Fig. 6

AAV2/8-APN^Tri treatment reduces amyloid pathology and microglia activation in the 5xFAD mice. A Immunohistochemistry analysis of Aβ (4G8; brown) in the hippocampus and cerebral cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (n = 6 mice for each experimental group) (Magnification: 10 × 10; Scale bar: 50μm). B Quantitative analysis of the Aβ loading and number of Aβ deposits in the hippocampus and cortex. C, D ELISA analysis of Aβ₄₂ and Aβ₄₀ levels in the hippocampus and the frontal cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (n = 5-6 mice for each experimental group). E Iba1 (red) and thioflavin S (green) double-immunofluorescent staining in the hippocampus of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (n = 6 mice for each experimental group) (Magnification: 10 × 10; Scale bar: 50μm). F Quantitative analysis of the Aβ loading in the hippocampus of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. G Relative intensity of Iba1 in the hippocampus of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. Data were presented as the mean ± s.e.m. n.s. not significant; *p < 0.05; **p < 0.01; ***p < 0.001. Statistical analysis was performed by unpaired t tests.