Introduction: The role of inflammatory factors in Parkinson's disease (PD) has not been consistently proven yet. Despite the presence of some potentially causative factors, the primary and initiating factor has not been determined. Therefore the influence of proinflammatory and antiphlogistic factors on the risk of PD remains unclear. The aim of the study was to evaluate the level of NT-proCNP as well as proinflammatory factors in peripheral blood of patients with PD and to compare the changes of cytokines and NT-proCNP profile of these patients with the profile within the control group.
Materials and methods: The study group consisted of 60 patients with the diagnosis of idiopathic PD, in the mean age of 59 ± 15.5 years, and control group of 24 persons, in the mean age of 64 ± 5.8 years, without neurodegenerative and inflammatory disorders. The quantitative determination of cytokines was evaluated with the fluorokine MAP cytokine multiplex kit and the Luminex 100 Platform. ELISA kits were used for the quantitative determination of human NT-proCNP.
Results: The levels of NT-proCNP and all measured cytokines were higher in serum of PD patients in comparison to the control group, though the significant differences were only observed in relation to serum level of NT-proCNP (p<0.05) and TNF-α (p<0.001). The mean serum level of NT-proCNP in PD patients correlates with the level of TNF-α (R=0.359, p<0.05) and IL-10 (R=-0.39, p=0.05). There are also other correlations in serum of PD group: between IL-10 and IL-12 (R=0.39, p=0.05), IL-6 and IL-1ß (R=0.65, p=0.05). The serum level of IL-6 is also in a positive relation with H&Y stage (R=0.27, p=0.05).
Conclusions: The concentration of NT-proCNP and TNF-α is essentially higher in parkinsonian patients than in healthy group. The levels of other anti- and proinflammatory cytokines also tend to be higher in PD patients in comparison to the control group. It confirms the significance of these factors' influence on molecular pathogenesis of PD and makes NT-proCNP a new potential determinant of inflammation in PD patients.
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