ArticleScience translational medicine2016
Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease.
Article in Science translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 556 papers.
What it found
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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.
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Who cites it
556 citing papers in PubMed, 955 citations in OpenAlex.
- Combined Effects ofInternational journal of molecular sciences · 2026Article
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- Pathological or preventative? Amyloid-β as an effector of innate immunity.Infection and immunity · 2026Review
- The γ-secretase complex: from discovery to a therapeutic target.RSC chemical biology · 2026Review
- A mechanistic framework linking the oral microbiome to Alzheimer's disease through neuroinflammation.Journal of Alzheimer's disease : JAD · 2026Review
- High reelin expression may explain why a subgroup of entorhinal cortex neurons functions as an initial nucleation site of Alzheimer's disease.PLoS computational biology · 2026Article
- Lung endothelial cytopathic tau is sufficient to impair long-term potentiation during infection.American journal of respiratory cell and molecular biology · 2026Article
- Chemokines in Alzheimer's Disease: Early Defence, Late Damage and the Impact of Sex and Infection.Basic & clinical pharmacology & toxicology · 2026Review
- Deep learning reveals antimicrobial peptides within prions.Nature microbiology · 2026Article
- Review
- Article
- Beyond association: A quantitative analysis of the infectious burden in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- TREM2 in neurodegeneration and diseases.Molecular psychiatry · 2026Review
- β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026Review
- Expansion Revealing of Pathology Resolves Nanostructures Associated with Inflammatory Phenotypes in COVID-19 Decedent Human Brain Tissue.bioRxiv : the preprint server for biology · 2026Article
- Protein Modifications and Quality Control System: Target for Alzheimer's Disease Therapy.International journal of molecular sciences · 2026Review
- Proteomic Analysis of Corpora Amylacea Extracted From Post-mortem Brain of MAiD-end-of-life Sporadic ALS Patients.Brain and behavior · 2026Article
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- Protection and Delivery of Phytochemicals from Passive Encapsulation to Guaranteed Self-Assembly Induced by Amyloid Template for Chronic Disease Prevention via Modulating Microbial-Host Crosstalk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Dual-functional self-assembled nanosystems with enhanced protease resistance: Promoting bacterial aggregation and immune activation for multidrug-resistant bacterial infection.Asian journal of pharmaceutical sciences · 2026Article
496 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The amyloid-β peptide (Aβ) is a key protein in Alzheimer's disease (AD) pathology. We previously reported in vitro evidence suggesting that Aβ is an antimicrobial peptide. We present in vivo data showing that Aβ expression protects against fungal and bacterial infections in mouse, nematode, and cell culture models of AD. We show that Aβ oligomerization, a behavior traditionally viewed as intrinsically pathological, may be necessary for the antimicrobial activities of the peptide. Collectively, our data are consistent with a model in which soluble Aβ oligomers first bind to microbial cell wall carbohydrates via a heparin-binding domain. Developing protofibrils inhibited pathogen adhesion to host cells. Propagating β-amyloid fibrils mediate agglutination and eventual entrapment of unatttached microbes. Consistent with our model, Salmonella Typhimurium bacterial infection of the brains of transgenic 5XFAD mice resulted in rapid seeding and accelerated β-amyloid deposition, which closely colocalized with the invading bacteria. Our findings raise the intriguing possibility that β-amyloid may play a protective role in innate immunity and infectious or sterile inflammatory stimuli may drive amyloidosis. These data suggest a dual protective/damaging role for Aβ, as has been described for other antimicrobial peptides.
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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.