Format

Send to

Choose Destination
J Neurol Sci. 2018 Jun 15;389:28-34. doi: 10.1016/j.jns.2018.02.011. Epub 2018 Feb 5.

Genetics of tardive dyskinesia: Promising leads and ways forward.

Author information

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.

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)

PMID:
29502799
DOI:
10.1016/j.jns.2018.02.011
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center