Antibiotic-induced perturbations in gut microbial diversity influences neuro-inflammation and amyloidosis in a murine model of Alzheimer’s disease
Open accessAbstract
Severe amyloidosis and plaque-localized neuro-inflammation are key pathological features of Alzheimer’s disease (AD). In addition to astrocyte and microglial reactivity, emerging evidence suggests a role of gut microbiota in regulating innate immunity and influencing brain function. Here, we examine the role of the host microbiome in regulating amyloidosis in the APP SWE /PS1 ΔE9 mouse model of AD. We show that prolonged shifts in gut microbial composition and diversity induced by long-term broad-spectrum combinatorial antibiotic treatment regime decreases Aβ plaque deposition. We also show that levels of soluble Aβ are elevated and that levels of circulating cytokine and chemokine signatures are altered in this setting. Finally, we observe attenuated plaque-localised glial reactivity in these mice and significantly altered microglial morphology. These findings suggest the gut microbiota community diversity can regulate host innate immunity mechanisms that impact Aβ amyloidosis.
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Antibiotic-induced perturbations in gut microbial diversity influence neuroinflammation with altered microglial morphology.
“antibiotic-induced perturbations in gut microbial diversity influence neuroinflammation with altered microglial morphology (105–107).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [105]
Antibiotics can reduce Aβ deposition and plaque-associated glial reactivity in an AD mouse model.
“However, antibiotics can reduce Aβ deposition and plaque-associated glial reactivity in an AD mouse model [585].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [585]
Eliminating gut bacteria can reduce plaque load and microglial activation in an amyloid model of Alzheimer's disease in mice.
“Eliminating gut bacteria can reduce plaque load and microglial activation in an amyloid model of AD in mice [80].”
From The endotoxin hypothesis of neurodegeneration (2019) · cites this paper as [80]
In Aβ-mice, altering gut microbiota affects Aβ deposition and changes microglial reactivity and morphology through unknown mechanisms.
“In Aβ-mice, manipulating gut microbiota influences Aβ deposition and alters microglial reactivity and morphology by unknown mechanisms149.”
From Microglia in neurodegeneration (2018) · cites this paper as [149]
APP/PS1ΔE9 mice given high-dose antibiotics have reduced Aβ plaque load and size, increased soluble Aβ42, and fewer plaque-associated microglia and reactive astrocytes.
“Indeed, one study demonstrated that APP/PS1ΔE9 mice chronically administered a cocktail of high dose antibiotics to modulate microbiome composition had significantly reduced Aβ plaque load, reduced plaque size, increased soluble Aβ42 levels and reduced plaque-associated microglia and reactive astrocytes (Minter et al., 2016).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Minter et al., 2016
Perturbations in microbial diversity due to antimicrobials influence pro-inflammatory cytokine secretion in the CNS and alter microglial morphology.
“Perturbations in microbial diversity, secondary to antimicrobials, have been shown to influence pro-inflammatory cytokine secretion in the CNS and alter microglial morphology (268–270).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [268]
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- Authors
- Minter, M. R., Zhang, C., Leone, V., Ringus, D. L., Zhang, X., Oyler-Castrillo, P., Musch, M. W., Liao, F., Ward, J. F., Holtzman, D. M., Chang, E. B., Tanzi, R. E., & Sisodia, S. S.
- Affiliations
- University of Chicago (US)
- Massachusetts General Hospital (US)
- Washington University in St. Louis (US)
- Corresponding author
- Sisodia, Sangram S.
- ORCID
- Venue
- Scientific Reports
- Published
- 2016-07-21
- Volume
- 6
- Issue
- 1
- Pages
- 30028-30028
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4956742
- OpenAlex
- W2479642761
- Cited by
- 655
- References
- 56
- Citations by year
- 2026: 40 · 2025: 63 · 2024: 76 · 2023: 66 · 2022: 102 · 2021: 89 · 2020: 74 · 2019: 59 · 2018: 47 · 2017: 33 · 2016: 6
- FWCI
- 38.90
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- University of Chicago (DK42086)
- Cure Alzheimer's Fund
- National Institute of Diabetes and Digestive and Kidney Diseases (DK42086, P30DK042086)
- Argonne National Laboratory
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, gut microbiota, antibiotic-induced dysbiosis, amyloid plaques, neuroinflammation, APPswe/PS1ΔE9 mice, soluble amyloid-beta, microglial morphology, glial activation, innate immunity, cytokines and chemokines, gut-brain axis
- MeSH terms
- Gastrointestinal Microbiome, Alzheimer Disease, Amyloidosis, Animals, Anti-Bacterial Agents, Disease Models, Animal, Immunity, Innate, Inflammation, Mice, Dysbiosis
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