Abstract: Objective To examine the changes of Aβ expression and its related metabolic enzymes in the brains of AD and T2DM mice, so as to explore the possible mechanism of type 2 diabetes mellitus combined with AD. Methods Five-month-old APP/PS1 double transgenic mice, ob/ob mice and the wild-type control mice were employed in this study. Immunohistochemical (IHC) staining, Elisa and Western blot were used to detect SP, Aβ and its related metabolic enzymes. Results A certain number of SPs were observed in the cerebral cortex and hippocampus of APP/PS1 mice; SPs were occasionally observed in the cortex of ob/ob mice, while no SP appeared in wild-type mice. Aβ40 and Aβ42 levels were significantly increased in APP/PS1 and ob/ob mice brains as compared with controls (P＜0.05), thought both Aβ40 and Aβ42 levels in AD mice were significantly higher than those of ob/ob mice (P＜0.05). APP expression level was highest in APP/PS1 mice among 3 groups, and its expressed higher in ob/ob mice than that of control mice (P＜0.05). BACE1 expression was notably increased in APP/PS1 and ob/ob mice as compared with control(P＜0.05), however, it expressed higher in APP/PS1 mice than ob/ob mice (P＜0.05). The expression of Aβ degradation enzyme IDE was reduced in APP/PS1 and ob/ob mice(P＜0.05), while lowest in ob/ob mice. Conclusions Abnormal production, degradation and gathering of Aβ are not only occurred in the early stage of AD, but also in the brain of T2DM. These results indicate that overexpression of Aβ may be one of main reasons for T2DM combined AD.

Key words: 【Key words】Aβ, Senile plaques, Alzheimer’s disease, Type 2 diabetes mellitus