Fig. 4: C3N nanodots reduce Aβ deposition levels in the brain of APP/PS1 mice.
From: C3N nanodots inhibits Aβ peptides aggregation pathogenic path in Alzheimer’s disease
After six months of treatment, the whole brains of APP/PS1 mice treated with/without C3N nanodots were collected. a 6E10-labeled mice brain sections immunostained for Aβ (6E10) and showing the amyloid plaque levels of the WT and APP/PS1 mice under different conditions. The cortex and hippocampus regions are marked with yellow and blue dashed lines, respectively. Scale bar = 500 μm. b 6E10-positive area (n = 16 images over 3 mice per group, P < 0.0001) and c number of 6E10-positive plaques in different sizes (n = 6 images over 3 mice per group, P < 0.0001, P = 0.0041) in the APP/PS1 mice untreated/treated with C3N nanodots at the doses of 1 mg/kg/d, respectively. d, e Levels of Aβ42/Aβ40 peptides in SDS‒, FA‒, and TBS‒ soluble forms in the cortex, n = 3 mice per group, P = 0.0285, 0.0007, 0.0021, 0.0498, 0.0021, and 0.0011 respectively. Statistical comparisons were performed between the APP/PS1 and C3N nanodots-treated groups, according to the Student’s t-test (two-tailed). Data are presented as mean ± SD.*P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001 vs APP/PS1 group. Source data are provided as a Source data file.
