...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Magnetic Resonance in Medicine >R-flurbiprofen improves axonal transport in the Tg2576 mouse model of Alzheimer's Disease as determined by MEMRI
【24h】

R-flurbiprofen improves axonal transport in the Tg2576 mouse model of Alzheimer's Disease as determined by MEMRI

机译：通过MEMRI确定，R-氟比洛芬可改善阿尔茨海默氏病Tg2576小鼠模型中的轴突转运

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

Axonal pathology is a prevalent feature of Alzheimer's disease (AD) and is thought to occur predominantly due to the accumulation of amyloid beta (Aβ). However, it remains unclear whether therapeutics geared toward reducing Aβ improves axonal deficits. We have previously used Manganese Enhanced MRI to demonstrate that axonal transport deficits occur before plaque formation in the Tg2576 mouse model of Alzheimer's disease. Here we tested whether axonal transport deficits in the Tg2576 mouse model improve in response to the Aβ42 selective lowering agent R-Flurbiprofen (R-F). We demonstrated that in young animals (before Aβ plaque formation), R-F treatment reduced Aβ42 levels and coincided with a significant improvement in axonal transport (P = 0.0186). However, in older animals (after plaque formation had occurred), we observed that R-F treatment did not reduce Aβ42 levels although we still observed a significant improvement in axonal transport as assessed with MEMRI (P = 0.0329). We then determined that R-F treatment reduced tau hyper-phosphorylation in the older animals. These data indicate that both Aβ42 and tau comprise a role in axonal transport rate deficits in the Tg2576 model of Alzheimer's Disease. Magn Reson Med, 2011. © 2010 Wiley-Liss, Inc.
机译：轴突病理是阿尔茨海默氏病（AD）的普遍特征，被认为主要是由于淀粉样β（Aβ）的积累所致。但是，尚不清楚用于降低Aβ的治疗药物是否能改善轴突缺乏症。我们以前使用锰增强MRI来证明在阿尔茨海默氏病的Tg2576小鼠模型中在形成斑块之前发生轴突运输缺陷。在这里，我们测试了Tg2576小鼠模型中的轴突运输缺陷是否响应Aβ42选择性降低剂R-Flurbiprofen（R-F）而得到改善。我们证明了在幼小的动物中（在Aβ斑块形成之前），R-F处理降低了Aβ42的水平，并伴随着轴突运输的显着改善（P = 0.0186）。然而，在年长的动物中（在发生斑块形成之后），我们观察到R-F治疗并未降低Aβ42水平，尽管我们仍观察到用MEMRI评估了轴突运输的显着改善（P = 0.0329）。然后，我们确定了R-F治疗可降低老年动物的tau过度磷酸化。这些数据表明，在阿尔茨海默氏病的Tg2576模型中，Aβ42和tau均在轴突运输速率缺陷中起作用。 Magn Reson Med，2011年。©2010 Wiley-Liss，Inc.。

著录项

  • 来源
    《Magnetic Resonance in Medicine》 |2011年第5期|p.1423-1429|共7页
  • 作者

    Karen D. B. Smith; Richard Paylor; Robia G. Pautler;

  • 作者单位

    Dept. Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA;

    Dept. Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA;

    Dept. Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA|Huffington Center on Aging, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA|Dept. Radiology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA|Dept. Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, USA;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    MEMRI; R-flurbiprofen; mouse; Tg2576; amyloid;

    机译：MEMRI;R-氟比洛芬;小鼠;Tg2576;淀粉样蛋白;

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