发现导致阿尔茨海默病发病最新毒性通路.docVIP

发现导致阿尔茨海默病发病的最新毒性通路 鉴于小鼠小胶质细胞 BV2即可对神经元起保护作用，又可间接分泌炎性细胞因子对神经元起毒性作用，是治疗神经炎症及神经退行性疾病的一个重要靶点。来自中国延边大学医学院许妍姬等设定了观察淀粉样类前体蛋白2-C端不同片段(Amyloid Precursor Like Protein 2-C Terminal Fragments，APLP2-CTFs)在BV2细胞中对S100A9表达影响APLP2-CTFs可上调BV2细胞中S100A9蛋白和mRNA表达为的神经元损伤与凋亡及修复和保护提供了一条新的毒性通路。文章发表在《中国神经再生研究（英文版）》杂志2014年11月第21期。 Article: Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells, by Guangzhe Li1, Hui Chen2, Lin Cheng2, Rongjie Zhao3, Junchang Zhao3, Yanji Xu2 (1 Department of Psychology, Yanbian Brain Hospital, Yanji, Jilin Province, China; 2 Department of Preventive Medicine, Medical College, Yanbian University, Yanji, Jilin Province, China; 3 Department of Pharmacology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, China) Li GZ, Chen H, Cheng L, Zhao RJ, Zhao JC, Xu YJ. Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells. Neural Regen Res. 2014;9(21):1923-1928. 欲获更多资讯：Neural Regen Res A novel toxic pathway by which Alzheimer’s disease occurs The murine microglial cell?line BV2 has neuroprotective effects, but is toxic to neurons by secreting inflammatory cytokines, and is an important target in the treatment of nerve inflammation and neurodegenerative diseases. Yanji Xu, Yanbian Brain Hospital, China investigated the influences of amyloid precursor like protein 2-C terminal fragments on S100A9 expression in BV2 cells (APLP2-CTFs). Results showed that APLP2-CTFs can up-regulate S100A9 protein and mRNA expression in BV2 cells. These results provide insights for investigating neuronal injury, apoptosis, repair and protection in Alzheimer’s disease. The relevant article was published in Neural Regeneration Research (Vol. 9, No. 21, 2014). Article: Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells, by Guangzhe Li1, Hui Chen2, Lin Cheng2, Rongjie Zhao3, Junchang Zhao3, Yanji Xu2 (1 Dep