The Influence of ADORA2A on Levodopa-Induced Dyskinesia.

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.

Uric acid: The role in the pathophysiology and the prediction in the diagnosis of Parkinson's disease: A Turkish-based study.

BACKGROUND AND PURPOSE: Oxidative stress has been associated as an essential contributor to the development of neurodegenerative diseases. Recent developments in the field of Parkinson's Disease (PD) pathophysiology have led to a renewed interest in this field. As an antioxidant, uric acid (UA) has arisen as a potential neuroprotectant. Higher concentrations of UA are linked to reducing the risk of the development of the disease and preventing its progression. However, the expositions are unsatisfactory because the outcomes of these reports have not been consistent. This study is set out to assess the association of whether lower UA concentrations increased the PD risk by investigating its relationship with patients' demographic and clinical data, and to determine whether previous studies are compatible with the Turkish-sampled population. Furthermore, we aimed to determine UA's probability of being an early-stage diagnostic marker. METHODS: A total of 305 patients and 100 healthy controls were included. Serum UA levels of patients and controls were compared with clinical features. We classified the patients into three motor subtypes and determined the disease severity by modified Hoehn&Yahr Staging Scale (mH&Y) and Unified Parkinson's Disease Rating Scale (UPDRS). Standardized Mini-Mental State Examination (MMSE-TR) was assessed for cognition. RESULTS: There were not any significant differences of age and sex between patients and controls (p=0.030, p=0.132). The mean UA was 5.06±1.33 mg/dL in patients and 5.46±1.44 in controls, and a statistical significance was detected (p=0.022). The mean MMSE-TR were 24.83±4.35 in patients and 27.09±2.13 in controls, and statictical significance was revealed (p=0.001). The mean duration of the disease was 6.31±4.16 years, mean UPDRS scores were 59.74±22.33, and mH&Y scores were 2.29±0.91. In binary comparisons, patients with tremor-dominant motor subtype had lower UA concentrations than controls (p=0.014). ROC curve analysis revealed UA's cut-off as ≤9.15, the specificity was 99.3, the sensitivity was 10.0, and the area under the curve was 0.576 (p<0.005). Regression analysis revealed age as an independent risk factor on UA values. Oxidative stress might be a factor in the development of PD, and UA may be a possible prospective protecting factor in the clinical course of the disease. However, it does not affect the severity. CONCLUSION: Our results support that lower uric acid concentrations are associated with PD; however, it is not a powerful indicator for predicting PD risk. As we reveal more about UA and its effect in further investigations, its significant role will become well-defined.

A Case of Pregabalin-Induced Parkinsonism.

Drug-induced parkinsonism is the second common movement disorder after Parkinson's disease. It occurs due to the use of not only neuroleptics but also some other medications as pregabalin. Pregabalin is an antiepileptic drug and a structural analog of gamma-aminobutyric acid (GABA), and its use decreases the release of several neurotransmitters. In this case report, we present a 53-year-old female patient with the signs of parkinsonism following pregabalin treatment. Drug-induced parkinsonism was diagnosed based on the clinical features, investigations, and resolution of the complaints. The symptoms relieved after the treatment stopped at a follow-up of 10 days. Due to the rare report of pregabalin-induced parkinsonism, we aim to enhance clinicians' awareness of pregabalin's probable side effects.