期刊
GUT
卷 70, 期 2, 页码 408-417出版社
BMJ PUBLISHING GROUP
DOI: 10.1136/gutjnl-2020-322429
关键词
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资金
- National Research Foundation of Korea (NRF) MRC - Korean government (MSIT) [2018R1A5A2020732]
- Research Foundation Flanders (FWO) [G0E1917N]
- Michael J. Fox Foundation [17194]
- National Research Foundation of Korea [2018R1A5A2020732] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Inflammatory bowel disease and Parkinson's disease have been shown to have a bidirectional link, with shared genetic loci such as LRRK2. Recent studies suggest that inflammatory bowel disease may increase the risk of developing Parkinson's disease. The underlying mechanisms of gut-brain interactions are still not fully understood, but recent findings are beginning to shed light on this connection.
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.
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