Relationshi̇p between serum glial fibrillary acidic prtotein and uric asid levels in parkinson's disease

Objectives: Parkinson's Disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. Pathological changes in Parkinson's disease are loss of dopaminergic cells that are containing melanin in the pars compacta of substantia nigra. The etiology of the disease and the nature of the pathophysiologic events that led to the loss of cells is not yet fully understood. We aimed to investigate the role and effects of serum Glial Fibrilary Asidic Protein (GFAP) and Uric asid (UA) levels in Parkinson's disease. Thus, we will try to find news options for the pathophysiology and treatment of Parkinson's disease. Material and Methods: All of the subjects (including patients and normal controls) were enrolled from the medical examination center of Medical Faculty Hospital of Dicle University. PD group The control group was 41 persons and selected from similar age and gender group. All controls and PD patients underwent a standardized neurological examination by movement disorder specialists, and the clinical diagnosis of PD was established according to the UK Parkinson's Disease Society Brain Bank criteria. Venous blood samples that taken from the patient and control groups were centrifuged and derived serum samples. The serum GFAP levels were measured by ELISA method and the serum UA concentrations were measured on an automatic biochemistry analyzer, by using commercially available kits according to manufacturers instructions. Results: The serum levels of GFAP and UA were significantly lower in the PD groups than in the normal control group (P < 0.05). There was no significant difference in serum GFAP and UA levels between the age and disease duration in PH group (P > 0.05). The serum level of both GFAP and UA of females in the PD group was significantly lower than the males in PD group (P < 0.05). Conclusion: GFAP has received much attention as a biological indicator in the central nervous system disease studies. It is not yet clear, however, whether the upregulation of GFAP following different pathological events in the CNS, may lead to GFAP release and emergence of detectable protein levels in peripheral blood. The treatment of serum UA levels may be a new therapeutic direction for PD. Randomized clinical trials targeting PD and conducting dopaminergic imaging may provide an attractive complementary opportunity to investigate potential effects of serum urate on PD risk.