Prevention of pathological change and cognitive degeneration of Tg2576 mice by inoculating Abeta(1-15) 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.
Hu
Jinjia
J
Department of Anatomy, Medical College of Shanghai Jiao Tong University, Shanghai 200025, China.
Li
Guoying
G
Wang
Huaqiao
H
Lin
Xian
X
Yao
Zhibin
Z
D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000276:immunology / Q000494:pharmacology; D000686:Amyloidosis / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D001921:Brain / Q000473:pathology; D004195:Disease Models, Animal; D006801:Humans; D007668:Kidney / Q000166:cytology; D008099:Liver / Q000166:cytology; D008168:Lung / Q000166:cytology; D018782:Maze Learning / Q000187:drug effects; D051379:Mice; D008822:Mice, Transgenic; D010446:Peptide Fragments / Q000276:immunology / Q000494:pharmacology; D011897:Random Allocation; D014612:Vaccines / Q000276:immunology*
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; D014612:Vaccines; C480626:amyloid beta-protein (1-15)