ArticleNature communications2023
Bacteroides Fragilis in the gut microbiomes of Alzheimer's disease activates microglia and triggers pathogenesis in neuronal C/EBPβ transgenic mice.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 5 of them syntheses that pooled it.
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Who cites it
81 citing papers in PubMed, 5 syntheses or guidelines pooled it, 87 citations in OpenAlex.
- Leveraging artificial intelligence for analysis of the gut microbiome for dementia diagnosis: a scoping review and discussion.Frontiers in dementia · 2026Pooled it
- Pooled it
- C/EBPβ as a master regulator of inflammasome signaling in neurodegenerative diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Pooled it
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- The impact of physical exercise on neuroinflammation mechanism in Alzheimer's disease.Frontiers in aging neuroscience · 2024Pooled it
- Mucin-degrading gut bacteria: context-dependent roles in intestinal homeostasis and disease.Gut microbes · 2026Review
- The microbiota-proteostasis axis: implications in neurodegenerative diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- From Dysbiosis to Blood-Brain Barrier Disruption: The Metabolite-Mediated Gut-Brain Axis in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Targeting C/EBPβ/ Calbindin 1 pathway bolsters the neural resilience to tau pathology and improves tau-impaired episodic memory.Molecular psychiatry · 2026Article
- Review
- Prostaglandins: Key players in immunomodulation of the nervous system.Neural regeneration research · 2026Article
- Modulating the Gut-Microbiota-Brain Axis in Alzheimer's Disease: Therapeutic Potential of Nutritional and Metabolic Factors.CNS neuroscience & therapeutics · 2026Review
- Oxyberberine-nanoparticle attenuates the cognitive deficits in a transgenic mouse model of Alzheimer's disease via modulating gut microbiota through suppressing CXCL10/CXCR3 pathway.Acta pharmacologica Sinica · 2026Article
- Bidirectional communication between the gut microbiota and the central nervous system.Neural regeneration research · 2026Article
- Aspirin alleviates long-term high-fat diet-induced depressive-like behavior in male mice via suppressing arachidonic acid-mediated microglial activation and neuroinflammation.Molecular psychiatry · 2026Article
- Microbiota-Targeted Chitooligosaccharides Intervention Restores Glucose Homeostasis After Islet Cell Transplantation in Rapamycin-Treated Mice.Food science & nutrition · 2026Article
- Gut dysbiosis associated with neonatal respiratory distress syndrome and biological plausibility of disease-specific probiotic intervention: a translational study.Journal of translational medicine · 2026Article
- Fecal virome transplantation alleviates weaning stress-induced behavioral alterations and intestinal health by reshaping the gut microbiome.Scientific reports · 2026Article
- Gut-Heart Axis: Microbiome Involvement in Wild-Type Transthyretin Amyloidosis.International journal of molecular sciences · 2026Article
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Gut dysbiosis contributes to Alzheimer's disease (AD) pathogenesis, and Bacteroides strains are selectively elevated in AD gut microbiota. However, it remains unknown which Bacteroides species and how their metabolites trigger AD pathologies. Here we show that Bacteroides fragilis and their metabolites 12-hydroxy-heptadecatrienoic acid (12-HHTrE) and Prostaglandin E2 (PGE2) activate microglia and induce AD pathogenesis in neuronal C/EBPβ transgenic mice. Recolonization of antibiotics cocktail-pretreated Thy1-C/EBPβ transgenic mice with AD patient fecal samples elicits AD pathologies, associated with C/EBPβ/Asparaginyl endopeptidase (AEP) pathway upregulation, microglia activation, and cognitive disorders compared to mice receiving healthy donors' fecal microbiota transplantation (FMT). Microbial 16S rRNA sequencing analysis shows higher abundance of proinflammatory Bacteroides fragilis in AD-FMT mice. Active components characterization from the sera and brains of the transplanted mice revealed that both 12-HHTrE and PGE2 activate primary microglia, fitting with poly-unsaturated fatty acid (PUFA) metabolites enrichment identified by metabolomics. Strikingly, recolonization with live but not dead Bacteroides fragilis elicited AD pathologies in Thy1-C/EBPβ transgenic mice, so did 12-HHTrE or PGE2 treatment alone. Collectively, our findings support a causal role for Bacteroides fragilis and the PUFA metabolites in activating microglia and inducing AD pathologies in Thy1- C/EBPβ transgenic mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.