Schizophrenia‐associated gene dysbindin‐1 and tardive dyskinesia. Issue 5 (11th May 2020)

• Record Type: Journal Article
• Authors: Maes, Miriam S.; Lu, Justin Y.; Tiwari, Arun K.; Freeman, Natalie; de Luca, Vincenzo; Müller, Daniel J.; Voineskos, Aristotle N.; Potkin, Steven G.; Lieberman, Jeffrey A.; Meltzer, Herbert Y.; Remington, Gary; Kennedy, James L.; Zai, Clement C.
• Other Names: Squassina Alessio guestEditor.
• Is Part Of: Drug development research. Volume 82:Issue 5(2021)
• Page Start: 678
• Page End: 684
• Publication Date: 2020-05-11
• Subjects: dysbindin‐1 (DTNBP1) -- pharmacogenetics -- schizophrenia -- tardive dyskinesia (TD); Drug development -- Periodicals; Drugs -- Research -- Periodicals; 615.19
• DOI: 10.1002/ddr.21681
• Languages: English
• ISSNs: 0272-4391

Abstract

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.