An A beta 3-10-KLH vaccine reduced Alzheimer's disease-like pathology and had a sustained effect in Tg-APPswe/PSEN1dE9 mice

作者：Meng, Yuan; Ding, Li; Zhang, Hui-Yi; Yin, Wen-Chao; Yan, Yi; Cao, Yun-Peng^*

来源：Brain Research, 2017, 1673: 72-77.

DOI：10.1016/j.brainres.2017.07.017

• Alzheimer's disease
• Synaptophysin
• NMDAR2B
• A beta 3-10-KLH vaccine
• A beta plaque

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. All 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 A beta plaques could improve synaptic plasticity and cognitive function. Researchers have developed various forms of vaccines to prevent A beta deposition or eliminate A beta plaques and have made some progress. We developed a new vaccine, A beta 3-10-KLH, to increase the level of the anti-A beta immune response, and we show that this vaccine resulted in a sustained prevention of A beta 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.

• 出版日期2017-10-15
• 单位中国医科大学