NMDA receptor genotypes associated with the vulnerability to develop dyskinesia

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 t...

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Bibliographic Details
Published in:Translational psychiatry 2012-01, Vol.2 (1), p.e67-e67
Main Authors: 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
Format: Article
Language:English
Subjects:
631/208/727/2000
631/378/1697
692/699/375/346
Age of Onset
Alleles
Antiparkinson Agents - adverse effects
Antipsychotic Agents - adverse effects
Behavioral Sciences
Biological Psychology
Dyskinesia, Drug-Induced - genetics
Dyskinesia, Drug-Induced - physiopathology
Dyskinesias - genetics
Dyskinesias - physiopathology
Gene Expression - genetics
Genetic Predisposition to Disease - genetics
Genotype
Humans
Huntington Disease - genetics
Huntington Disease - physiopathology
Levodopa - adverse effects
Long-Term Care
Medicine
Medicine & Public Health
Motor Cortex - physiopathology
Movement Disorders - genetics
Movement Disorders - physiopathology
Neurosciences
Original
original-article
Pharmacotherapy
Polymorphism, Single Nucleotide - genetics
Psychiatry
Receptors, N-Methyl-D-Aspartate - genetics
Schizophrenia - drug therapy
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Summary: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.
ISSN:2158-3188
2158-3188
DOI:10.1038/tp.2011.66