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Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Int+J+Mol+Sci 2015 ; 16 (5): 10526-36 Nephropedia Template TP
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Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid ?-Mediated Neurotoxicity #MMPMID26006224
Dai X; Hou W; Sun Y; Gao Z; Zhu S; Jiang Z
Int J Mol Sci 2015[May]; 16 (5): 10526-36 PMID26006224show ga
Alzheimer?s disease (AD) is characterized by a large number of amyloid-? (A?) deposits in the brain. Therefore, inhibiting A? 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 A?-induced neurotoxicity and oxidative stress in rat hippocampal neurons. However, the potential mechanism that COS reduce A?-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 A? 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 A?1-42-induced neurotoxicity in rat cortical neurons. Taken together, our results demonstrated for the first time that COS could inhibit A?1-42 fibrils formation and disaggregate preformed fibrils, suggesting that COS may have anti-A? fibrillogenesis and fibril-destabilizing properties. These findings highlight the potential role of COS as novel therapeutic agents for the prevention and treatment of AD.