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Schizophrenia-associated gene dysbindin-1 and tardive dyskinesia.

Miriam S MaesJustin Y LuArun K TiwariNatalie FreemanVincenzo de LucaDaniel J MüllerAristotle N VoineskosSteven G PotkinJeffrey A LiebermanHerbert Y MeltzerGary RemingtonJames L KennedyClement C Zai
Published in: Drug development research (2020)
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.
Keyphrases
  • copy number
  • bipolar disorder
  • genome wide
  • binding protein
  • uric acid
  • risk assessment
  • metabolic syndrome
  • drug delivery
  • replacement therapy
  • drug induced
  • genome wide association study