Contemporary pathogenetic aspects of parkinson’s disease development

Abstract

The article presents modern views on the role of apoptosis, necrosis, oxidative stress and inflammatory processes, as well as their combination in the pathogenesis of Parkinson’s disease. The Parkinson’s disease remains one of the global medical and social problems. According to most authors, the number of patients worldwide who suffer from Parkinson’s disease exceeds 6 million. The disease is diagnosed in 1% of the population under the age of 60 and 3% at the age of 80 and older. In Ukraine, the prevalence of the disease is 133 cases per 100 thousand populations. High rates of disability, a steady increase in the incidence, still insufficient treatment effectiveness, significant economic costs of treatment, given the relatively high cost of drugs, the need for constant dynamic monitoring of the doctor, the development of rehabilitation measures, make the problem of Parkinson’s disease in Ukraine a national one. According to modern ideas about the pathogenetic changes that are characteristic of Parkinson’s disease, one of the leading roles in the development of neurodegeneration in it is played by the presynaptic protein α-synuclein. However, the exact functions of this protein are still insufficiently studied. The key moment of the molecular pathogenesis of Parkinson’s disease is the change in the native spatial stacking of α-synuclein with the formation of β-structures and oligomers that have neurotoxicity followed by their fibrillation with the formation of increasing cytoplasmic aggregates. There is evidence that even before the manifestation of a typical clinic for Parkinson’s disease pathological synuclein inclusions is found in the olfactory bulbs and neurons of the dorsal motor nucleus n. vagus, after which they can be found in more rostral sections – the nuclei of the suture and the reticular pharmacy, the black substance, etc. Of great importance is the presence of exogenous factors that can reduce the risk of disease, which include smoking, drinking coffee, taking non-steroidal anti-inflammatory drugs, vitamin E, etc. Such changes can be explained by their effect on the molecular properties of α-synuclein. It has been shown that, for example, hydroquinone stabilizes soluble oligomeric forms of α-synuclein and has an inhibitory effect on the formation of fibrils.