| Literature DB >> 18473158 |
Frederike Schirmbeck1, Alexander Georgi, Jana Strohmaier, Christine Schmael, Katja V Boesshenz, Thomas W Mühleisen, Stefan Herms, Per Hoffmann, Rami Abou Jamra, Johannes Schumacher, Wolfgang Maier, Peter Propping, Markus M Nöthen, Sven Cichon, Marcella Rietschel, Thomas G Schulze.
Abstract
Whereas Dysbindin is considered a schizophrenia vulnerability gene, there is no consistency of findings. Phenotype refinement approaches may help to increase the genetic homogeneity and thus reconcile conflicting results. Premorbid adjustment (PMA) has been suggested to aid the phenotypic dissection. Gornick et al. (J Autism Dev Disord 35:831-838, 2005) reported an association between Dysbindin and PMA in US-Caucasian individuals with childhood-onset psychosis. In a sample of 222 adult-onset schizophrenia inpatients from Germany, we could not detect an association between PMA and 36 SNPs in Dysbindin. Our results suggest that genetic variation in Dysbindin may not contribute to the schizophrenia phenotype with an onset beyond childhood. Further studies including even larger samples and more SNPs may be warranted to clarify the relationship between Dysbindin and PMA.Entities:
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Year: 2008 PMID: 18473158 DOI: 10.1007/s10803-008-0582-6
Source DB: PubMed Journal: J Autism Dev Disord ISSN: 0162-3257