Figure 4

Expression levels of APP, cleavage enzymes and fragments of APP in STZ-treated transgenic mouse brain. (A) RT-PCR analysis was performed to determine the levels of APP mRNA in APP/PS1 transgenic mouse brain. GAPDH was used as an internal reference gene. (B) There were no significant differences in expression levels of APP mRNA between in the STZ- and vehicle-treated transgenic mouse brain. (C) Immunoblotting showing the expression levels of APP695 in vehicle control and STZ-treated APP/PS1 transgenic mouse brain. β-actin was used as a loading control. (D) Administration of STZ significantly increased the expression level of APP695 in the transgenic mouse brain. (E) Immunoblotting showing the expression levels of ADAM10, BACE1, PS1 in transgenic mouse brain. β-actin was used as a loading control. (F) STZ treatment did not affect the expression level of ADAM10 protein. (G) STZ-induced insulin deficiency resulted in a marked increase in BACE1 protein in the transgenic mouse brain. (H) STZ treatment resulted in an increased level of PS1 protein, but the difference was not statistically significant, compared with the vehicle control. (I) Immunoblotting showing the expression levels of sAPPα, sAPPβ and CTFs in transgenic mouse brain. β-actin was used as a loading control. (J) STZ-induced insulin deficiency significantly reduced the levels of sAPPα. (K) STZ treatment resulted in a markedly increased level of sAPPβ in transgenic mouse brain. (L) STZ treatment significantly increased the level of CTFs. *p < 0.05, **p < 0.01 (n = 7).