ArticleJournal of Alzheimer's disease : JAD2017
Evidence that the Human Innate Immune Peptide LL-37 may be a Binding Partner of Amyloid-β and Inhibitor of Fibril Assembly.
Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Pooled it
- Article
- The neuroimmune system and cognition.Nature immunology · 2026Review
- β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026Review
- Human cathelicidin peptide LL-37 compacts nucleic acids and alters neutrophil extracellular trap structure.Scientific reports · 2026Article
- The dysregulation of innate immunity by Porphyromonas gingivalis in the etiology of Alzheimer's disease.Journal of internal medicine · 2026Review
- Investigation of Regulation and Binding Patterns of the Human Cathelicidin Peptide LL-37 in Complexation with Nucleic Acids, and its Impact on Neutrophil Extracellular Traps.bioRxiv : the preprint server for biology · 2026Article
- Antimicrobial Peptides as Cross-Seeding Modulators at the Neurodegenerative-Infectious Interface.Research (Washington, D.C.) · 2026Review
- Rationally Designed Pentapeptide Analogs of Aβ19-23 Fragment as Potent Inhibitors of Aβ42 Aggregation.Molecules (Basel, Switzerland) · 2025Article
- Emerging roles of antimicrobial peptides in innate immunity, neuronal function, and neurodegeneration.Trends in neurosciences · 2024Review
- Between good and evil: Complexation of the human cathelicidin LL-37 with nucleic acids.Biophysical journal · 2024Review
- LL-37: Structures, Antimicrobial Activity, and Influence on Amyloid-Related Diseases.Biomolecules · 2024Review
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- A Review of the Common Neurodegenerative Disorders: Current Therapeutic Approaches and the Potential Role of Bioactive Peptides.Current protein & peptide science · 2024Review
- Selective protein aggregation confines and inhibits endotoxins in wounds: Linking host defense to amyloid formation.iScience · 2023Article
- A cationic amphiphilic peptide chaperone rescues AβRSC medicinal chemistry · 2023Article
- Repeated truncation of a modular antimicrobial peptide gene for neural context.PLoS genetics · 2022Article
- Antimicrobial Peptides (AMPs) in the Pathogenesis of Alzheimer's Disease: Implications for Diagnosis and Treatment.Antibiotics (Basel, Switzerland) · 2022Review
- Metagenomic and Functional Characterization of Two Chilean Kefir Beverages Reveals a Dairy Beverage Containing Active Enzymes, Short-Chain Fatty Acids, Microbial β-Amyloids, and Bio-Film Inhibitors.Foods (Basel, Switzerland) · 2022Article
- Regulatory Roles of Antimicrobial Peptides in the Nervous System: Implications for Neuronal Aging.Frontiers in cellular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdentifying physiologically relevant binding partners of amyloid-β (Aβ) that modulate in vivo fibril formation may yield new insights into Alzheimer's disease (AD) etiology. Human cathelicidin peptide, LL-37, is an innate immune effector and modulator, ubiquitous in human tissues and expressed in myriad cell types.
objectiveWe present in vitro experimental evidence and discuss findings supporting a novel hypothesis that LL-37 binds to Aβ42 and can modulate Aβ fibril formation.
methodsSpecific interactions between LL-37 and Aβ (with Aβ in different aggregation states, assessed by capillary electrophoresis) were demonstrated by surface plasmon resonance imaging (SPRi). Morphological and structural changes were investigated by transmission electron microscopy (TEM) and circular dichroism (CD) spectroscopy. Neuroinflammatory and cytotoxic effects of LL-37 alone, Aβ42 alone, and LL-37/Aβ complexes were evaluated in human microglia and neuroblastoma cell lines (SH-SY5Y).
resultsSPRi shows binding specificity between LL-37 and Aβ, while TEM shows that LL-37 inhibits Aβ42 fibril formation, particularly Aβ's ability to form long, straight fibrils characteristic of AD. CD reveals that LL-37 prevents Aβ42 from adopting its typical β-type secondary structure. Microglia-mediated toxicities of LL-37 and Aβ42 to neurons are greatly attenuated when the two peptides are co-incubated prior to addition. We discuss the complementary biophysical characteristics and AD-related biological activities of these two peptides.
conclusionBased on this body of evidence, we propose that LL-37 and Aβ42 may be natural binding partners, which implies that balanced (or unbalanced) spatiotemporal expression of the two peptides could impact AD initiation and progression.
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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.