| Literature DB >> 32394511 |
Miriam S Maes1, Justin Y Lu1, Arun K Tiwari1,2, Natalie Freeman1, Vincenzo de Luca1,2,3, Daniel J Müller1,2,3, Aristotle N Voineskos1,2,3, Steven G Potkin4, Jeffrey A Lieberman5, Herbert Y Meltzer6, Gary Remington1,2,3, James L Kennedy1,2,3, Clement C Zai1,2,3,7.
Abstract
Tardive dyskinesia (TD) is a potentially irreversible movement disorder observed following long-term antipsychotic exposure. Its cause is unknown; however, a genetic component has been supported by studies of affected families. Dysbindin-1, encoded by the dystrobrevin-binding protein 1 DTNBP1 gene, has been associated with schizophrenia and is potentially involved in dopamine neurotransmission through its regulation of dopamine release and dopamine D2 receptor recycling, making it a candidate for investigation in TD. We investigated common variants across the DTNBP1 gene in our schizophrenia/patients with schizoaffective disorder of European ancestry. We found a number of DTNBP1 three-marker haplotypes to be associated with TD occurrence and TD severity (p < 0.05). These preliminary findings, if replicated in larger independent samples, would suggest that drugs targeting dysbindin-1 may be an option in the prevention and treatment of TD.Entities:
Keywords: dysbindin-1 (DTNBP1); pharmacogenetics; schizophrenia; tardive dyskinesia (TD)
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Year: 2020 PMID: 32394511 DOI: 10.1002/ddr.21681
Source DB: PubMed Journal: Drug Dev Res ISSN: 0272-4391 Impact factor: 4.360