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Genetics of early-onset obsessive-compulsive disorder

Walitza, Susanne ; Wendland, Jens ; Gruenblatt, Edna ; Warnke, Andreas ; Sontag, Thomas ; Tucha, Oliver ; Lange, Klaus

In: European Child & Adolescent Psychiatry, 2010, vol. 19, no. 3, p. 227-235

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    Titre
    • Genetics of early-onset obsessive-compulsive disorder
    Auteur
    • Walitza, Susanne. Department of Child and Adolescent Psychiatry, University of Zurich, Zurich, Switzerland
    • Wendland, Jens. Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, USA
    • Gruenblatt, Edna. Department of Child and Adolescent Psychiatry, University of Zurich, Zurich, Switzerland
    • Warnke, Andreas. Department of Child and Adolescent Psychiatry and Psychotherapy, University of Würzburg, Wurzburg, Germany
    • Sontag, Thomas. Department of Experimental Psychology, University of Regensburg, Regensburg, Germany
    • Tucha, Oliver. Department of Psychology, University of Groningen, Groningen, The Netherlands
    • Lange, Klaus. Department of Experimental Psychology, University of Regensburg, Regensburg, Germany
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • European Child & Adolescent Psychiatry, 2010, vol. 19, no. 3, p. 227-235. Springer-Verlag
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:310547
    Summary
    Obsessive-compulsive disorder (OCD) is characterized by recurrent, intrusive and disturbing thoughts as well as by repetitive stereotypic behaviors. Epidemiological data are similar in children and adults, i.e., between 1 and 3% of the general population suffer from OCD. Children with OCD are often seriously impaired in their development. OCD, especially of early onset, has been shown to be familial. Several candidate genes of predominantly neurotransmitter systems have been analyzed and a total of three genome-wide linkage scans have been performed until now. Analyses of candidate genes in linkage regions have not provided evidence for their involvement in OCD, with the exception of the glutamate transporter gene SLC1A1 on 9p24. Genome-wide association analyses are in progress and the results will promote further independent replication studies. The consideration of subtypes regarding age of onset, symptom dimensions and/or comorbid disorders is needed