The Influence of ADORA2A on Levodopa-Induced Dyskinesia
Neurology India, cilt.70, sa.2, ss.633-637, 2022 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 70 Sayı: 2
- Basım Tarihi: 2022
- Doi Numarası: 10.4103/0028-3886.344646
- Dergi Adı: Neurology India
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Veterinary Science Database
- Sayfa Sayıları: ss.633-637
- Anahtar Kelimeler: ADORA2A, genetics, levodopa, levodopa-induced dyskinesia, motor complications, neurogenetics, Parkinson's disease, polymorphism
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Background: Dopamine deficiency causes Parkinson's disease (PD), and on treatment, levodopa is the gold standard. Various drug-metabolizing enzymes and drug receptors are believed to be involved in prompting dyskinesias due to the extended usage of levodopa. Shreds of evidence in genomic studies have presented that ADORA2A receptor antagonism has beneficial outcomes to avoid these drug-induced side effects. Objective: The aim of this study was to study the polymorphisms of rs2298383, rs35060421, and rs5751876 in the ADORA2A in patients diagnosed as PD and describe their possible relationships with levodopa-induced dyskinesias (LID). Methods: One-hundred and seventy-two patients were recruited and separated as the study and the control group. DNA was achieved from peripheral venous blood, high resolution melting analysis, and reverse-transcriptase PCR was performed. Results: The allele differences among the groups were not statistically significant. Although it was not statistically significant, the rs35060421 allele was observed to repeat more frequently. However, we did not find an association between such polymorphisms of ADORA2A and LID. Conclusions: Although this result showed that a higher sample number might produce different results as possible, current results in the Turkish sample indicated that these alleles of ADORA2A might not be related to LID in patients.