@entity195 ( @entity195 ) is characterized by a large number of amyloid-b (Ab) deposits in the brain. Therefore, inhibiting @entity1423 or destabilizing preformed aggregates could be a promising therapeutic target for halting/slowing the progression of @entity195 . Chitosan oligosaccharides (COS) have previously been reported to exhibit antioxidant and neuroprotective effects. Recent study shows that COS could markedly decrease oligomeric Ab-induced @entity2359 and oxidative stress in @entity35 hippocampal neurons. However, the potential mechanism that COS reduce Ab-mediated @entity2359 remains unclear. In the present study, our findings from circular dichroism spectroscopy, transmission electron microscope and @entity7732 fluorescence assay suggested that COS act as an inhibitor of @entity1423 and this effect shows dose-dependency. Moreover, data from @entity7732 assay indicated that COS could significantly inhibit fibrils formation and disrupt preformed fibrils in a dose-dependent manner. Furthermore, the addition of COS attenuated Ab1-42-induced @entity2359 in @entity35 cortical neurons. Taken together, our results demonstrated for the first time that COS could inhibit Ab1-42 fibrils formation and disaggregate preformed fibrils, suggesting that COS may have anti-Ab fibrillogenesis and fibril-destabilizing properties. These findings highlight the potential role of COS as novel therapeutic agents for the prevention and treatment of @entity195 .

Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid b-Mediated XXXX .

@entity1423 :: ('MESH:D001791', 'Disease') :: ['Ab aggregation'] @entity195 :: ('MESH:D000544', 'Disease') :: ['AD', "Alzheimer's disease"] @entity35 :: ('10116', 'Species') :: ['rat'] @entity7732 :: ('MESH:C009462', 'Chemical') :: ['thioflavin T'] @entity2359 :: ('MESH:D020258', 'Disease') :: ['neurotoxicity']
@entity2359 :: (MESH:D020258,Disease) :: ['Neurotoxicity']
