Implications of gut and oral microbiota in neuroinflammatory responses in Alzheimer's disease

被引:16
作者
Bello-Corral, Laura [1 ,2 ]
Alves-Gomes, Lisa [3 ]
Fernandez-Fernandez, Jesus Antonio [1 ,2 ]
Fernandez-Garcia, Daniel [1 ,2 ]
Casado-Verdejo, Ines [1 ,4 ]
Sanchez-Valdeon, Leticia [1 ,2 ,5 ]
机构
[1] Univ Leon, Hlth Res Nursing Grp GREIS, Leon 24071, Spain
[2] Univ Leon, Dept Nursing & Physiotherapy, Leon 24071, Spain
[3] Univ Minho, Nursing Sch, Braga, Portugal
[4] Univ Leon, Dept Nursing & Physiotherapy, Ponferrada 24401, Spain
[5] Univ Leon, Campus Vegazana, Leon 24071, Spain
关键词
Alzheimer 's; Gut microbiota; Oral microbiota; Dysbiosis; Neuroinflammation; NLRP3; MOUSE MODEL; PERIODONTITIS; PROBIOTICS; AXIS;
D O I
10.1016/j.lfs.2023.122132
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
A diverse and stable microbiota promotes a healthy state, nevertheless, an imbalance in gut or oral bacterial composition, called dysbiosis, can cause gastrointestinal disorders, systemic inflammatory states and oxidative stress, among others. Recently, gut and oral dysbiosis has been linked to Alzheimer's disease (AD), which is considered the most common form of dementia and a public health priority due to its high prevalence and incidence. The aim of this review is to highlight the implications of gut and oral microbiota in the neuro-inflammation characteristic of AD pathology and the subsequent cognitive impairment. It is a systematic review of the current literature obtained by searching the PubMed, Web of Science and Scopus databases. The char-acteristic intestinal dysbiosis in AD patients leads to increased permeability of the intestinal barrier and activates immune cells in the central nervous system due to translocation of microbiota-derived metabolites and/or bacteria into the circulation leading to increased neuroinflammation and neuronal loss, thus generating the cognitive impairment characteristic of AD. The presence in the central nervous system of Porphyromonas gingivalis can cause an increased neuroinflammation and beta-amyloid peptide accumulation.
引用
收藏
页数:13
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