...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Epilepsy currents >“Untangling” Alzheimer's Disease and Epilepsy
【24h】

“Untangling” Alzheimer's Disease and Epilepsy

机译：“解开”阿尔茨海默氏病和癫痫病

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

There is a substantial body of evidence that spontaneous recurrent seizures occur in a subset of patients with Alzheimer disease (AD), especially the familial forms that have an early onset. In transgenic mice that simulate these genetic forms of AD, seizures or reduced seizure threshold have also been reported. Mechanisms underlying the seizures or reduced seizure threshold in these mice are not yet clear and are likely to be complex, because the synthesis of amyloid β (Aβ) involves many peptides and proteases that influence excitability. Based on transgenic mouse models of AD where Aβ and its precursor are elevated, it has been suggested that seizures are caused by the downregulation of the Nav1.1 sodium channel in a subset of GABAergic interneurons, leading to a reduction in GABAergic inhibition. Another mechanism of hyperexcitability appears to involve tau, because deletion of tau reduces seizures in some of the same transgenic mouse models of AD. Therefore, altered excitability may be as much a characteristic of AD as plaques and tangles—especially for the familial forms of AD.
机译：有大量证据表明，一部分阿尔茨海默氏病（AD）患者，尤其是发病较早的家族形式，会发生自发性反复发作。在模拟这些遗传形式的AD的转基因小鼠中，也有癫痫发作或癫痫发作阈值降低的报道。这些小鼠中癫痫发作或癫痫发作阈值降低的潜在机制尚不清楚，可能很复杂，因为淀粉样蛋白β（Aβ）的合成涉及许多影响兴奋性的肽和蛋白酶。基于Aβ及其前体水平升高的AD转基因小鼠模型，已表明癫痫发作是由GABA能性中间神经元子集中Nav1.1钠通道的下调引起的，从而导致了GABA能抑制的降低。过度兴奋的另一种机制似乎涉及tau，因为在某些相同的AD转基因小鼠模型中tau的缺失减少了癫痫发作。因此，兴奋性改变可能与斑块和缠结一样是AD的特征，尤其是对于AD的家族形式。

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