...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Increased Amyloid Precursor Protein and Tau Expression Manifests as Key Secondary Cell Death in Chronic Traumatic Brain Injury
【24h】

Increased Amyloid Precursor Protein and Tau Expression Manifests as Key Secondary Cell Death in Chronic Traumatic Brain Injury

机译：增加了淀粉样前体蛋白和τ表达表现为关键辅助细胞死亡在慢性创伤性脑损伤

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

In testing the hypothesis of Alzheimer's disease (AD)-like pathology in late stage traumatic brain injury (TBI), we evaluated AD pathological markers in late stage TBI model. Sprague-Dawley male rats were subjected to moderate controlled cortical impact (CCI) injury, and 6 months later euthanized and brain tissues harvested. Results from H&E staining revealed significant 33% and 10% reduction in the ipsilateral and contralateral hippocampal CA3 interneurons, increased MHCII-activated inflammatory cells in many gray matter (8-20-fold increase) and white matter (6-30-fold increased) regions of both the ipsilateral and contralateral hemispheres, decreased cell cycle regulating protein marker by 1.6- and 1-fold in the SVZ and a 2.3- and 1.5-fold reductions in the ipsilateral and contralateral dentate gyrus, diminution of immature neuronal marker by two- and onefold in both the ipsilateral and contralateral SVZ and dentate gyrus, and amplified amyloid precursor protein (APP) distribution volumes in white matter including corpus callosum, fornix, and internal capsule (4-38-fold increase), as well as in the cortical gray matter, such as the striatum hilus, SVZ, and dentate gyrus (6-40-fold increase) in TBI animals compared to controls (P's<0.001). Surrogate AD-like phenotypic markers revealed a significant accumulation of phosphorylated tau (AT8) and oligomeric tau (T22) within the neuronal cell bodies in ipsilateral and contralateral cortex, and dentate gyrus relative to sham control, further supporting the rampant neurodegenerative pathology in TBI secondary cell death. These findings indicate that AD-like pathological features may prove to be valuable markers and therapeutic targets for late stage TBI. J. Cell. Physiol. 232: 665-677, 2017. (c) 2016 Wiley Periodicals, Inc.
机译：在测试中阿尔茨海默病的假说(广告)——在后期创伤性脑病理病理损伤,我们评估广告标记在后期创伤性脑损伤模型。雄性老鼠受到适度控制皮质影响损伤(CCI), 6个月以后安乐死和大脑组织收获。从他走时染色显示33%,很大身体的同侧的和减少10%侧海马CA3中间神经元,增加MHCII-activated炎性细胞许多灰质(8-20-fold增加)和白色(6-30-fold增加)地区的问题身体的同侧的侧半球,减少细胞周期调节蛋白标记1.6 - 2.3和1-fold SVZ的,降低身体的同侧的1.5倍侧齿状回,减少的未成熟神经元标记的两年期和单一的同侧和对侧的两个SVZ和齿状回和放大淀粉样前体蛋白(APP)分布在白色卷问题包括胼胝体、穹窿和内囊(4-38-fold增加),以及灰质皮层、纹状体等门、SVZ和齿状回(6-40-fold在创伤性脑损伤动物相比,控制增加)(P < 0.001)。揭示了一个重要的积累磷酸化τ(AT8)和寡聚τ(T22)在神经元细胞体在同侧和对侧皮层和齿状回相对于虚假的控制,进一步支持猖獗的神经退行性创伤性脑损伤的病理辅助细胞死亡。这个广告可能病理特征是有价值的标记和治疗的目标后期创伤性脑损伤。2017.

著录项

相似文献

  • 外文文献
  • 中文文献
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