ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Pathological or preventative? Amyloid-β as an effector of innate immunity.Infection and immunity · 2026Review
- Bidirectional relationship between the biofilm ofMicrobiology spectrum · 2026Article
- Infection-driven gut dysbiosis and epigenetic programming of microglia: toward a systems level framework linking microbial metabolites, neuroinflammation, synaptic dysfunction, and probiotic modulation.Frontiers in cellular and infection microbiology · 2026Review
- The Importance of Being Imperfect: Structure and Function of Bacterial Amyloid.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Microbiota-Gut-Brain Axis in Neurodegenerative Diseases: The Role of Bacterial Amyloids.Cellular and molecular gastroenterology and hepatology · 2026Review
- Artificial intelligence empowers gut microbiota research in neurodegenerative diseases molecular mechanisms and precision therapy.iScience · 2025Review
- Photochemically synthesized gold nanoparticles conjugated with Boswellic acid inhibit alpha synuclein aggregation and delay fibrillation kinetics.Scientific reports · 2025Article
- Lifelong partners: Gut microbiota-immune cell interactions from infancy to old age.Mucosal immunology · 2025Review
- Shattering the Amyloid Illusion: The Microbial Enigma of Alzheimer's Disease Pathogenesis-From Gut Microbiota and Viruses to Brain Biofilms.Microorganisms · 2025Review
- Helicobacter pylori outer membrane vesicles directly promote Aβ aggregation and enhance Aβ toxicity in APP/PS1 mice.Communications biology · 2024Article
- Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
Abstract
Alzheimer's disease (AD) is a leading form of dementia where the presence of extra-neuronal plaques of Amyloid-β (Aβ) is a pathological hallmark. However, Aβ peptide is also observed in the intestinal tissues of AD patients and animal models. In this study, it is reported that Aβ monomers can target and disintegrate microbial amyloids of FapC and CsgA formed by opportunistic gut pathogens, Pseudomonas aeruginosa and Escherichia coli, explaining a potential role of Aβ in the gut-brain axis. Employing a zebrafish-based transparent in vivo system and whole-mount live-imaging, Aβ is observed to diffuse into the vasculature and subsequently localize with FapC or CsgA fibrils that were injected into the tail muscles of the fish. FapC aggregates, produced after Aβ treatment (Faβ), present selective toxicity to SH-SY5Y neuronal cells while the intestinal Caco-2 cells are shown to phagocytose Faβ in a non-toxic cellular process. After remodeling by Aβ, microbial fibrils lose their native function of cell adhesion with intestinal Caco-2 cells and Aβ dissolves and detaches the microbial fibrils already attached to the cell membrane. Taken together, this study strongly indicates an anti-biofilm role for Aβ monomers that can help aid in the future development of selective anti-Alzheimer's and anti-infective medicine.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.