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Updated: Jan 31, 2026

Oral Administration of Rotenone using a Gavage and Image Analysis of Alpha-synuclein Inclusions in the Enteric Nervous System
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Acute inflammation down-regulates alpha-synuclein expression in enteric neurons.

Alice Prigent1,2, Jacques Gonzales1,2, Tony Durand1

  • 1Inserm, U1235, Nantes, France.

Journal of Neurochemistry
|December 28, 2018
PubMed
Summary

Inflammation decreases alpha-synuclein expression in the enteric nervous system (ENS) via the p38 pathway. This finding offers new insights into Parkinson's disease (PD) development and the role of gastrointestinal inflammation.

Keywords:
LPSalpha-synucleincolitisenteric nervous systempro-inflammatory cytokines

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Area of Science:

  • Neuroscience
  • Gastroenterology
  • Immunology

Background:

  • Alpha-synuclein protein expression is linked to Parkinson's disease (PD).
  • Alpha-synuclein is found in both the central nervous system (CNS) and the enteric nervous system (ENS).
  • Gastrointestinal inflammation is increasingly recognized as a potential factor in PD development.

Purpose of the Study:

  • To investigate the impact of inflammation on alpha-synuclein expression in the ENS.
  • To explore the molecular mechanisms, specifically the p38 pathway, involved in inflammation-induced changes in alpha-synuclein expression.

Main Methods:

  • Primary cultures of rat ENS and CNS cells were treated with inflammatory stimuli (lipopolysaccharide, TNF-α/IL-1β).
  • Mice were subjected to dextran sulfate sodium (DSS)-induced colitis (acute and chronic models).
  • Alpha-synuclein expression levels were quantified using Western blot and qPCR; p38 pathway involvement was assessed using inhibitors.

Main Results:

  • Inflammatory stimuli (LPS, TNF-α/IL-1β) reduced alpha-synuclein expression in rat ENS cultures, an effect blocked by p38 inhibitors.
  • These inflammatory agents did not affect alpha-synuclein expression in rat CNS cultures or human erythroid leukemia cells.
  • Acute DSS-induced colitis in mice correlated with decreased colonic alpha-synuclein expression, while chronic colitis did not show this effect.

Conclusions:

  • Acute inflammatory insults down-regulate ENS alpha-synuclein expression through a p38-dependent pathway.
  • These findings contribute to understanding alpha-synuclein's role in the ENS in PD.
  • The study highlights the potential involvement of gastrointestinal inflammation in the pathogenesis of Parkinson's disease.