ArticleJournal of Alzheimer's disease : JAD2022
Bacterial Amyloid Curli Associated Gut Epithelial Neuroendocrine Activation Predominantly Observed in Alzheimer's Disease Mice with Central Amyloid-β Pathology.
Article in Journal of Alzheimer's disease : JAD, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Microbiota-Gut-Brain Axis in Neurodegenerative Diseases: The Role of Bacterial Amyloids.Cellular and molecular gastroenterology and hepatology · 2026Review
- Host-gut microbiota interactions in health and disease: mechanisms and intervention strategies.Frontiers in microbiology · 2026Review
- The Evolution of Functional Amyloids and Their Impact on Host-Microbe Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The Interplay of Inflammation and Gut-Microbiota Dysbiosis in Alzheimer's Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Stool-derived extracellular vesicles increase inflammasome signaling and regulate the gut-brain axis after stroke in Alzheimer's disease transgenic mice.Experimental neurology · 2025Article
- Bacterial Amyloids as Hubs for Nucleic Acid Interactions: Implications and Mechanisms.International journal of molecular sciences · 2025Review
- Linkage of circadian rhythm disruptions with Alzheimer's disease and therapeutic interventions.Acta pharmaceutica Sinica. B · 2025Review
- Effects of Prebiotic Phytocompound Administration in Gestational Diabetic Dams and Its Influence on Offspring Cognitive Outcomes.International journal of molecular sciences · 2025Article
- Advances in molecular mechanisms and therapeutic strategies for central nervous system diseases based on gut microbiota imbalance.Journal of advanced research · 2025Review
- Iron Homeostasis Dysregulation, Oro-Gastrointestinal Microbial Inflammatory Factors, and Alzheimer's Disease: A Narrative Review.Microorganisms · 2025Review
- Shattering the Amyloid Illusion: The Microbial Enigma of Alzheimer's Disease Pathogenesis-From Gut Microbiota and Viruses to Brain Biofilms.Microorganisms · 2025Review
- Gut microbial metabolism in Alzheimer's disease and related dementias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- Interconnections between the Gut Microbiome and Alzheimer's Disease: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2024Review
- The menace within: bacterial amyloids as a trigger for autoimmune and neurodegenerative diseases.Current opinion in microbiology · 2024Review
- Amyloid, Crohn's disease, and Alzheimer's disease - are they linked?Frontiers in cellular and infection microbiology · 2024Review
- Disease- and stage-specific alterations of the oral and fecal microbiota in Alzheimer's disease.PNAS nexus · 2024Article
- Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Common Signaling Pathways Involved in Alzheimer's Disease and Stroke: Two Faces of the Same Coin.Journal of Alzheimer's disease reports · 2023Review
- The potential of the gut microbiome for identifying Alzheimer's disease diagnostic biomarkers and future therapies.Frontiers in neuroscience · 2023Review
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSubstantial evidence from recent research suggests an influential and underappreciated force in Alzheimer's disease (AD) pathogenesis: the pathological signals originate from outside the brain. Pathogenic bacteria produce amyloid-like proteins "curli" that form biofilms and show functional similarities to human amyloid-β (Aβ). These proteins may contribute to neurological disease progression via signaling cascade from the gut to the brain.
objectiveWe propose that curli causes neuroendocrine activation from the gut to brain that promotes central Aβ pathology.
methodsPGP9.5 and TLR2 levels in response to curli in the lumen of Tg2576 AD mice were analyzed by immunohistochemical and qRT-PCR analysis. Western blot and human 3D in vitro enteroids culture systems were also used. 16S rRNA gene sequencing was used to investigate bacterial dysbiosis.
resultsWe found significant increase in bacterial-amyloid curli with elevated TLR2 at the mRNA level in the pre- and symptomatic Tg-AD gut compared to littermate WT controls. This data associates with increased gram-positive bacterial colonization in the ileum of the symptomatic AD mice. We found fundamental evidence for vagus nerve activation in response to bacterial curli. Neuroendocrine marker PGP9.5 was significantly elevated in the gut epithelium of symptomatic AD mice, and this was colocalized with increased TLR2 expression. Enteroids, 3D-human ileal mini-gut monolayer in vitro model system also revealed increase levels of TLR2 upon stimulation with purified bacterial curli fibrils.
conclusionThese findings reveal the importance of pathological changes within the gut-vagus-brain signaling in response to luminal bacterial amyloid that might play a vital role in central Aβ pathogenesis seen in the AD brain.
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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.