پديد آورندگان :
Ivanova، Svetlana A. نويسنده Mental Health Research Institute, Tomsk, Russian Federation Ivanova, Svetlana A. , Fedorenko، Olga Yu نويسنده Mental Health Research Institute, Tomsk, Russian Federation Fedorenko, Olga Yu , Freidin، Maxim B. نويسنده Research Institute for Medical Genetics, Tomsk, Russian Federation Freidin, Maxim B. , Alifirova، Valentina M. نويسنده Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation Alifirova, Valentina M. , Zhukova، Natalia G نويسنده Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation Zhukova, Natalia G , Zhukova، Irina A نويسنده Department of Neurology and Neurosurgery, Siberian State Medical University, Tomsk, Russian Federation Zhukova, Irina A , Al Hadithy، Asmar F.Y. نويسنده Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands Al Hadithy, Asmar F.Y. , Brouwers، Jacobus R.B.J. نويسنده Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands Brouwers, Jacobus R.B.J. , Bokhan، Nikolay A. نويسنده Mental Health Research Institute, Tomsk, Russian Federation Bokhan, Nikolay A. , Wilffert، Bob نويسنده Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands Wilffert, Bob , Loonen، Anton J.M. نويسنده Department of Pharmacotherapy and Pharmaceutical Care, University of Groningen, Groningen, The Netherlands Loonen, Anton J.M.
كليدواژه :
Parkinson’s disease , Genetic variants , Serotonergic receptors , Levodopa-induced dyskinesia , Dopaminergic receptors
چكيده لاتين :
Introduction: Long-term levodopa treatment of Parkinson’s disease (PD) is frequently complicated by spontaneously occurring involuntary muscle movements called dyskinesia. The exact pathological mechanism of this complication has not yet been elucidated. We have previously demonstrated that in PD patients the vulnerability to develop peripheral but not orofacial dyskinesia is associated with the presence of two variants of the GRIN2A gene. Moreover, we have shown that in tardive dyskinesia (TD) orofacial dyskinesia is associated with other polymorphisms as compared with peripheral dyskinesia. In the present study we investigate whether the peripheral versus orofacial nature of levodopa-induced dyskinesia (LID) in PD can be explained by considering polymorphisms for dopaminergic and serotonergic receptors.
Materials and Methods: 101 Russian patients with PD (38M/63F) were examined. Genotyping was carried out on 19 SNPs for 3 neurotransmitter genes: 10 SNPs for DRD3 gene (rs11721264, rs167770, rs3773678, rs963468, rs7633291, rs2134655, rs9817063, rs324035, rs1800828, rs167771), 1 SNP for DRD4 gene (rs3758653), and 8 SNPs for HTR2C gene (rs6318, rs5946189, rs569959, rs17326429, rs4911871, rs3813929, rs1801412, rs12858300).
Results: Genotyping patients with PD and LID revealed that only rs3773678 (DRD3, dominant, p = 0.042) was associated with orofacial dyskinesia.
Conclusion: The findings of the current study are not related to LID in PD itself, but to other forms of orofacial dyskinesia in this patient group.
Abbreviations: PD – Parkinson’s disease; TD – Tardive dyskinesia; LID – Levodopa-induced dyskinesia; MSN – Medium Spiny Neuron; NMDA – N-methyl-D-aspartate;
HD – Huntington’s disease; SNP – Single nucleotide polymorphism
