonenberger ; Haukur Pálmason ; Christiane Seitz ; Jobst Meyer ; Christine M. FreitagSource :
- Psychiatry research [ 1872-7123 ] ; 2016.
Abstract
Stress results in a variety of neuroendocrine, immune and behavioral responses and represents a risk factor for many disorders. Following exposure to stress, glucocorticoids are secreted from the adrenal cortex and act via the ligand-activated glucocorticoid receptor (GR). Several polymorphisms of the GR-encoding gene NR3C1 have been described and functionally investigated. However, the impact of these variants on complex diseases such as Attention-Deficit/Hyperactivity Disorder (ADHD) is still unclear. In this study, 251 children with ADHD, 19 affected and 35 unaffected siblings, and their parents were included in a family-based association study assessing seven common variants of NR3C1 (TthIIII_rs10052957; NR3C1-I_rs10482605; ER22/23EK_rs6189/rs6190; N363S_rs56149945; BclI_rs41423247; GR-9beta_rs6198). A four-marker haplotype (TthIIII-NR3C1-I-ER22/23EK) was nominally associated with ADHD. In addition, in index children with ADHD, associations with comorbid disorders, inattentive and hyperactive-impulsive symptoms were explored. N363S minor allele carriers were more likely to show comorbid conduct disorder (CD). In our study, NR3C1 variants moderately affected ADHD and had a significant effect on comorbid CD. Therefore, NR3C1 as an important gene of the hypothalamic-pituitary-adrenal axis seems to be particularly relevant for the pathophysiology of ADHD combined with comorbid CD. For a deeper understanding, investigations in larger samples of healthy, ADHD and CD individuals are warranted.
DOI: 10.1016/j.psychres.2016.10.001
PubMed: 27741480
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Electronic address: schotefrese@uni-trier.de.</nlm:affiliation></affiliation></author><author><name sortKey="Bonenberger, Martina" sort="Bonenberger, Martina" uniqKey="Bonenberger M" first="Martina" last="Bonenberger">Martina Bonenberger</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Palmason, Haukur" sort="Palmason, Haukur" uniqKey="Palmason H" first="Haukur" last="Pálmason">Haukur Pálmason</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Seitz, Christiane" sort="Seitz, Christiane" uniqKey="Seitz C" first="Christiane" last="Seitz">Christiane Seitz</name><affiliation><nlm:affiliation>Department of Child and Adolescent Psychiatry and Psychotherapy, Saarland University Hospital, Homburg, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Meyer, Jobst" sort="Meyer, Jobst" uniqKey="Meyer J" first="Jobst" last="Meyer">Jobst Meyer</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Freitag, Christine M" sort="Freitag, Christine M" uniqKey="Freitag C" first="Christine M" last="Freitag">Christine M. 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Schote</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany. Electronic address: schotefrese@uni-trier.de.</nlm:affiliation></affiliation></author><author><name sortKey="Bonenberger, Martina" sort="Bonenberger, Martina" uniqKey="Bonenberger M" first="Martina" last="Bonenberger">Martina Bonenberger</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Palmason, Haukur" sort="Palmason, Haukur" uniqKey="Palmason H" first="Haukur" last="Pálmason">Haukur Pálmason</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Seitz, Christiane" sort="Seitz, Christiane" uniqKey="Seitz C" first="Christiane" last="Seitz">Christiane Seitz</name><affiliation><nlm:affiliation>Department of Child and Adolescent Psychiatry and Psychotherapy, Saarland University Hospital, Homburg, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Meyer, Jobst" sort="Meyer, Jobst" uniqKey="Meyer J" first="Jobst" last="Meyer">Jobst Meyer</name><affiliation><nlm:affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Freitag, Christine M" sort="Freitag, Christine M" uniqKey="Freitag C" first="Christine M" last="Freitag">Christine M. Freitag</name><affiliation><nlm:affiliation>Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, JW Goethe University, Frankfurt am Main, Germany.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Psychiatry research</title><idno type="eISSN">1872-7123</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Stress results in a variety of neuroendocrine, immune and behavioral responses and represents a risk factor for many disorders. Following exposure to stress, glucocorticoids are secreted from the adrenal cortex and act via the ligand-activated glucocorticoid receptor (GR). Several polymorphisms of the GR-encoding gene NR3C1 have been described and functionally investigated. However, the impact of these variants on complex diseases such as Attention-Deficit/Hyperactivity Disorder (ADHD) is still unclear. In this study, 251 children with ADHD, 19 affected and 35 unaffected siblings, and their parents were included in a family-based association study assessing seven common variants of NR3C1 (TthIIII_rs10052957; NR3C1-I_rs10482605; ER22/23EK_rs6189/rs6190; N363S_rs56149945; BclI_rs41423247; GR-9beta_rs6198). A four-marker haplotype (TthIIII-NR3C1-I-ER22/23EK) was nominally associated with ADHD. In addition, in index children with ADHD, associations with comorbid disorders, inattentive and hyperactive-impulsive symptoms were explored. N363S minor allele carriers were more likely to show comorbid conduct disorder (CD). In our study, NR3C1 variants moderately affected ADHD and had a significant effect on comorbid CD. Therefore, NR3C1 as an important gene of the hypothalamic-pituitary-adrenal axis seems to be particularly relevant for the pathophysiology of ADHD combined with comorbid CD. For a deeper understanding, investigations in larger samples of healthy, ADHD and CD individuals are warranted.