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Inflammatory bowel disease and Parkinson’s disease: common pathophysiological links
  1. Ho-Su Lee1,2,
  2. Evy Lobbestael3,
  3. Séverine Vermeire4,5,
  4. João Sabino4,5,
  5. Isabelle Cleynen1
  1. 1 Department of Human Genetics, KU Leuven, Leuven, Belgium
  2. 2 Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul, Republic of Korea
  3. 3 Laboratory for Neurobiology and Gene Therapy, KU Leuven, Leuven, Belgium
  4. 4 Department of Chronic diseases, Metabolism and Ageing, KU Leuven, Leuven, Belgium
  5. 5 Department of Gastroenterology and Hepatology, University Hospitals Leuven, KU Leuven, Leuven, Belgium
  1. Correspondence to Professor Isabelle Cleynen, Department of Human Genetics, KU Leuven, Leuven 3000, Belgium; isabelle.cleynen{at}


Inflammatory bowel disease and Parkinson’s disease are chronic progressive disorders that mainly affect different organs: the gut and brain, respectively. Accumulating evidence has suggested a bidirectional link between gastrointestinal inflammation and neurodegeneration, in accordance with the concept of the ‘gut–brain axis’. Moreover, recent population-based studies have shown that inflammatory bowel disease might increase the risk of Parkinson's disease. Although the precise mechanisms underlying gut–brain interactions remain elusive, some of the latest findings have begun to explain the link. Several genetic loci are shared between both disorders with a similar direction of effect on the risk of both diseases. The most interesting example is LRRK2 (leucine-rich repeat kinase 2), initially identified as a causal gene in Parkinson's disease, and recently also implicated in Crohn’s disease. In this review, we highlight recent findings on the link between these seemingly unrelated diseases with shared genetic susceptibility. We discuss supporting and conflicting data obtained from epidemiological and genetic studies along with remaining questions and concerns. In addition, we discuss possible biological links including the gut–brain axis, microbiota, autoimmunity, mitochondrial function and autophagy.

  • inflammatory bowel disease
  • IBD - genetics
  • epidemiology
  • IBD basic research
  • Parkinson's disease

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  • Twitter @hosu_lee, @ICleynen

  • H-SL and EL contributed equally.

  • Contributors H-SL and EL performed a systematic literature search. H-SL, EL and IC wrote the manuscript and created the table and figures. JS and SV provided intellectual input and critical revision of the manuscript. All authors have approved the final version of this article.

  • Funding H-SL was supported by a National Research Foundation of Korea (NRF) MRC grant funded by the Korean government (MSIT) (2018R1A5A2020732). EL is supported by the Research Foundation Flanders (FWO) (G0E1917N) and Michael J. Fox Foundation (17194).

  • Competing interests JS reports receiving speaker’s fees from Nestle Health Sciences, Abbvie and Takeda; receiving consultancy fees from Janssen. SV reports receiving speaker’s fees from AbbVie, Takeda, Genentech/Roche, Pfizer and Janssen; receiving consultancy fees from AbbVie, MSD, Takeda, Ferring, Genentech/Roche, Shire, Pfizer, Galapagos, Mundipharma, Hospira, Celgene, Second Genome, Progenity, Lilly, Arena, Gilead and Janssen; receiving financial support for research from MSD, Abbvie, Janssen and Pfizer.

  • Patient consent for publication Not required.

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