Prevention of pathological change and cognitive degeneration of Tg2576 mice by inoculating Aβ1–15 vaccine

This study aims to discuss the effect of preventing pathological changes and cognitive degeneration of Tg2576 mice by inoculating the subunit fragment of Abeta vaccine. Thirty-two Tg2576 mice were randomly divided into four groups, each having eight mice: Group I, the control group, inoculated with adjuvants; Group II, the Abeta(42) group, inoculated with Abeta(42) vaccine; Group III, the Abeta(1-15) group, inoculated with Abeta(1-15) vaccine; and Group IV, the Abeta(36-42) group, inoculated with Abeta(36-42) vaccine. The titer of the serum antibody against Abeta(42) (Group II) was significantly higher than that of the control group (Group I), and a low level of antibodies could be detected in the brain homogenate in the three vaccine-inoculated groups. Morris water maze test showed that the Abeta(42) group, Abeta(1-15) group and Abeta(36-42) group were obviously improved compared with the control group. The cultured splenocytes sampled from each group were induced by Con A or their respective antigens, and the cell proliferation of the three vaccine-inoculated groups was significantly higher than that of the control group. In the Abeta(42) group, IL2 and IFN-gamma were relatively low and IL4 and IL10 were relatively high. By contrast, IL4 and IL10 were much higher in the Abeta(1-15) group and IL2 and IFN-gamma were much higher in the Abeta(36-42) group. The immunohistochemical test showed a large number of senile plaques in the brain cortex and hippocampus of the mice in the control group, no senile plaque in the brain of the Abeta(1-15) group and Abeta(42) group mice, and a small number of senile plaques in the brain of the Abeta(36-42) group mice. The results suggest that the subunit fragment of Abeta(1-15) vaccine could prevent not only cognitive and behavioral degeneration but also Abeta deposition and formation of senile plaques in Tg2576 mice.