Meng Yuan, Ding Li, Zhang Hui-Yi, Yin Wen-Chao, Yan Yi, Cao Yun-Peng
Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning Province, China.
Brain Res. 2017 Oct 15;1673:72-77. doi: 10.1016/j.brainres.2017.07.017. Epub 2017 Aug 2.
Alzheimer's disease is a neurodegenerative disease that affects many patients worldwide. The amyloid cascade hypothesis has been adopted by most researchers as the mechanism underlying Alzheimer's disease. Aβ plaques have been considered the core factor in the neurotoxic effect in Alzheimer's disease, though some controversy remains. Further effort is necessary to elucidate the mechanism and to develop effective treatments. Previous studies have indicated that eliminating Aβ plaques could improve synaptic plasticity and cognitive function. Researchers have developed various forms of vaccines to prevent Aβ deposition or eliminate Aβ plaques and have made some progress. We developed a new vaccine, Aβ3-10-KLH, to increase the level of the anti-Aβ immune response, and we show that this vaccine resulted in a sustained prevention of Aβ deposition at 4 months after cessation of the vaccine treatment. At the same time point, the expression of synaptophysin and NMDAR2B in APP/PS1 transgenic mice was increased by immunization.
阿尔茨海默病是一种影响全球众多患者的神经退行性疾病。淀粉样蛋白级联假说已被大多数研究人员采纳为阿尔茨海默病的潜在发病机制。尽管仍存在一些争议，但β淀粉样蛋白（Aβ）斑块已被视为阿尔茨海默病神经毒性作用的核心因素。仍需进一步努力来阐明其机制并开发有效的治疗方法。先前的研究表明，清除Aβ斑块可改善突触可塑性和认知功能。研究人员已开发出各种形式的疫苗来预防Aβ沉积或清除Aβ斑块，并取得了一些进展。我们开发了一种新疫苗Aβ3-10-KLH，以提高抗Aβ免疫反应水平，并且我们表明该疫苗在停止疫苗治疗后4个月可持续预防Aβ沉积。在同一时间点，免疫接种可增加APP/PS1转基因小鼠中突触素和NMDAR2B的表达。
