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10.3390/ijms160510526 http://scihub22266oqcxt.onion/10.3390/ijms160510526 C4463660!4463660 !26006224     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26006224 &cmd=llinks): Failed to open stream: HTTP request failed! 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Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid ?-Mediated Neurotoxicity |pdf=|usr=}}{{26006224 }} gab.com Text Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid -Mediated Neurotoxicity JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=26006224 #FOAvip 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. Twit Text FOAVip Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid -Mediated Neurotoxicity ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=26006224 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26006224 #FOAvip English Wikipedia <ref>{{Cite pmid|26006224 }}</ref> 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 PMID26006224 show 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. |Amyloid beta-Peptides/antagonists & inhibitors/*metabolism/ultrastructure [MESH] |Animals [MESH] |Cell Survival/drug effects [MESH] |Cells, Cultured [MESH] |Chitosan/analogs & derivatives/*pharmacology [MESH] |Neurons/*drug effects/metabolism/*pathology [MESH] |Neuroprotective Agents/chemistry/*pharmacology [MESH] |Oligosaccharides/chemistry/*pharmacology [MESH] |Peptide Fragments/antagonists & inhibitors/*metabolism/ultrastructure [MESH] |Protein Aggregates/drug effects [MESH] |Protein Aggregation, Pathological/drug therapy/metabolism/pathology [MESH] |Rats [MESH]Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate A(epmc).pdf DeepDyve Pubget Overpricing