Abstract
Abstract—One of the priorities of neuroscience is the fight against socially relevant neurodegenerative diseases, including Parkinson’s disease (PD). Given the limited possibilities of studying the pathogenesis of this disease, the creation and detailed study of appropriate experimental models is of great importance. Therefore, the purpose of this work was to continue the long-term study of the cellular and molecular mechanisms of the pathogenesis of Parkinson’s disease and their systemic manifestations in a model of this disease in mice which is based on the use of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Here, using Western blotting, it was shown that in the blood plasma of mice with MPTP-induced clinical stage of PD, the ratio of monomeric to oligomeric α-synuclein is almost halved, and there is a tendency toward a decrease in the ratio of total α-synuclein to α-synuclein phosphorylated at serine-129. According to several studies, these changes are typical in patients with PD. Unlike plasma, no change in the ratio of these proteins was found in lymphocytes. From the alignment of our data on the content of α-synuclein and its isoforms in the blood of Parkinsonian mice, and the literature data on the content of α-synuclein in PD patients, it follows that our PD model can be used for an in-depth assessment of the peripheral manifestations of this disease, as well as for improving the differential diagnosis of PD, analyzing the effectiveness therapy, and screening for new drugs.
Published Version
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