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

doi:10.1038/tp.2011.66

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

^*Corresponding author for this work

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Abstract

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 language	English
Article number	e67
Number of pages	4
Journal	Translational Psychiatry
Volume	2
DOIs	https://doi.org/10.1038/tp.2011.66
Publication status	Published - 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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NMDA receptor genotypes associated with the vulnerability to develop dyskinesiaFinal publisher's version, 217 KBLicence: CC BY-NC-SA

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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. (2012). NMDA receptor genotypes associated with the vulnerability to develop dyskinesia. Translational Psychiatry, 2, Article e67. https://doi.org/10.1038/tp.2011.66

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title = "NMDA receptor genotypes associated with the vulnerability to develop dyskinesia",

abstract = "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.",

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",

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

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doi = "10.1038/tp.2011.66",

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AU - Ivanova, S. A.

AU - Loonen, A. J. M.

AU - Pechlivanoglou, P.

AU - Freidin, M. B.

AU - Al Hadithy, A. F. Y.

AU - Rudikov, E. V.

AU - Zhukova, I. A.

AU - Govorin, N. V.

AU - Sorokina, V. A.

AU - Fedorenko, O. Y.

AU - Alifirova, V. M.

AU - Semke, A. V.

AU - Brouwers, J. R. B. J.

AU - Wilffert, B.

PY - 2012/1/10

Y1 - 2012/1/10

N2 - 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.

AB - 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.

KW - extra-pyramidal

KW - GRIN2A

KW - levodopa-induced dyskinesia

KW - medium spiny neuron

KW - NMDA

KW - tardive dyskinesia

KW - VARIATIONS MODIFY AGE

KW - TARDIVE-DYSKINESIA

KW - HUNTINGTONS-DISEASE

KW - PARKINSONS-DISEASE

KW - GENETIC ASSOCIATION

KW - PATHOGENESIS

KW - MECHANISMS

KW - ONSET

KW - SCHIZOPHRENIA

KW - NR2A

U2 - 10.1038/tp.2011.66

DO - 10.1038/tp.2011.66

M3 - Article

C2 - 22832729

SN - 2158-3188

VL - 2

JO - Translational Psychiatry

JF - Translational Psychiatry

M1 - e67

ER -

NMDA receptor genotypes associated with the vulnerability to develop dyskinesia

Abstract

Keywords

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