Figure 7. Nasal administration of IFNγ accelerates Aβ deposition in the brains of APP/PS1 mice by inducing the expression of BACE-1 and PS2.
IFNγ (10 ng/20 μl/d) was nasally administered to 3-months-old WT mice for 7 days (A–C). In select experiments, n2a cells were treated with IFNγ (10 ng/ml) for 24 h before extracting total mRNA and protein (D,E). In separate experiments, 3-months-old APP/PS1 mice was nasally administered with IFNγ (10 ng/20 μl/d) for 3 or 6 months before determining the Aβ deposition in APs (F–I). The protein and mRNA expression of BACE-1, PS1 and PS2 were determined by western blot and qRT-PCR (A,D). Total amounts of β-actin and GAPDH served as an internal control. The production of sAPPα, sAPPβ and Aβ1–42 was determined by western blot and Aβ1–42 enzyme immunoassay kits (B,E). Total amounts of β-actin and protein served as an internal control. The immunoactivity of Aβ was determined by an immunohistochemistry assay (C,F,G). APs/field in cerebral cortex and hippocampus of APP/PS1 mice were analyzed by counting the number of APs in the images of immunohistochemistry assay (H,I). The data represent the means ± S.E. of atleast three independent experiments. *p < 0.05; **p < 0.01 and ***p < 0.001 with respect to vehicle-treated controls.