Interlink between the gut microbiota and inflammation in the context of oxidative stress in Alzheimer’s disease progression

ABSTRACT

The microbiota-gut-brain axis is an important pathway of communication and may dynamically contribute to Alzheimer’s disease (AD) pathogenesis. Pathological commensal gut microbiota alterations, termed as dysbiosis, can influence intestinal permeability and break the blood–brain barrier which may trigger AD pathogenesis via redox signaling, neuronal, immune, and metabolic pathways. Dysbiosis increases the oxidative stress. Oxidants affect the innate immune system through recognizing microbial-derived pathogens by Toll-like receptors and initiating the inflammatory process. Most of the gut microbiome research work highlights the relationship between the gut microbiota and AD, but the contributory connection between precise bacteria and brain dysfunction in AD pathology cannot be fully demonstrated. Here, we summarize the current information of the fundamental connections between oxidative stress, inflammation, and gut dysbiosis in AD. This review emphasizes on the involvement of gut microbiota in the regulation of oxidative stress, inflammation, immune responses including central and peripheral cross-talk. It provides insights for novel preventative and therapeutic approaches in AD.

KEYWORDS:

• Microbiota-gut-brain axis
• gut microbiota
• dysbiosis
• oxidative stress
• inflammation
• Alzheimer’s disease

Acknowledgments

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Disclosure statement

No potential conflict of interest was reported by the author(s).

Author Contributions

T.K.D. and B.P.G. constructed the design and outlined the content. T.K.D. reviewed and analyzed the literatures, drafted the manuscript, and prepared the figures; B.P.G. obtained the funding, editing and supervised the writing of the review. All authors critically revised the manuscript. All authors have read and agreed to the published version of the manuscript.

Additional information

Funding

This was supported by the National Institutes of Health (NIA 5R01AG070934-03 to B.P.G)