...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurobiology of disease >Age-dependent neurovascular abnormalities and altered microglial morphology in the YAC128 mouse model of Huntington disease.
【24h】

Age-dependent neurovascular abnormalities and altered microglial morphology in the YAC128 mouse model of Huntington disease.

机译：亨廷顿病的YAC128小鼠模型中年龄依赖性神经血管异常和小胶质细胞形态改变。

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

Central nervous system (CNS) inflammatory processes including microglial activation have been implicated in the pathogenesis of neurodegenerative diseases such as Huntington Disease (HD). We report age-dependent changes in striatal microglial morphology and vasculature in the YAC128 mouse model of HD. Decreases in microglial ramification along with a decrease in vessel diameter and increased vessel density and length suggest the presence of microgliosis and proangiogenic activity in YAC128 mice. Our hypothesis for this study was that the changes in microglial morphology and perturbations in vasculature may be involved in the pathogenesis of HD and that peripheral challenge with the bacterial endotoxin, lipopolysaccharide (LPS), will exacerbate these microglial and vascular changes as well as the HD phenotype in YAC128 mice at 12 months. Chronic peripheral LPS (1mg/kg) potentiated microglial activation indicated by an increase in microglial cell body size and retraction of processes. This potentiation in microglial activation with chronic peripheral LPS challenge was paralleled with vascular remodeling including dilatation, increased vessel wall thickness, increased BBB permeability and fibrinogen deposition in YAC128 striatum. Although peripheral LPS caused an increase in microglial activation and degenerative changes in cerebrovasculature, the phenotypic hallmarks of HD in YAC128 mice such as motor coordination deficits and decreased striatal volume were not exacerbated by chronic peripheral LPS exposure. This study identifies age-dependent increases in microglial activation and angiogenesis in YAC128 at 12 months. Peripheral inflammation induced by chronic LPS causes similar changes but does not influence the HD phenotype in YAC128 mice.
机译：包括小胶质细胞活化在内的中枢神经系统（CNS）炎症过程已与诸如亨廷顿病（HD）等神经退行性疾病的发病机理有关。我们报告高清的YAC128小鼠模型中纹状体小胶质细胞形态和脉管系统的年龄依赖性变化。小胶质细胞分枝的减少，以及血管直径的减少以及血管密度和长度的增加表明，YAC128小鼠存在小胶质细胞增生和促血管生成活性。我们这项研究的假设是，小胶质细胞形态和脉管系统的变化可能参与了HD的发病机制，而细菌内毒素，脂多糖（LPS）引起的外周挑战将加剧这些小胶质和血管变化以及HD YAC128小鼠在12个月时的表型。慢性周围性LPS（1mg / kg）增强了小胶质细胞的活化，其表现为小胶质细胞体大小的增加和过程的回缩。与慢性外周LPS刺激有关的小胶质细胞活化增强作用与血管重塑平行，包括扩张，血管壁厚度增加，BBB通透性增加和YAC128纹状体中纤维蛋白原沉积。尽管外周脂多糖引起小胶质细胞活化的增加和脑血管系统的退行性改变，但慢性外周脂多糖暴露不会加剧YAC128小鼠的HD的表型特征，例如运动协调障碍和纹状体体积减少。这项研究确定了12个月时YAC128中小胶质细胞激活和血管生成的年龄依赖性增加。慢性LPS引起的周围炎症会引起类似的变化，但不会影响YAC128小鼠的HD表型。

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