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What role does inflammation play in the development of Parkinson's disease?

Correlation between parkinson's disease and inflammation in the human body.

Author: Akhmetova Aigerim 

Editor: Merentsova Anastasia 

 

 

According to numerous data, there is a connection between the development of Parkinson's disease and inflammatory processes in the human body. An increase in pro-inflammatory cytokines in blood serum and CSF samples was noted in patients with Parkinson's disease. Cytokines are biologically active factors that are released in response to external influences. This study correlates with epidemiological observations of the effective use of anti-inflammatory drugs to reduce the risk of Parkinson's disease. 

 

According to empirical studies in mouse models conducted at the Bethesda National Institutes of Health (Maryland, USA), there was a direct contribution of neuroinflammation to the Parkinson's disease phenotype associated with mutations in the PRKN and PINK1 genes. Assuming that neuroinflammation causes neurodegeneration in patients with PRKN or PINK1 mutations, targeted anti-inflammatory treatment may be a strategy for slowing the progression of the disease in this group of individuals. 

 

The question of the origin of inflammation remains unclear: from peripheral tissues or from the central nervous system. If the source of the inflammatory process is the central nervous system, then additional research is needed to find an answer to the question: does the observed inflammation cause the loss of dopaminergic neurons (characteristic of the disease) as a primary event or is it secondary - a consequence of neurodegeneration. In any case, there is evidence that cytokines, such as interleukin-6 (IL6), cross the blood-brain barrier and are transported from brain tissue to blood and vice versa. According to the authors of the work, this study can serve as a "starting point" for the search for the most effective therapy, as well as preventive measures for Parkinson's disease. 

 

Source: https://pubmed.ncbi.nlm.nih.gov/33029617/ 

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