Figure 5

STZ-induced insulin deficiency accelerates plaque formation and Aβ secretion in the APP/PS1 mouse brain. (A) Twenty weeks after STZ administration, the senile plaques were detected using Aβ immunohistochemistry, and Aβ levels were measured by ELISA in APP/PS1 transgenic mouse brain. The representative images of Aβ-immunostained brain sections from vehicle control and STZ-treated transgenic mice, respectively. Note the number and size of Aβ-positive plaques were increased in the cortex and hippocampus in STZ-treated mice, compared with the control. Scale bar = 100 μm. (B) STZ-induced insulin deficiency significantly increased the number of plaques in the cortex and hippocampus in the transgenic mouse. (C) Insulin deficiency led to an increase in the plaque burden in the cortex and hippocampus of the mouse brain. (D) The level of soluble Aβ1-42 was measured using an ELISA kit. STZ treatment significantly increased the levels of Aβ1-42 peptide in APP/PS1 transgenic mouse brain. * p < 0.05, ** p < 0.01 (n = 7).