Inflammatory bowel disease and Parkinson's disease: common pathophysiological links

被引:114
作者
Lee, Ho-Su [1 ,2 ]
Lobbestael, Evy [3 ]
Vermeire, Severine [4 ,5 ]
Sabino, Joao [4 ,5 ]
Cleynen, Isabelle [1 ]
机构
[1] Katholieke Univ Leuven, Dept Human Genet, B-3000 Leuven, Belgium
[2] Univ Ulsan, Dept Biochem & Mol Biol, Coll Med, Seoul, South Korea
[3] Katholieke Univ Leuven, Lab Neurobiol & Gene Therapy, Leuven, Belgium
[4] Katholieke Univ Leuven, Dept Chron Dis Metab & Ageing, Leuven, Belgium
[5] Katholieke Univ Leuven, Univ Hosp Leuven, Dept Gastroenterol & Hepatol, Leuven, Belgium
基金
新加坡国家研究基金会;
关键词
ALPHA-SYNUCLEIN; GUT MICROBIOTA; LRRK2; G2019S; RISK; ASSOCIATION; STRESS; DEGRADATION; DYSFUNCTION; IMPAIRMENT; PREVALENCE;
D O I
10.1136/gutjnl-2020-322429
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:408 / 417
页数:10
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