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.
Original language | English (US) |
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Pages (from-to) | 678-684 |
Number of pages | 7 |
Journal | Drug Development Research |
Volume | 82 |
Issue number | 5 |
DOIs | |
State | Published - Aug 2021 |
Keywords
- dysbindin-1 (DTNBP1)
- pharmacogenetics
- schizophrenia
- tardive dyskinesia (TD)
ASJC Scopus subject areas
- Drug Discovery