Gut Microbiota and Dysbiosis in Alzheimer's Disease: Implications for Pathogenesis and Treatment

被引:332
作者
Liu, Shan [1 ]
Gao, Jiguo [1 ]
Zhu, Mingqin [1 ,2 ,3 ,4 ]
Liu, Kangding [1 ]
Zhang, Hong-Liang [5 ]
机构
[1] Jilin Univ, Dept Neurol, First Hosp Jilin Univ, Xinmin St 71, Changchun 130021, Peoples R China
[2] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA
[3] Mayo Clin, Dept Neurol, Rochester, MN USA
[4] Mayo Clin, Dept Immunol, Rochester, MN USA
[5] Natl Nat Sci Fdn China, Dept Life Sci, Shuangqing Rd 83, Beijing 100085, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; Gut microbiota; Microbiota-gut-brain axis; Gut dysbiosis; TRANSGENIC MICE CORRELATE; TRAUMATIC BRAIN-INJURY; INTESTINAL MICROBIOTA; MEDITERRANEAN DIET; MOUSE MODEL; BILE-ACIDS; IMMUNE; HEALTH; EXPRESSION; BEHAVIOR;
D O I
10.1007/s12035-020-02073-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term "microbiota-gut-brain axis" from "gut-brain axis" underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer's disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.
引用
收藏
页码:5026 / 5043
页数:18
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