The present paper delivers informative data on impaired metabolism in the sections the brain, representative of Parkinson’s disease. It’s considered to be an established fact, that at all the stage of Parkinson’s disease the level of aliphatic polyamines - putrescine, spermidine and spermine - the highest concentrations of which are known to be of cytotoxic spectrum activity, increases in dopaminergic neurons. The role of α-synuclein in the development of dystrophic processes in dopaminergic neurons of the brain is also presented in the article. According the introduced in the paper the newest literature data, the association between the incidence of neurodegenerative disorder symptomocomplex occurrence in Parkinson’s disease and Helicobacter pylori long-term persistence in the organs of gastrointestinal tract disease can be precisely traced. In this regard, the subject under wide discussion is the current hypothesis, according to
which as a result of Helicobacter pylori persistence in neuritis, localized in the organs of gastrointestinal tract, α-synucleins begin to cumulate and undergo aggregation. The main postulate of the hypothesis is based on the fact, that namely similar aggregates of α-synucleins enter the sections of the brain by means of perineural penetration or/and through hematoencephalic barrier, causing neurodegenerative disorders, characteristic of Parkinson’s disease. This hypothesis is considered by the authors from a critical point of view. Thus, more acceptable is the assumption, that it’s not α-synucleins but α-synuclein autoantibodies produced in the organs of immunogenesis that penetrate through hematoencephalic barrier. In this regard, the role of the resident conditional pathogenic microorganisms, produced in the gastrointestinal tract, in the genesis of
Parkinson’s disease, in our opinion, should be observed from qualitatively new viewpoints. In this aspect, a special attention of the researchers should be paid particularly to the processes of E. coly bacterial translocation, the products of secretion and decomposition (putrescine, lipopolysaccharide) of which can induce the symptomocomplex, characteristic of Parkinson’s disease by entering the brain through hematoencephalic barrier.
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