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">27741480</PMID><DateCreated><Year>2016</Year><Month>10</Month><Day>14</Day></DateCreated><DateRevised><Year>2016</Year><Month>12</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7123</ISSN><JournalIssue CitedMedium="Internet"><Volume>246</Volume><PubDate><Year>2016</Year><Month>Dec</Month><Day>30</Day></PubDate></JournalIssue><Title>Psychiatry research</Title><ISOAbbreviation>Psychiatry Res</ISOAbbreviation></Journal><ArticleTitle>Glucocorticoid receptor variants in childhood attention-deficit/hyperactivity disorder and comorbid psychiatric disorders.</ArticleTitle><Pagination><MedlinePgn>275-283</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0165-1781(15)30748-4</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.psychres.2016.10.001</ELocationID><Abstract><AbstractText NlmCategory="UNASSIGNED">Stress results in a variety of neuroendocrine, immune and behavioral responses and represents a risk factor for many disorders. Following exposure to stress, glucocorticoids are secreted from the adrenal cortex and act via the ligand-activated glucocorticoid receptor (GR). Several polymorphisms of the GR-encoding gene NR3C1 have been described and functionally investigated. However, the impact of these variants on complex diseases such as Attention-Deficit/Hyperactivity Disorder (ADHD) is still unclear. In this study, 251 children with ADHD, 19 affected and 35 unaffected siblings, and their parents were included in a family-based association study assessing seven common variants of NR3C1 (TthIIII_rs10052957; NR3C1-I_rs10482605; ER22/23EK_rs6189/rs6190; N363S_rs56149945; BclI_rs41423247; GR-9beta_rs6198). A four-marker haplotype (TthIIII-NR3C1-I-ER22/23EK) was nominally associated with ADHD. In addition, in index children with ADHD, associations with comorbid disorders, inattentive and hyperactive-impulsive symptoms were explored. N363S minor allele carriers were more likely to show comorbid conduct disorder (CD). In our study, NR3C1 variants moderately affected ADHD and had a significant effect on comorbid CD. Therefore, NR3C1 as an important gene of the hypothalamic-pituitary-adrenal axis seems to be particularly relevant for the pathophysiology of ADHD combined with comorbid CD. For a deeper understanding, investigations in larger samples of healthy, ADHD and CD individuals are warranted.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schote</LastName><ForeName>Andrea B</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany. Electronic address: schotefrese@uni-trier.de.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bonenberger</LastName><ForeName>Martina</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pálmason</LastName><ForeName>Haukur</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Seitz</LastName><ForeName>Christiane</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Child and Adolescent Psychiatry and Psychotherapy, Saarland University Hospital, Homburg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meyer</LastName><ForeName>Jobst</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurobehavioral Genetics, Institute of Psychobiology, University of Trier, Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Freitag</LastName><ForeName>Christine M</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, JW Goethe University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>10</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Psychiatry Res</MedlineTA><NlmUniqueID>7911385</NlmUniqueID><ISSNLinking>0165-1781</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ADHD</Keyword><Keyword MajorTopicYN="N">Association</Keyword><Keyword MajorTopicYN="N">Conduct disorder</Keyword><Keyword MajorTopicYN="N">Cortisol</Keyword><Keyword MajorTopicYN="N">NR3C1</Keyword><Keyword MajorTopicYN="N">SNPs</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>11</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>08</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>10</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>10</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27741480</ArticleId><ArticleId IdType="pii">S0165-1781(15)30748-4</ArticleId><ArticleId IdType="doi">10.1016/j.psychres.2016.10.001</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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