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Schizophrenia‐associated gene dysbindin‐1 and tardive dyskinesia
Author(s) -
Maes Miriam S.,
Lu Justin Y.,
Tiwari Arun K.,
Freeman Natalie,
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.
Publication year - 2021
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.21681
Subject(s) - tardive dyskinesia , schizophrenia (object oriented programming) , dopamine , schizoaffective disorder , psychosis , haplotype , dyskinesia , antipsychotic , genetics , atypical antipsychotic , neuroscience , gene , psychology , biology , medicine , psychiatry , disease , allele , parkinson's disease
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.