Cited by 153Gut microbiota and healthAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Inflammatory pathways in Alzheimer’s disease mediated by gut microbiota

Qian, Xiao-hang, Song, Xiao-xuan, Liu, Xiao-li, Chen, Sheng-di, Tang, Hui-dong·2021·Ageing Research Reviews

Abstract

In the past decade, numerous studies have demonstrated the close relationship between gut microbiota and the occurrence and development of Alzheimer's disease (AD). However, the specific mechanism is still unclear. Both the neuroinflammation and systemic inflammation serve as the key hubs to accelerate the process of AD by promoting pathology and damaging neuron. What's more, the gut microbiota is also crucial for the regulation of inflammation. Therefore, this review focused on the role of gut microbiota in AD through inflammatory pathways. Firstly, this review summarized the relationship and interaction among gut microbiota, inflammation, and AD. Secondly, the direct and indirect regulatory effects of gut microbiota on AD through inflammatory pathways were described. These effects were mainly mediated by the component of the gut microbiota (lipopolysaccharides (LPS) and amyloid peptides), the metabolites of bacteria (short-chain fatty acids, branched amino acids, and neurotransmitters) and functional by-products (bile acids). In addition, potential treatments (fecal microbiota transplantation, antibiotics, probiotics, prebiotics, and dietary interventions) for AD were also discussed through these mechanisms. Finally, according to the current research status, the key problems to be solved in the future studies were proposed.

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Crossref · 10.1016/j.arr.2021.101317

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  • Various pathological factors, such as Aβ plaques, pro-inflammatory cytokines, and oxidative stress, activate microglia, leading to release of pro-inflammatory mediators that exacerbate neurotoxicity.

    “This hypothesis posits that various pathological factors, such as Aβ plaques, pro-inflammatory cytokines, and oxidative stress, activate microglia, the central nervous system’s innate immune cells. Upon activation, microglia undergo morphological changes and initiate a variety of inflammatory responses, which can lead to the release of pro-inflammatory mediators that exacerbate neurotoxicity.”
  • The inflammatory hypothesis suggests that chronic neuroinflammation plays a significant role in the pathogenesis of AD.

    “The inflammatory hypothesis suggests that chronic neuroinflammation plays a significant role in the pathogenesis of AD.”
  • Persistent activation of microglia may result in failure to resolve inflammation, contributing to neuronal damage and cognitive decline associated with AD.

    “The persistent activation of microglia may result in a failure to resolve inflammation, contributing to neuronal damage and the cognitive decline associated with AD [15,16].”

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Authors
Qian, X.-H., Song, X.-X., Liu, X.-L., Chen, S.-D., & Tang, H.-D.
Venue
Ageing Research Reviews
Publisher
Elsevier BV
Published
2021-07
Volume
68
Pages
101317
ISSN
1568-1637 (ISSN-L)
OpenAlex
W3134448216
Cited by
153
References
209
Citations by year
2026: 12 · 2025: 31 · 2024: 35 · 2023: 40 · 2022: 28 · 2021: 7
FWCI
2.89
Type
journal article
Language
en
Open access
closed
Locations
  • Ageing Research Reviews (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, gut microbiota, neuroinflammation, systemic inflammation, lipopolysaccharide, amyloid peptides, short-chain fatty acids, branched-chain amino acids, neurotransmitters, bile acids, fecal microbiota transplantation, probiotics, prebiotics, dietary intervention, antibiotics
MeSH terms
Gastrointestinal Microbiome, Fecal Microbiota Transplantation, Alzheimer Disease, Amyloid, Humans, Probiotics

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