Gut dysbiosis in stroke and its implications on Alzheimer's disease-like cognitive dysfunction.
Gut dysbiosis in stroke and its implications on Alzheimer's disease-like cognitive dysfunction.
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DOI：
10.1111/cns.13613
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发表时间：
2021-05
影响因子：
5.5
通讯作者：
Borlongan CV
中科院分区：
文献类型：
--
作者：
Cho J;Park YJ;Gonzales-Portillo B;Saft M;Cozene B;Sadanandan N;Borlongan CV
各种神经疾病，如中风和阿尔茨海默病(AD)，涉及神经炎性反应。肠道-脑轴的出现加强了我们对神经系统疾病进展和继发性细胞死亡的理解。肠道微生物群，特别是那些与炎症相关的微生物群，可能反映大脑和肠道的生态失调，从而为利用炎性微生物群作为生物标志物和治疗靶点提供了可能性。肠道-脑轴可能是疾病病理的一个促成因素，并为神经疾病的治疗提供基于细胞的再生医学的创新方法。在回顾中风和阿尔茨海默病的发病机制时，我们还讨论了肠道微生物区系对认知功能减退和脑病理的影响。尽管两种疾病的原代细胞死亡的潜在机制明显不同，但两者都可能与肠道微生物功能障碍有关，这是每种疾病特有的一种相应的异常。针对加重疾病症状的外周细胞死亡途径，例如由肠道引起的那些，再加上传统的中枢治疗方法，可能会改善中风和AD的预后。肠道微生物区系和中风。一种潜在的中风治疗方法包括通过益生元和益生菌改变肠道微生物区系，触发治疗性代谢物(即抗炎因子)的产生，从而可能隔离与中风相关的继发性细胞死亡。
Various neurological disorders, such as stroke and Alzheimer's disease (AD), involve neuroinflammatory responses. The advent of the gut‐brain axis enhances our understanding of neurological disease progression and secondary cell death. Gut microbiomes, especially those associated with inflammation, may reflect the dysbiosis of both the brain and the gut, opening the possibility to utilize inflammatory microbiomes as biomarkers and therapeutic targets. The gut‐brain axis may serve as a contributing factor to disease pathology and offer innovative approaches in cell‐based regenerative medicine for the treatment of neurological diseases. In reviewing the pathogenesis of stroke and AD, we also discuss the effects of gut microbiota on cognitive decline and brain pathology. Although the underlying mechanism of primary cell death from either disease is clearly distinct, both may be linked to gut‐microbial dysfunction as a consequential aberration that is unique to each disease. Targeting peripheral cell death pathways that exacerbate disease symptoms, such as those arising from the gut, coupled with conventional central therapeutic approach, may improve stroke and AD outcomes. Gut microbiota and stroke. A potential stroke therapy involves modification of the gut microbiota via prebiotics and probiotics, triggering the production of therapeutic metabolites (i.e., anti‐inflammatory factors) that may sequester the secondary cell death associated with stroke.
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影响因子：
82.9
作者：
Benakis C;Brea D;Caballero S;Faraco G;Moore J;Murphy M;Sita G;Racchumi G;Ling L;Pamer EG;Iadecola C;Anrather J
通讯作者：
Anrather J
多重分析物测定以表征不同的痴呆症：脑抑制后和其他痴呆症中的脑炎症细胞因子。
影响因子：
4.2
作者：
Chen A;Oakley AE;Monteiro M;Tuomela K;Allan LM;Mukaetova-Ladinska EB;O'Brien JT;Kalaria RN
通讯作者：
Kalaria RN
影响因子：
4.6
作者：
Cheemalapati SV;Winskas J;Wang H;Konnaiyan K;Zhdanov A;Roth A;Adapa SR;Deonarine A;Noble M;Das T;Gatenby R;Westerheide SD;Jiang RH;Pyayt A
通讯作者：
Pyayt A
影响因子：
6.1
作者：
Castelli V;d'Angelo M;Quintiliani M;Benedetti E;Cifone MG;Cimini A
通讯作者：
Cimini A
影响因子：
6.3
作者：
Chi, Laiting;Du, Kairong;Li, Wenzhi
通讯作者：
Li, Wenzhi