Abstract: The objective of the present study was to evaluate the protective effect of chitosan oligosaccharides
(COS) against cognitive deficits and oxidative damage induced by bilateral intrahippocampal (IH) injections of aggregated
amyloid-β1-42 (Aβ1–42) and to explore the underlying molecular mechanisms. Methods: Morris water maze test was performed
to observe the effect of COS on learning and memory in Alzheimer’s disease rats. At the same time, serum super oxide
dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and protein carbonyl and malondialdehyde (MDA)
contents were measured to evaluate the antioxidant capacity of COS. Results: Compared with the sham operation control
group, Aβ1–42-exposed rats showed remarkable memory impairment in ethological experiments. In contrast, compared with
the model group, the learning and memory functions of the COS-treated patients were improved. Besides, the rats in the
model group showed significantly lower serum activities of SOD and GSH-Px as well as significantly higher MDA and
protein carbonyl contents compared with the sham operation group. After the intervention of COS, the activities of SOD and
GSH-Px significantly were increased, and MDA and protein carbonyl contents were reduced significantly compared with
the model group. Conclusion: COS has potential therapeutic effect on Aβ1-42-induced cognitive impairment via inhibiting
oxidative stress.

Key words: chitosan oligosaccharide, β-amyloid protein, Alzheimer’s disease, oxidative stress