Features of the mitochondrial dysfunction development in Parkinson’s disease, possibilities of drug correction for ultrastructural disorders
Authors: Rozova K.V. , Gonchar O.O. , Karaban I.M. , Karasevich N.V. , Khodakovska M.A. , Melnik N.O. 
Published: November 2024

Background. The studied mitochondrial ultrastructure disorders in Parkinson’s disease (PD) are evidence of the formation of mitochondrial dysfunction (MD). They can be considered in a pathogenetic connection with the level of oxidative-prooxidant processes. The purpose was to study and evaluate the effectiveness and tolerability of the original EGb 761® in the comprehensive treatment of PD patients with cognitive impairment, the effect of the medicine on MD and oxidative stress manifestations. Materials and methods. The effectiveness of the EGb 761® course was studied in 22 patients with PD diagnosed according to the UK Brain Bank criteria (Hughes A., 1992), aged 45–74 years, with disease stage 1.5–3.0 (by Hoehn-Yahr). There were general clinical, neurological studies with assessment of motor activity by MDS-UPDRS, a sensorimotor reaction and motor tempo, neuropsychological research, evaluation of biochemical indicators of the state of oxidative stress, electron microscopy and morphometric studies of blood cells before and after a course of the original EGb 761®. Results. The EGb 761® course treatment of PD patients improved motor activity and cognitive functions. A significant increase in lipid peroxidation intensity and oxidative-prooxidant processes ratio was found, i.e. oxidative stress levels markers. The EGb 761® use for 1 month led to a decrease in the pro-oxidant processes intensity. Increasing the duration of drug use to 2 months caused a reduction in the thiobarbituric acid reactive substances in the patient’s plasma by almost 50 % compared to the indicator before treatment. The superoxide dismutase and catalase activity decreased by 28 and 42 % (p < 0.05), respectively, in comparison with baseline. Studies have revealed changes in the mitochondrial ultrastructure and the MD formation in blood cells. A decrease in the dense δ-granules was observed in platelets. This indicates the serotonergic system dysfunction and disturbances in the serotonin regulatory effects regarding the vascular wall contractility. The large α-granules number in platelets was higher than in healthy people, indicating a risk of thrombosis in PD patients. Significant disturbances were found in the mitochondrial ultrastructure with the MD formation. The EGb 761® use contributed to the formation of a mitochondrial intact structure, i.e. elimination of MD structural manifestations. Conclusions. The course treatment with original EGb 761® against the background of comprehensive pathogenetic therapy of PD patients with cognitive impairment improved motor activity, mental functions and eliminated the structural manifestations of MD in blood cells. It should be assumed that the mechanism of this phenomenon is due to a decrease in the pro-oxidative and oxidative processes intensity, reduced reactive oxygen species generation, and, eventually, a decrease in the oxidative process level that a key link in the PD pathogenesis.