The gut microbiome in Alzheimer’s disease: what we know and what remains to be explored
Open accessAbstract
Alzheimer’s disease (AD), the most common cause of dementia, results in a sustained decline in cognition. There are currently few effective disease modifying therapies for AD, but insights into the mechanisms that mediate the onset and progression of disease may lead to new, effective therapeutic strategies. Amyloid beta oligomers and plaques, tau aggregates, and neuroinflammation play a critical role in neurodegeneration and impact clinical AD progression. The upstream modulators of these pathological features have not been fully clarified, but recent evidence indicates that the gut microbiome (GMB) may have an influence on these features and therefore may influence AD progression in human patients. In this review, we summarize studies that have identified alterations in the GMB that correlate with pathophysiology in AD patients and AD mouse models. Additionally, we discuss findings with GMB manipulations in AD models and potential GMB-targeted therapeutics for AD. Lastly, we discuss diet, sleep, and exercise as potential modifiers of the relationship between the GMB and AD and conclude with future directions and recommendations for further studies of this topic.
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Gut microbiome alterations and intestinal barrier impairment have been observed in patients with MCI, AD, PD, and ALS.
“Gut microbiome alterations and intestinal barrier impairment have been observed in patients with MCI, AD, PD, and ALS patients.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [624]
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Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases
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Emerging diagnostics and therapeutics for Alzheimer disease
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“…fl ammatory response and the hyperphosphorylation of tau protein via activation of the GSK-3 β pathway, ultimately leading to cognitive impairment [104]. astrocytes and microglia, which in turn induces an inflammatory response and the hyperphosphorylation of tau protein via activation of the GSK-3…”
BackgroundChandra, S., Di Meco, A., Dodiya, H. B., Popovic, J., Cuddy, L. K., Weigle, I. Q., Zhang, X., Sadleir, K., Sisodia, S. S., & Vassar, R. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00635-2 · Cited by 58 · see citing works
Self-citation
- Authors
- Chandra, S., Sisodia, S. S., & Vassar, R. J.
- Affiliations
- Northwestern University (US)
- University of Chicago (US)
- Corresponding author
- Vassar, Robert J.
- Venue
- Molecular Neurodegeneration
- Published
- 2023-02-01
- Volume
- 18
- Issue
- 1
- Pages
- 9-9
- ISSN
- 1750-1326 (ISSN-L)
- PMC
- PMC9889249
- OpenAlex
- W4318680477
- Cited by
- 278
- References
- 228
- Citations by year
- 2026: 56 · 2025: 100 · 2024: 84 · 2023: 38
- FWCI
- 7.37
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Molecular Neurodegeneration (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Knowledge@UChicago (University of Chicago) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- University of Chicago (cc-by)
- Funders
- Good ventures foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, gut microbiota, amyloid-beta, tau aggregates, neuroinflammation, neurodegeneration, gut-brain axis, microbiota-based therapy, diet, sleep, physical activity, mouse models of Alzheimer's disease
- MeSH terms
- Gastrointestinal Microbiome, Alzheimer Disease, Animals, Cognition, Disease Models, Animal, Humans, Amyloid beta-Peptides, Mice
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