Bacterial Metabolites Mirror Altered Gut Microbiota Composition in Patients with Parkinson's Disease

J Parkinsons Dis. 2019;9(s2):S359-S370. doi: 10.3233/JPD-191780.

Abstract

Increasing evidence is supporting the hypothesis of α-synuclein pathology spreading from the gut to the brain although the exact etiology of Parkinson's disease (PD) is unknown. Furthermore, it has been proposed that inflammation, via the gastrointestinal tract, potentially through infections, may contribute to α-synuclein pathogenesis, and thus to the risk of developing PD. Recently, many studies have shown that PD patients have an altered microbiota composition compared to healthy controls. Inflammation in the gut might drive microbiota alterations or vice versa. Many studies focused on the detection of biomarkers of the etiology, onset, or progression of PD however also report metabolites from bacterial origin. These metabolites might reflect the bacterial composition and as well play an important role in immune homeostasis, ultimately affecting the progression of PD. Besides the bacterial metabolites, pharmacological treatment of PD might play a crucial role during the progression and thus treatment of the disease on the immune system. This review aims to establish a link between the microbial composition with the observed alterations of bacterial metabolites and their impact on the immune system, which could have influential effect in onset, progression and etiology of PD.

Keywords: Microbiota composition; Parkinson’s disease; bacterial metabolites; dopamine; immune modulators; levodopa.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Dysbiosis* / complications
  • Dysbiosis* / immunology
  • Dysbiosis* / metabolism
  • Dysbiosis* / microbiology
  • Gastrointestinal Microbiome*
  • Humans
  • Immune System* / immunology
  • Immune System* / metabolism
  • Immune System* / microbiology
  • Metabolome*
  • Parkinson Disease* / etiology
  • Parkinson Disease* / immunology
  • Parkinson Disease* / metabolism
  • Parkinson Disease* / microbiology