Fig. 3: C3N nanodots rescues the cognition deficits of the APP/PS1 mice.
From: C3N nanodots inhibits Aβ peptides aggregation pathogenic path in Alzheimer’s disease
a, b Temporal changes in fluorescence intensity of C3N-Cy5.5 in the mouse brain following intraperitoneal injection (i.p.) at a relatively high dosage of 200 mg/kg to ensure optimal imaging. n = 3 mice per group. The P value represents the significant difference between the C3N nanodots-treated groups and the control group determined by one-way ANOVA (P = 0.0331, 0.0106, and 0.0003, respectively). c Time to reach hidden platform in Morris water maze of the WT and APP/PS1 mice treated without/with C3N nanodots (Two-way ANOVA for groups, P = 0.0396, 0.0019, and 0.0001). d The average swimming velocity of each group. e Representative swimming paths of escape latency in the fifth day. f Representative 60 s swimming paths of mice treated with various regimens to locate the escape platform after platform retrieval. g Accumulated time spent by mice treated with different regimens in all four quadrants. (P = 0.0016 and 0.0257). h Frequency of mice traversing the platform position after platform retrieval (P = 0.0024 and 0.0209). i The novel object recognition index (RI) of mice in each group mice (P = 0.0311 and 0.0168). j Representative paths of novel object recognition. All data are presented as mean ± SD. n.s. = no significants, n = 6 mice each group. Statistical significance was determined by one-way ANOVA in (g–i) with P < 0.05 considered statistically significant. *P < 0.05, **P < 0.01 and ***P < 0.001. Source data are provided as a Source data file.
