Fig. 5

AAV2/8-APN^Tri treatment improve memory functions and reduces dystrophic neurites in the 5xFAD mice. A The escape latency of different treatment group in the visible platform of Morris water maze (MWM) test. (n = 9 mice for wildtype and n = 11 for both AAV-treated groups). B The escape latency in 5-day sessions performed by different treatment group in MWM test. (n = 9 mice for wildtype and n = 11 for both AAV-treated groups). C Representative tracks of different treatment groups in the hidden sessions (H1, H3 & H5). D Probe test indicates the percentage of time spent in the target quadrant (platform location) by different mouse treatment groups. (n = 9 mice for wildtype and n = 11 for both AAV-treated groups). E Representative images of co-staining of Aβ and Lamp1 in the cortex and hippocampus of AAV2/8-GFP-treated (n = 6), and AAV2/8-APN^Tri-treated 5xFAD (n = 6) (Total 780 plaques were analyzed; Magnification: 10 × 40; Scale bar: 10μm). F, G Quantification of total dystrophic volume represented by Lamp1 staining surrounding the compact Aβ and filamentous Aβ. Data were presented as the mean ± s.e.m. *p < 0.05; **p < 0.01; ***p < 0.001. Statistical analysis of MWM tests (A, B) was analyzed with two-way ANOVA followed by Bonferroni’s post hoc test. Statistical analysis in (D) was performed by one-way ANOVA followed with Bonferroni’s post hoc comparison tests and in (F, G) were performed by unpaired t test.