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帕金森病和其他路易体病中的胃肠道疾病

Gastrointestinal disorders in Parkinson's disease and other Lewy body diseases.

作者信息

Hirayama Masaaki, Nishiwaki Hiroshi, Hamaguchi Tomonari, Ohno Kinji

机构信息

Department of Pathophysiological Laboratory Sciences, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Division of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Japan.

出版信息

NPJ Parkinsons Dis. 2023 May 5;9(1):71. doi: 10.1038/s41531-023-00511-2.

Abstract

Parkinson's disease (PD) is pathologically characterized by the abnormal accumulation of α-synuclein fibrils (Lewy bodies) in the substantia nigra and other brain regions, although the role of Lewy bodies remains elusive. Constipation usually precedes the motor symptoms in PD, which is in accordance with the notion that α-synuclein fibrils start from the intestinal neural plexus and ascend to the brain in at least half of PD patients. The gut microbiota is likely to be involved in intestinal and brain pathologies. Analyses of the gut microbiota in PD, rapid-eye-movement sleep behavior disorder, and dementia with Lewy bodies suggest three pathological pathways. First, Akkermansia, which is increased in PD, degrades the intestinal mucus layer and increases intestinal permeability, which triggers inflammation and oxidative stress in the intestinal neural plexus. Second, decreased short-chain fatty acids (SCFAs)-producing bacteria in PD reduce the number of regulatory T cells. Third, SCFAs also aggravate microglial activation with an unelucidated pathway. In addition, in dementia with Lewy bodies (DLB), which is another form of α-synucleinopathies, increased genera, Ruminococcus torques and Collinsella, may mitigate neuroinflammation in the substantia nigra by increasing secondary bile acids. Interventions for the gut microbiota and their metabolites may potentially delay or mitigate the development and progression of PD and other Lewy body diseases.

摘要

帕金森病(PD)的病理特征是黑质和其他脑区出现α-突触核蛋白纤维(路易小体)异常聚集,尽管路易小体的作用仍不清楚。便秘通常先于PD的运动症状出现,这与至少半数PD患者中α-突触核蛋白纤维从肠神经丛开始并向脑内上行的观点一致。肠道微生物群可能参与肠道和脑部病变。对PD、快速眼动睡眠行为障碍和路易体痴呆患者的肠道微生物群分析提示了三条病理途径。首先,在PD中增加的阿克曼氏菌会降解肠道黏液层并增加肠道通透性,从而引发肠神经丛的炎症和氧化应激。其次,PD中产生短链脂肪酸(SCFAs)的细菌减少会降低调节性T细胞的数量。第三,SCFAs还会通过一条不明途径加重小胶质细胞的激活。此外,在另一种α-突触核蛋白病——路易体痴呆(DLB)中,瘤胃球菌属和柯林斯菌属的增加可能通过增加次级胆汁酸来减轻黑质中的神经炎症。对肠道微生物群及其代谢产物的干预可能会潜在地延缓或减轻PD和其他路易体病的发生和发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc0f/10163029/8a62ea9c73a5/41531_2023_511_Fig1_HTML.jpg

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