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Upregulation of enteric alpha-synuclein as a possible link between inflammatory bowel disease and Parkinson’s disease
  1. Pascal Derkinderen1,
  2. Wendy Noble2,
  3. Michel Neunlist1,
  4. Malvyne Rolli-Derkinderen1
  1. 1 Université de Nantes, Inserm, TENS, The Enteric Nervous System in Gut and Brain Diseases, IMAD, Nantes, France
  2. 2 Department of Basic and Clinical Neuroscience, King's College London, Institute of Psychiatry, Psychology and Neuroscience, London, London, UK
  1. Correspondence to Dr Pascal Derkinderen, University of Nantes, Nantes, France; derkinderenp{at}

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With interest, we read the review by Lee et al on the possible link between inflammatory bowel disease and Parkinson’s disease.1 After reviewing the recent evidence showing that inflammatory bowel disease and Parkinson’s disease are epidemiologically and genetically linked, the authors discuss the potential shared biological mechanisms between these two seemingly unrelated disorders. In this context, they briefly discuss the possible role of alpha-synuclein, a neuronal protein which is not only expressed in both the gut and brain but that is also a key component of Parkinson’s disease pathology.2 They summarise their literature analysis by saying that ‘Expression of α-synuclein in both the gut and brain of Parkinson’s disease patients represents a possible link between Parkinson’s disease and inflammatory bowel disease. However, the precise mechanism and role of enteric alpha-synuclein remain unknown’.1

Although we agree with the authors that the mechanisms by which gastrointestinal inflammation might …

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  • Contributors All authors contributed to the text. PD prepared the figure.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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