What is the role of genetics in the etiology of tardive dyskinesia (TD)?

Updated: Oct 17, 2018
  • Author: James Robert Brasic, MD, MPH; Chief Editor: Selim R Benbadis, MD  more...
  • Print


A genetic basis for TD has not been identified. In particular, a functional polymorphism of the gene coding for human glutathione S-transferase P1 (GSTP1) does not appear to be associated with TD. [22] Additionally, CYP3A4 and CYP2D6 gene polymorphisms are apparently unassociated with TD. [23] TD has been associated with polymorphisms of the dopamine D3 receptor Ser9Gly [24] and of the serotonin 2A [1] and 2C receptor genes [24, 1] .

Reports of associations between TD and polymorphisms of nicotinamide adenine dinucleotide phosphate (NADPH) quinine oxidoreductase 1 (NQO1) and superoxide dismutase 2 (SOD2, MnSOD) genes have not consistently been confirmed by subsequent studies. [25]

Brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms may be associated with the development of TD and the severity of TD in whites. [26] Thus, the enhancement of BDNF may be protective against the development of TD, particularly in whites. [26]

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!