Immunization of Tg-APPswe/PSEN1dE9 mice with A beta 3-10-KLH vaccine prevents synaptic deficits of Alzheimer's disease
Immunization of Tg-APPswe/PSEN1dE9 mice with A beta 3-10-KLH vaccine prevents synaptic deficits of Alzheimer's disease
复制标题
使用 A beta 3-10-KLH 疫苗免疫 Tg-APPswe/PSEN1dE9 小鼠可预防阿尔茨海默病的突触缺陷
DOI：
10.1016/j.bbr.2017.05.056
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发表时间：
2017
影响因子：
2.7
通讯作者：
Cao YunPeng
中科院分区：
文献类型：
--
作者：
Meng Yuan;Ding Li;Zhang HuiYi;Yin WenChao;Yan Yi;Cao YunPeng
淀粉样蛋白级联假说被研究者广泛接受为阿尔茨海默病的发病机制。主动免疫消除Aβ沉积已用于临床前和临床研究。a - β3-10-KLH是a - β3-10肽与锁孔帽贝血青素（KLH）结合的疫苗。我们用Aβ3-10- klh肽和Aβ1-42肽免疫2.5月龄Tg-APPswe/PSEN1dE9小鼠，消除这些转基因小鼠脑内的Aβ沉积。免疫组化染色和透射电镜检测结果表明，新疫苗在保护突触功能和结构方面比Aβ1-42肽更有优势。β3-10- klh肽是治疗阿尔茨海默病的有效疫苗。
The amyloid cascade hypothesis is widely accepted by researchers as the mechanism of Alzheimer’s disease. Active immunization to eliminate Aβ depositions has been used in preclinical and clinical studies. Aβ3-10-KLH is a vaccine of the Aβ3-10 peptide combined with keyhole limpet hemocyanin (KLH). We immunized 2.5-month-old Tg-APPswe/PSEN1dE9 mice with Aβ3-10-KLH peptide and Aβ1-42 peptide to eliminate Aβ deposits in the brains of these transgenic mice. The results of immunohistochemical staining and transmission electron microscopy detection indicated that our new vaccine was more advantageous in protecting synaptic function and structure than the Aβ1-42 peptide. Aβ3-10-KLH peptide is an effective vaccine in the treatment of Alzheimer’s disease.