A common microdeletion affecting a hippocampus- and amygdala-specific isoform of tryptophan hydroxylase 2 is not associated with affective disorders
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 4377207
Author(s) Hammer, Christian; Degenhardt, Franziska; Priebe, Lutz; Stutz, Adrian M.; Heilmann, Stefanie; Waszak, Sebastian M.; Schlattl, Andreas; Mangold, Elisabeth; Hoffmann, Per; MooDS Consortium,; Nöthen, Markus M.; Rietschel, Marcella; Rappold, Gudrun; Korbel, Jan O.; Cichon, Sven; Niesler, Beate
Author(s) at UniBasel Cichon, Sven
Year 2014
Title A common microdeletion affecting a hippocampus- and amygdala-specific isoform of tryptophan hydroxylase 2 is not associated with affective disorders
Journal Bipolar disorders
Volume 16
Number 7
Pages / Article-Number 764-768
Keywords Amygdala/*pathology; Female; Genetic Predisposition to Disease/*genetics; Hippocampus/*pathology; Humans; Linkage Disequilibrium; Male; Mood Disorders/*genetics/*pathology; Polymorphism, Single Nucleotide/*genetics; Tryptophan Hydroxylase/*genetics; 5-hydroxytryptamine (5-HT); bipolar affective disorder (BPAD); copy number polymorphism (CNP); deletion; major depressive disorder (MDD); serotonin; tryptophan hydroxylase 2 (TPH2)
Abstract OBJECTIVES: Copy number variants (CNVs) have been shown to affect susceptibility for neuropsychiatric disorders. To date, studies implicating the serotonergic system in complex conditions have just focused on single nucleotide polymorphisms (SNPs). We therefore sought to identify novel common genetic copy number polymorphisms affecting genes of the serotonergic system, and to assess their putative role in bipolar affective disorder (BPAD) and major depressive disorder (MDD). METHODS: A selection of 41 genes of the serotonergic system encoding receptors, the serotonin transporter, metabolic enzymes and chaperones were investigated using a paired-end mapping (PEM) approach on next-generation sequencing data from the pilot project of the 1000 Genomes Project. For association testing, 593 patients with MDD, 1,145 patients with BPAD, and 1,738 healthy controls were included in the study. RESULTS: PEM led to the identification of a microdeletion in the gene encoding tryptophan hydroxylase 2 (TPH2), affecting an amygdala- and hippocampus-specific isoform. It was not associated with BPAD or MDD using a case-control association approach. CONCLUSIONS: We did not find evidence for a role of the TPH2 microdeletion in the pathoetiology of affective disorders. Further studies examining its putative role in behavioral traits regulated by the limbic system are warranted.
Publisher Wiley-Blackwell
ISSN/ISBN 1398-5647 ; 1399-5618
edoc-URL https://edoc.unibas.ch/61550/
Full Text on edoc No
Digital Object Identifier DOI 10.1111/bdi.12207
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/24754353
ISI-Number WOS:000344373100011
Document type (ISI) Article
 
   

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