...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease.
【24h】

Cell cycle re-entry mediated neurodegeneration and its treatment role in the pathogenesis of Alzheimer's disease.

机译：细胞周期再进入介导的神经退行性变及其在阿尔茨海默氏病发病机理中的治疗作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

As one of the earliest pathologic changes, the aberrant re-expression of many cell cycle-related proteins and inappropriate cell cycle control in specific vulnerable neuronal populations in Alzheimer's disease (AD) is emerging as an important component in the pathogenesis leading to AD and other neurodegenerative diseases. These events are clearly representative of a true cell cycle, rather than epiphenomena of other processes since, in AD and other neurodegenerative diseases, there is a true mitotic alteration that leads to DNA replication. While the exact role of cell cycle re-entry is unclear, recent studies using cell culture and animal models strongly support the notion that the dysregulation of cell cycle in neurons leads to the development of AD-related pathology such as hyperphosphorylation of tau and amyloid-beta deposition and ultimately causes neuronal cell death. Importantly, cell cycle re-entry is also evident in mutant amyloid-beta precursor protein and tau transgenic mice and, as in human disease, occurs prior to the development of the pathological hallmarks, neurofibrillary tangles and amyloid-beta plaques. Therefore, the study of aberrant cell cycle regulation in model systems, both cellular and animal, may provide extremely important insights into the pathogenesis of AD and also serve as a means to test novel therapeutic approaches.
机译：作为最早的病理学改变之一，在阿尔茨海默氏病（AD）的特定易感神经元群体中，许多细胞周期相关蛋白的异常重新表达和不适当的细胞周期控制正在成为导致AD和其他疾病的发病机理中的重要组成部分神经退行性疾病。这些事件显然代表了真正的细胞周期，而不是其他过程的现象，因为在AD和其他神经退行性疾病中，存在着导致DNA复制的真正的有丝分裂改变。虽然细胞周期再进入的确切作用尚不清楚，但最近使用细胞培养和动物模型进行的研究强烈支持以下观点：神经元中细胞周期失调会导致AD相关病理的发展，例如tau和磷酸化淀粉样蛋白的过度磷酸化。 β沉积并最终导致神经元细胞死亡。重要的是，在突变的淀粉样蛋白-β前体蛋白和tau转基因小鼠中，细胞周期的再进入也很明显，并且像在人类疾病中一样，发生在病理学标志，神经原纤维缠结和淀粉样蛋白-斑块发展之前。因此，在细胞和动物模型系统中异常细胞周期调控的研究可能为AD的发病机理提供极为重要的见解，也可以作为测试新型治疗方法的手段。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号