2. Academic Validation
  3. Genetics of tardive dyskinesia: Promising leads and ways forward

Genetics of tardive dyskinesia: Promising leads and ways forward

  • J Neurol Sci. 2018 Jun 15:389:28-34. doi: 10.1016/j.jns.2018.02.011.
Clement C Zai 1,  Miriam S Maes 2,  Arun K Tiwari 3,  Gwyneth C Zai 3,  Gary Remington 4,  James L Kennedy 5
Affiliations

Affiliations

  • 1 Neurogenetics Section, Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Canada; Department of Psychiatry, University of Toronto, Canada; Institute of Medical Science, University of Toronto, Canada; Laboratory Medicine and Pathobiology, University of Toronto, Canada. Electronic address: clement.zai@camh.ca.
  • 2 Neurogenetics Section, Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Canada.
  • 3 Neurogenetics Section, Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Canada; Department of Psychiatry, University of Toronto, Canada.
  • 4 Neurogenetics Section, Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Canada; Department of Psychiatry, University of Toronto, Canada; Institute of Medical Science, University of Toronto, Canada.
  • 5 Neurogenetics Section, Tanenbaum Centre for Pharmacogenetics, Molecular Brain Science, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Canada; Department of Psychiatry, University of Toronto, Canada; Institute of Medical Science, University of Toronto, Canada. Electronic address: jim.kennedy@camh.ca.
PMID: 29502799 DOI: 10.1016/j.jns.2018.02.011
Abstract

Tardive dyskinesia (TD) is a potentially irreversible and often debilitating movement disorder secondary to chronic use of Dopamine Receptor blocking medications. Genetic factors have been implicated in the etiology of TD. We therefore have reviewed the most promising genes associated with TD, including DRD2, DRD3, VMAT2, HSPG2, HTR2A, HTR2C, and SOD2. In addition, we present evidence supporting a role for these genes from preclinical models of TD. The current understanding of the etiogenesis of TD is discussed in the light of the recent approvals of valbenazine and deutetrabenazine, VMAT2 inhibitors, for treating TD.

Keywords

Dopamine D(2) receptor gene (DRD2); Dopamine D(3) receptor gene (DRD3); Heparan sulfate proteoglycan 2 (HSPG2); Manganese superoxide dismutase (SOD2); Pathophysiology; Pharmacogenetics; Serotonin 2A receptor (HTR2A); Serotonin 2C receptor (HTR2C); Tardive dyskinesia (TD); Vesicular monoamine transporter 2 gene (VMAT2/SLC18A2).

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