Acta clinica Belgica · 2016
Serum levels of homocysteine, asymmetric dimethylarginine and nitric oxide in patients with Parkinson's disease.
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Kirbas Serkan, Kirbas Aynur, Tufekci Ahmet, Cumhur Cure Medine, Cakmak Sevim, Yazici Tarkan, Cure Erkan
Аннотация
OBJECTIVES: Endothelial dysfunction has been implicated as a crucial event in the development of several neurodegenerative diseases. The aim of this study was to investigate the serum homocysteine, asymmetric dimethylarginine (ADMA) and nitric oxide (NO) levels in patients with Parkinson's disease (PD) and to compare the results with data from healthy controls.
METHODS: A total of 132 subjects, including 82 idiopathic PD patients who were newly diagnosed and untreated (47 males, 35 females, mean age of 60.8 ± 7.1 years) and 50 healthy controls (28 males, 22 females, mean age of 60.2 ± 6.7 years) were enrolled in this study. The serum ADMA and NO levels were determined using enzyme-linked immunosorbent assay (ELISA), while the homocysteine levels were determined by chemiluminescent microparticle immunoassay.
RESULTS: The ADMA and NO levels of the PD patients were significantly higher than those of the healthy controls. The serum ADMA levels were 0.70 ± 0.15 μmol/L in the PD patients and 0.50 ± 0.12 μmol/L in the healthy controls (p < 0.001). The serum NO levels were 78.7 ± 10.3 μmol/L in the PD patients and 59.9 ± 9.5 μmol/L in the healthy controls (p < 0.001). In addition, the ADMA and NO levels were significantly correlated with the serum homocysteine levels in patients with PD (r = 0.874, p < 0.001, r = 0.803, p = 0.005, respectively).
CONCLUSION: In our study, the high ADMA and NO levels of patients with PD indicate endothelial dysfunction, and this dysfunction may play a role in PD pathogenesis. Larger studies, including randomised clinical trials in humans and animal studies, are needed to validate our findings and help in developing a better understanding of the pathogenesis of PD.
METHODS: A total of 132 subjects, including 82 idiopathic PD patients who were newly diagnosed and untreated (47 males, 35 females, mean age of 60.8 ± 7.1 years) and 50 healthy controls (28 males, 22 females, mean age of 60.2 ± 6.7 years) were enrolled in this study. The serum ADMA and NO levels were determined using enzyme-linked immunosorbent assay (ELISA), while the homocysteine levels were determined by chemiluminescent microparticle immunoassay.
RESULTS: The ADMA and NO levels of the PD patients were significantly higher than those of the healthy controls. The serum ADMA levels were 0.70 ± 0.15 μmol/L in the PD patients and 0.50 ± 0.12 μmol/L in the healthy controls (p < 0.001). The serum NO levels were 78.7 ± 10.3 μmol/L in the PD patients and 59.9 ± 9.5 μmol/L in the healthy controls (p < 0.001). In addition, the ADMA and NO levels were significantly correlated with the serum homocysteine levels in patients with PD (r = 0.874, p < 0.001, r = 0.803, p = 0.005, respectively).
CONCLUSION: In our study, the high ADMA and NO levels of patients with PD indicate endothelial dysfunction, and this dysfunction may play a role in PD pathogenesis. Larger studies, including randomised clinical trials in humans and animal studies, are needed to validate our findings and help in developing a better understanding of the pathogenesis of PD.