Abstract
L-dopa–induced dyskinesia (LID) is a frequent motor complication of Parkinson’s disease (PD), associated with a negative prognosis. Previous studies showed an association between dopamine receptor (DR) gene (DR) variants and LID, the results of which have not been confirmed. The present study is aimed to determine whether genetic differences of DR are associated with LID in a small but well-characterized cohort of PD patients. To this end we enrolled 100 PD subjects, 50 with and 50 without LID, matched for age, gender, disease duration and dopaminergic medication in a case-control study. We conducted polymerase chain reaction for single nucleotide polymorphisms (SNP) in both D1-like (DRD1A48G; DRD1C62T and DRD5T798C) and D2-like DR (DRD2G2137A, DRD2C957T, DRD3G25A, DRD3G712C, DRD4C616G and DRD4nR VNTR 48bp) analyzed genomic DNA. Our results showed that PD patients carrying allele A at DRD3G3127A had an increased risk of LID (OR 4.9; 95% CI 1.7–13.9; p = 0.004). The present findings may provide valuable information for personalizing pharmacological therapy in PD patients.
Highlights
Levodopa-induced dyskinesia (LID) is a disabling motor complication of long-term levodopa therapy in Parkinson’s disease (PD) [1,2]
Work from our group showed that the TT genotype at DRD1 rs686 may predispose PD patients to developing visual hallucinations (VHs) while subjects with GG at DRD1 rs4532 display a shorter time to VHs [10]
One study showed that PD patients carrying the rs6280 single nucleotide polymorphism (SNP) at DRD3 have earlier onset of peak dose dyskinesia [11]
Summary
Levodopa-induced dyskinesia (LID) is a disabling motor complication of long-term levodopa therapy in Parkinson’s disease (PD) [1,2]. One study showed that PD patients carrying the rs6280 single nucleotide polymorphism (SNP) at DRD3 have earlier onset of peak dose dyskinesia [11]. Due to the lack of confirmed results on the role of polymorphic DR variants in LID development, the present pilot study was designed to further investigate DR genetics in a small but accurately characterized cohort of Italian PD patients. To this end, we selected a panel of DR variants, giving priority to the most frequent and functionally characterized ones, and compared the frequency of all variants in two matched subgroups of PD patients with and without LID
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