4.7 Review

Crosstalk between Gut and Brain in Alzheimer's Disease: The Role of Gut Microbiota Modulation Strategies

Journal

NUTRIENTS
Volume 13, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/nu13020690

Keywords

gut dysbiosis; microbial metabolites; diet; probiotics; neurodegenerative diseases

Funding

  1. Brain Korea (BK) 21 Plus Project - Korean Government, Republic of Korea [22A20153713433]

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The gut microbiota can influence brain immune homeostasis through the microbiota-gut-brain axis and play a key role in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). Modulating GM through diet, probiotics, or fecal microbiota transplantation may represent potential therapeutic strategies in treating AD.
The gut microbiota (GM) represents a diverse and dynamic population of microorganisms and about 100 trillion symbiotic microbial cells that dwell in the gastrointestinal tract. Studies suggest that the GM can influence the health of the host, and several factors can modify the GM composition, such as diet, drug intake, lifestyle, and geographical locations. Gut dysbiosis can affect brain immune homeostasis through the microbiota-gut-brain axis and can play a key role in the pathogenesis of neurodegenerative diseases, including dementia and Alzheimer's disease (AD). The relationship between gut dysbiosis and AD is still elusive, but emerging evidence suggests that it can enhance the secretion of lipopolysaccharides and amyloids that may disturb intestinal permeability and the blood-brain barrier. In addition, it can promote the hallmarks of AD, such as oxidative stress, neuroinflammation, amyloid-beta formation, insulin resistance, and ultimately the causation of neural death. Poor dietary habits and aging, along with inflammatory responses due to dysbiosis, may contribute to the pathogenesis of AD. Thus, GM modulation through diet, probiotics, or fecal microbiota transplantation could represent potential therapeutics in AD. In this review, we discuss the role of GM dysbiosis in AD and potential therapeutic strategies to modulate GM in AD.

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