NMDA receptor genotypes associated with the vulnerability to develop dyskinesia

S. A. Ivanova, A. J M Loonen, P. Pechlivanoglou, M. B. Freidin, A. F Y Al Hadithy, E. V. Rudikov, I. A. Zhukova, N. V. Govorin, V. A. Sorokina, O. Y. Fedorenko, V. M. Alifirova, A. V. Semke, J. R B J Brouwers, B. Wilffert

Research output: Contribution to journalArticlepeer-review

34 Citations (Scopus)


Dyskinesias are involuntary muscle movements that occur spontaneously in Huntington's disease (HD) and after long-term treatments for Parkinson's disease (levodopa-induced dyskinesia; LID) or for schizophrenia (tardive dyskinesia, TD). Previous studies suggested that dyskinesias in these three conditions originate from different neuronal pathways that converge on overstimulation of the motor cortex. We hypothesized that the same variants of the N-methyl-D-aspartate receptor gene that were previously associated with the age of dyskinesia onset in HD were also associated with the vulnerability for TD and not LID. Genotyping patients with LID and TD revealed, however, that these two variants were dose-dependently associated with susceptibility to LID, but not TD. This suggested that LID, TD and HD might arise from the same neuronal pathways, but TD results from a different mechanism.

Original languageEnglish
Article numbere67
JournalTranslational Psychiatry
Publication statusPublished - 2012


  • extra-pyramidal
  • GRIN2A
  • levodopa-induced dyskinesia
  • medium spiny neuron
  • NMDA
  • tardive dyskinesia

ASJC Scopus subject areas

  • Psychiatry and Mental health
  • Biological Psychiatry
  • Cellular and Molecular Neuroscience

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