Abstract

While the pathogenesis of Parkinson's disease is not fully understood, there is increasing evidence that inflammatory responses in the brain are implicated in both disease initiation and progression. The inflammatory process in Parkinson's disease is, however, not limited to the brain but also involves the gastrointestinal tract. High amounts of cytokines and inflammatory markers are found in the colon of Parkinson's disease patients and there is now strong epidemiological and genetical evidence linking Parkinson's disease to inflammatory bowel diseases. Recent findings obtained in both experimental inflammatory bowel diseases and Parkinson's disease further support a bidirectional link between gastrointestinal inflammation and brain neurodegeneration. Altogether, these observations suggest a role for gastrointestinal inflammation in the initiation and progression of Parkinson's disease.

Highlights

  • While the pathogenesis of Parkinson’s disease is not fully understood, there is increasing evidence that inflammatory responses in the brain are implicated in both disease initiation and progression

  • While a small monocentric retrospective study did not observe any increased occurrence of Crohn’s disease (CD) in Parkinson’s disease (PD) patients [11], four large nationwide surveys showed that inflammatory bowel disease (IBD) patients had an increased risk of subsequent PD compared to controls [12,13,14,15]

  • After combining the data of these four studies, a recent meta-analysis showed that the overall risk of PD in IBD was significantly higher than controls, with a 28% and 30% increased risk of PD for CD and ulcerative colitis (UC), respectively [16]

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Summary

Introduction

While the pathogenesis of Parkinson’s disease is not fully understood, there is increasing evidence that inflammatory responses in the brain are implicated in both disease initiation and progression. We analyzed the expression levels of the main pro-inflammatory cytokines (tumor necrosis factor-𐀀, interferon-𐀀, interleukin-6 and interleukin-1𐀀) in colonic 4 biopsies from 19 PD patients and 14 age-matched healthy controls.

Results
Conclusion

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