Structural damage of myelin in experimental Parkinsonism and prospects for their drug correction in the clinic of Parkinson's disease
Changes in myelin ultrastructure under experimental Parkinsonism in the tissues of the medulla oblongata and striatum were performed under experimental Parkinsonism induced by rotenone administration in 30 adult rats of the Wistar line. Clinico-electromyographic studies were performed on patients with Parkinson's disease with a stage of disease 2.0 -3.0 (Hoehn a. Yahr).
Efficacy of Cerebrolysin has been shown to correct myelin abnormalities to elucidate the effect on the muscle reflex response to irritation of sensitive nerve fibres of the mixed nerve with subsequent monosynaptic activation of motor neurons and spinal cord neurons. One of the mechanisms associated with myelin damage in Parkinsonism is the development of mitochondrial dysfunction, in any case, its ultrastructural component. The use of Cerebrolysin leads to a significant elimination of mitochondrial dysfunction and myelin damage. It can be assumed that the positive effect of the drug lies in the antioxidant effect, which, in turn, effect the transmembrane conductivity, which should be considered one of the neuroprotective effects of the drug.
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