...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Current drug targets. CNS and neurological disorders >Amyloid associated proteins in Alzheimer's and prion disease.
【24h】

Amyloid associated proteins in Alzheimer's and prion disease.

机译：阿尔茨海默氏病和病毒病中的淀粉样蛋白相关蛋白。

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

Clustering of activated microglia in Abeta deposits is related to accumulation of amyloid associated factors and precedes the neurodegenerative changes in AD. Microglia-derived pro-inflammatory cytokines are suggested to be the driving force in AD pathology. Inflammation-related proteins, including complement factors, acute-phase proteins, pro-inflammatory cytokines, that normally are locally produced at low levels, are increasingly synthesized in Alzheimer's disease (AD) brain. Similar to AD, in prion diseases (Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker disease and experimentally scrapie infected mouse brain) amyloid associated factors and activated glial cells accumulate in amyloid deposits of conformational changed prion protein (PrPres). Biological properties of Abeta and prion (PrP) peptides, including their potential to activate microglia, relate to Abeta and PrP peptide fibrillogenic abilities that are influenced by certain amyloid associated factors. However, since small oligomers of amyloid forming peptides are more toxic to neurons than large fibrils, certain amyloid associated factors that enhance fibril formation, may sequester the potentially harmful Abeta and PrP peptides from the neuronal microenvironment. In this review the positive and negative actions of amyloid associated factors on amyloid peptide fibril formation and on the fibrillation state related activation of microglia will be discussed. Insight in these mechanisms will enable the design of specific therapies to prevent neurodegenerative diseases in which amyloid accumulation and glial activation are prominent early features.
机译：Abeta沉积物中活化的小胶质细胞的聚集与淀粉样蛋白相关因子的积累有关，并且先于AD的神经退行性变化。小胶质细胞来源的促炎细胞因子被认为是AD病理学的驱动力。炎症相关蛋白，包括补体因子，急性期蛋白，促炎细胞因子，通常以低水平局部产生，在阿尔茨海默病（AD）脑中越来越多地合成。与AD相似，在病毒病（Creutzfeldt-Jakob病，Gerstmann-Straussler-Scheinker病和实验上被瘙痒病感染的小鼠大脑）中，淀粉样蛋白相关因子和活化的神经胶质细胞积聚在构象改变的ion病毒蛋白（PrPres）的淀粉样蛋白沉积物中。 Abeta和病毒（PrP）肽的生物学特性，包括它们激活小胶质细胞的潜力，与受某些淀粉样蛋白相关因素影响的Abeta和PrP肽原纤维形成能力有关。但是，由于淀粉样蛋白形成肽的小寡聚物对神经元的毒性比大纤维小，因此某些增强淀粉样蛋白形成的淀粉样蛋白相关因子可从神经元微环境中隔离潜在有害的Abeta和PrP肽。在这篇综述中，将讨论淀粉样蛋白相关因子对淀粉样蛋白肽原纤维形成以及对与小胶质细胞的纤颤状态相关的激活的正作用和负作用。对这些机制的深入了解将有助于设计特定的疗法，以预防淀粉样蛋白堆积和神经胶质细胞活化是突出的早期特征的神经退行性疾病。

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