ArticleInternational journal of molecular sciences2015
Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid β-Mediated Neurotoxicity.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 52 citations in OpenAlex.
- Chitosan-Based Nose-to-Brain Drug Delivery for Management of Neurological Disorders: Intrinsic Neuroprotective Action and Carrier Capabilities.AAPS PharmSciTech · 2026Review
- Chitooligosaccharide and Its Derivatives: Potential Candidates as Food Additives and Bioactive Components.Foods (Basel, Switzerland) · 2023Review
- The Ability of Some Polysaccharides to Disaggregate Lysozyme Amyloid Fibrils and Renature the Protein.Pharmaceutics · 2023Article
- Polysaccharides: potential bioactive macromolecules for Alzheimer's disease.Frontiers in nutrition · 2023Review
- Molecular Mechanisms of Inhibition of Protein Amyloid Fibril Formation: Evidence and Perspectives Based on Kinetic Models.International journal of molecular sciences · 2022Review
- Potential Medical Applications of Chitooligosaccharides.Polymers · 2022Review
- Selenide Chitosan Sulfate Improved the Hepatocyte Activity, Growth Performance, and Anti-oxidation Capacity by Activating the Thioredoxin Reductase of Chickens In Vitro and In Vivo.Biological trace element research · 2022Article
- Synthetic phosphoethanolamine-modified oligosaccharides reveal the importance of glycan length and substitution in biofilm-inspired assemblies.Nature communications · 2022Article
- Chitin and Chitosan Derivatives as Biomaterial Resources for Biological and Biomedical Applications.Molecules (Basel, Switzerland) · 2020Review
- Use of Biodegradable, Chitosan-Based Nanoparticles in the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2020Review
- Chitosan Oligosaccharides Attenuate Amyloid Formation of hIAPP and Protect Pancreatic β-Cells from Cytotoxicity.Molecules (Basel, Switzerland) · 2020Article
- Icariside II inhibits lipopolysaccharide-induced inflammation and amyloid production in rat astrocytes by regulating IKK/IκB/NF-κB/BACE1 signaling pathway.Acta pharmacologica Sinica · 2020Article
- Crosstalk between chitosan and cell signaling pathways.Cellular and molecular life sciences : CMLS · 2019Review
- A Review of the Preparation, Analysis and Biological Functions of Chitooligosaccharide.International journal of molecular sciences · 2018Review
- Application of Chitosan, Chitooligosaccharide, and Their Derivatives in the Treatment of Alzheimer's Disease.Marine drugs · 2017Review
- An Overview of the Protective Effects of Chitosan and Acetylated Chitosan Oligosaccharides against Neuronal Disorders.Marine drugs · 2017Review
- Effects of a Standardized Phenolic-Enriched Maple Syrup Extract on β-Amyloid Aggregation, Neuroinflammation in Microglial and Neuronal Cells, and β-Amyloid Induced Neurotoxicity in Caenorhabditis elegans.Neurochemical research · 2016Article
- Vitamin k3 inhibits protein aggregation: Implication in the treatment of amyloid diseases.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by a large number of amyloid-β (Aβ) deposits in the brain. Therefore, inhibiting Aβ aggregation or destabilizing preformed aggregates could be a promising therapeutic target for halting/slowing the progression of AD. Chitosan oligosaccharides (COS) have previously been reported to exhibit antioxidant and neuroprotective effects. Recent study shows that COS could markedly decrease oligomeric Aβ-induced neurotoxicity and oxidative stress in rat hippocampal neurons. However, the potential mechanism that COS reduce Aβ-mediated neurotoxicity remains unclear. In the present study, our findings from circular dichroism spectroscopy, transmission electron microscope and thioflavin T fluorescence assay suggested that COS act as an inhibitor of Aβ aggregation and this effect shows dose-dependency. Moreover, data from thioflavin T assay indicated that COS could significantly inhibit fibrils formation and disrupt preformed fibrils in a dose-dependent manner. Furthermore, the addition of COS attenuated Aβ1-42-induced neurotoxicity in rat cortical neurons. Taken together, our results demonstrated for the first time that COS could inhibit Aβ1-42 fibrils formation and disaggregate preformed fibrils, suggesting that COS may have anti-Aβ fibrillogenesis and fibril-destabilizing properties. These findings highlight the potential role of COS as novel therapeutic agents for the prevention and treatment of AD.
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