ArticleSchizophrenia research2010
A reappraisal of the association between Dysbindin (DTNBP1) and schizophrenia in a large combined case-control and family-based sample of German ancestry.
Article in Schizophrenia research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies.Frontiers in pharmacology · 2021Review
- Developmental Genes and Regulatory Proteins, Domains of Cognitive Impairment in Schizophrenia Spectrum Psychosis and Implications for Antipsychotic Drug Discovery: The Example of Dysbindin-1 Isoforms and Beyond.Frontiers in pharmacology · 2019Review
- Neurodevelopmental disease mechanisms, primary cilia, and endosomes converge on the BLOC-1 and BORC complexes.Developmental neurobiology · 2018Review
- Genetic association of single nucleotide polymorphisms in dystrobrevin binding protein 1 gene with schizophrenia in a Malaysian population.Genetics and molecular biology · 2015Article
- Dysbindin-associated proteome in the p2 synaptosome fraction of mouse brain.Journal of proteome research · 2014Article
- Behavioral characterization of mice overexpressing human dysbindin-1.Molecular brain · 2014Article
- Dysbindin is a potent inducer of RhoA-SRF-mediated cardiomyocyte hypertrophy.The Journal of cell biology · 2013Article
- The DTNBP1 (dysbindin-1) gene variant rs2619522 is associated with variation of hippocampal and prefrontal grey matter volumes in humans.European archives of psychiatry and clinical neuroscience · 2013Article
- Cell biology of the BLOC-1 complex subunit dysbindin, a schizophrenia susceptibility gene.Molecular neurobiology · 2011Review
- Neuroplasticity signaling pathways linked to the pathophysiology of schizophrenia.Neuroscience and biobehavioral reviews · 2011Review
- Current Strategies in Diagnosis of Inherited Storage Pool Defects.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2010Article
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundDysbindin (DTNBP1) is a widely studied candidate gene for schizophrenia (SCZ); however, inconsistent results across studies triggered skepticism towards the validity of the findings. In this HapMap-based study, we reappraised the association between Dysbindin and SCZ in a large sample of German ethnicity.
methodSix hundred thirty-four cases with DSM-IV SCZ, 776 controls, and 180 parent-offspring trios were genotyped for 38 Dysbindin SNPs. We also studied two phenotypically-defined subsamples: 147 patients with a positive family history of SCZ (FH-SCZ+) and SCZ patients characterized for cognitive performance with Trail-Making Tests A and B (TMT-A: n=219; TMT-B: n=247). Given previous evidence of gene-gene interactions in SCZ involving the COMT gene, we also assessed epistatic interactions between Dysbindin markers and 14 SNPs in COMT.
resultsNo association was detected between Dysbindin markers and SCZ, or in the FH-SCZ+ subgroup. Only one marker (rs1047631, previously reported to be part of a risk haplotype), showed a nominally significant association with performance on TMT-A and TMT-B; these findings did not remain significant after correction for multiple comparisons. Similarly, no pair-wise epistatic interactions between Dysbindin and COMT markers remained significant after correction for 504 pair-wise comparisons.
conclusionsOur results, based on one of the largest samples of European Caucasians and using narrowly-defined criteria for SCZ, do not support the etiological involvement of Dysbindin markers in SCZ. Larger samples may be needed in order to unravel Dysbindin's possible role in the genetic basis of proposed intermediate phenotypes of SCZ or to detect epistatic interactions.
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