Diet Patterns, the Gut Microbiome, and Alzheimer's Disease.

A. McGrattan, C. Stewart, A. Cassidy, J. Woodside, C. McEvoy
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引用次数: 7

Abstract

Given the complex bidirectional communication system that exists between the gut microbiome and the brain, there is growing interest in the gut microbiome as a novel and potentially modifiable risk factor for Alzheimer's disease (AD). Gut dysbiosis has been implicated in the pathogenesis and progression of AD by initiating and prolonging neuroinflammatory processes. The metabolites of gut microbiota appear to be critical in the mechanism of the gut-brain axis. Gut microbiota metabolites, such as trimethylamine-n-oxide, lipopolysaccharide, and short chain fatty acids, are suggested to mediate systemic inflammation and intracerebral amyloidosis via endothelial dysfunction. Emerging data suggest that the fungal microbiota (mycobiome) may also influence AD pathology. Importantly,  60% of variation in the gut microbiome is attributable to diet, therefore modulating the gut microbiome through dietary means could be an effective approach to reduce AD risk. Given that people do not eat isolated nutrients and instead consume a diverse range of foods and combinations of nutrients that are likely to be interactive, studying the effects of whole diets provides the opportunity to account for the interactions between different nutrients. Thus, dietary patterns may be more predictive of real-life effect on gut microbiome and AD risk than foods or nutrients in isolation. Accumulating evidence from experimental and animal studies also show potential effects of gut microbiome on AD pathogenesis. However, data from human dietary interventions are lacking. Well-designed intervention studies are needed in diverse populations to determine the influence of diet on gut microbiome and inform the development of effective dietary strategies for prevention of AD.
饮食模式,肠道微生物群和阿尔茨海默病。
鉴于肠道微生物群和大脑之间存在复杂的双向通信系统,肠道微生物群作为阿尔茨海默病(AD)的一种新的、潜在的可改变的危险因素越来越受到关注。肠道生态失调通过启动和延长神经炎症过程与阿尔茨海默病的发病和进展有关。肠道微生物群的代谢物似乎在肠脑轴的机制中至关重要。肠道微生物代谢物,如三甲胺-n-氧化物、脂多糖和短链脂肪酸,被认为通过内皮功能障碍介导全身炎症和脑内淀粉样变性。新出现的数据表明,真菌微生物群(mycobiome)也可能影响AD的病理。重要的是,60%的肠道微生物组变化可归因于饮食,因此通过饮食调节肠道微生物组可能是降低AD风险的有效方法。考虑到人们不吃孤立的营养物质,而是吃各种各样的食物和可能相互作用的营养物质的组合,研究整体饮食的影响提供了解释不同营养物质之间相互作用的机会。因此,饮食模式可能比单独的食物或营养素更能预测肠道微生物群和AD风险的实际影响。来自实验和动物研究的越来越多的证据也表明肠道微生物群对阿尔茨海默病发病机制的潜在影响。然而,缺乏人类饮食干预的数据。需要在不同人群中进行精心设计的干预研究,以确定饮食对肠道微生物组的影响,并为制定预防AD的有效饮食策略提供信息。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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