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Article

Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid β-Mediated Neurotoxicity

1
Beijing Key Laboratory of Bioactive Substances and Functional Foods, Beijing Union University, Beijing 100191, China
2
College of Life Sciences, Capital Normal University, Beijing 100048, China
3
Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, Beijing 100191, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Vassilios Roussis
Int. J. Mol. Sci. 2015, 16(5), 10526-10536; https://doi.org/10.3390/ijms160510526
Received: 6 March 2015 / Revised: 19 April 2015 / Accepted: 3 May 2015 / Published: 8 May 2015
(This article belongs to the Special Issue Bioactivity of Marine Natural Products)
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. View Full-Text
Keywords: Alzheimer’s disease; amyloid-β peptide; chitosan oligosaccharides; aggregation; neurotoxicity Alzheimer’s disease; amyloid-β peptide; chitosan oligosaccharides; aggregation; neurotoxicity
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MDPI and ACS Style

Dai, X.; Hou, W.; Sun, Y.; Gao, Z.; Zhu, S.; Jiang, Z. Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid β-Mediated Neurotoxicity. Int. J. Mol. Sci. 2015, 16, 10526-10536. https://doi.org/10.3390/ijms160510526

AMA Style

Dai X, Hou W, Sun Y, Gao Z, Zhu S, Jiang Z. Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid β-Mediated Neurotoxicity. International Journal of Molecular Sciences. 2015; 16(5):10526-10536. https://doi.org/10.3390/ijms160510526

Chicago/Turabian Style

Dai, Xueling, Wanqi Hou, Yaxuan Sun, Zhaolan Gao, Shigong Zhu, and Zhaofeng Jiang. 2015. "Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid β-Mediated Neurotoxicity" International Journal of Molecular Sciences 16, no. 5: 10526-10536. https://doi.org/10.3390/ijms160510526

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