...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neuron >Abeta42 is essential for parenchymal and vascular amyloid deposition in mice.
【24h】

Abeta42 is essential for parenchymal and vascular amyloid deposition in mice.

机译：Abeta42对于小鼠的实质和血管淀粉样蛋白沉积至关重要。

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

Considerable circumstantial evidence suggests that Abeta42 is the initiating molecule in Alzheimer's disease (AD) pathogenesis. However, the absolute requirement for Abeta42 for amyloid deposition has never been demonstrated in vivo. We have addressed this by developing transgenic models that express Abeta1-40 or Abeta1-42 in the absence of human amyloid beta protein precursor (APP) overexpression. Mice expressing high levels of Abeta1-40 do not develop overt amyloid pathology. In contrast, mice expressing lower levels of Abeta1-42 accumulate insoluble Abeta1-42 and develop compact amyloid plaques, congophilic amyloid angiopathy (CAA), and diffuse Abeta deposits. When mice expressing Abeta1-42 are crossed with mutant APP (Tg2576) mice, there is also a massive increase in amyloid deposition. These data establish that Abeta1-42 is essential for amyloid deposition in the parenchyma and also in vessels.
机译：大量的间接证据表明，Abeta42是阿尔茨海默氏病（AD）发病机理的起始分子。但是，Abeta42淀粉样蛋白沉积的绝对需求尚未在体内得到证明。我们已经通过开发在不存在人类淀粉样β蛋白前体（APP）过表达的情况下表达Abeta1-40或Abeta1-42的转基因模型来解决此问题。表达高水平的Abeta1-40的小鼠不会发展明显的淀粉样蛋白病理。相比之下，表达较低水平的Abeta1-42的小鼠会积聚不溶的Abeta1-42，并形成致密的淀粉样蛋白斑块，嗜血性淀粉样血管病（CAA）和弥漫性Abeta沉积物。当表达Abeta1-42的小鼠与突变APP（Tg2576）小鼠杂交时，淀粉样蛋白的沉积也大量增加。这些数据表明，Abeta1-42对于淀粉样蛋白在薄壁组织以及血管中的沉积至关重要。

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