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Intestinal alterations in patients with Parkinson’s disease

Presented by
Dr Gabriele Bellini, University of Pisa, Italy
EAN 2022

Patients with Parkinson’s disease (PD) can demonstrate mild intestinal inflammation, accompanied by an increase in faecal tumour necrosis factor (TNF), faecal IL-1beta, collagen fibres, and S100-expression. PD patients can also show an impairment of the intestinal epithelial barrier, expressed by an increase in acidic mucins, a decrease in Claudin-1-expression, and alterations in the microbiota.

PD is characterised by alpha-synuclein accumulation, changes in gut microbiota composition, impairment of the intestinal epithelial barrier (IEB), and enteric neurogenic/immune/inflammatory changes. “The intestinal system is not only impaired by PD, but can also be a culprit,” said Dr Gabriele Bellini (University of Pisa, Italy) [1]. An imbalance in neuro-immune, brain-gut axis could lead to neuroinflammation and intestinal dysmotility. Furthermore, gut microbiota alterations, frequently found in PD patients, could very well favour bacterial translocation with an increased intestinal permeability. This could result in enteric neuroinflammation which could favour the misfolding and aggregation of alpha-synuclein. Dr Bellini and his group therefore set up a study to evaluate:

  • Changes in faecal microbiota composition;
  • Changes in the intestinal mucosal barrier that are capable of altering intestinal permeability;
  • Alterations of inflammatory markers in plasma and stool.

Enrolled were 19 PD patients (14 men) and 19 healthy controls. They underwent motor and cognitive evaluations, laboratory (plasma and stool) evaluations, as well as morphological evaluations using colon biopsies: epithelial mucins, collagen fibres, Claudin-1 tight junction, and S-100-positive glial cells.

Looking at changes in faecal microbiota, PD patients had a significantly different alpha-diversity, which was not the case for beta-diversity. Butyricimonas, a short-chain fatty acid-producing bacterium that plays an important role in colonic T cell differentiation, was reduced. Morphological results in PD patients showed an increase in acidic mucin production and in collagen density, a reduced expression of Claudin-1, and an increase of S-100-positive glial cells. The endoscopic exam did not reveal a macroscopic inflammatory process. Compared with controls however, there were significantly higher levels of faecal IL-1beta (P<0.01) and of faecal TNF (P<0.05). Dr Bennini: “This allows for the hypothesis that PD patients have a mild form of intestinal inflammation.”

  1. Bellini G, et al. Intestinal histomorphological and molecular alterations in patients with Parkinson’s disease: results from a pilot study. OPR-059, EAN 2022, 25–28 April, Vienna, Austria.

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