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NMDA receptor genotypes associated with the vulnerability to develop dyskinesia

Ivanova, S. A., Loonen, A. J. M., Pechlivanoglou, P., Freidin, M. B., Al Hadithy, A. F. Y., Rudikov, E. V., Zhukova, I. A., Govorin, N. V., Sorokina, V. A., Fedorenko, O. Y., Alifirova, V. M., Semke, A. V., Brouwers, J. R. B. J. & Wilffert, B., 10-Jan-2012, In : Translational Psychiatry. 2, 4 p., e67.

Research output: Contribution to journalArticleAcademicpeer-review

  • 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
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
Number of pages4
JournalTranslational Psychiatry
Volume2
Publication statusPublished - 10-Jan-2012

    Keywords

  • extra-pyramidal, GRIN2A, levodopa-induced dyskinesia, medium spiny neuron, NMDA, tardive dyskinesia, VARIATIONS MODIFY AGE, TARDIVE-DYSKINESIA, HUNTINGTONS-DISEASE, PARKINSONS-DISEASE, GENETIC ASSOCIATION, PATHOGENESIS, MECHANISMS, ONSET, SCHIZOPHRENIA, NR2A

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