Enhanced expression of I-κB with neurofibrillary pathology in Alzheimer's disease
Enhanced expression of I-κB with neurofibrillary pathology in Alzheimer's disease
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DOI：
10.1097/00001756-200108280-00011
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发表时间：
2001-08
期刊：
影响因子：
1.7
通讯作者：
Y. Yoshiyama;K. Arai;T. Hattori
中科院分区：
文献类型：
--
作者：
Y. Yoshiyama;K. Arai;T. Hattori
众所周知，炎症和免疫反应与阿尔茨海默病（AD）的发病机制有关。 NF-κB 是一种主要转录因子，在炎症和免疫反应中发挥核心作用，并通过自动调节反馈系统受 I-κB 调节。我们的研究中的西南免疫组织化学和免疫组织化学证明 AD 大脑中激活了 NF-κB。然而，I-κB 的表达也被激活，其分布与 AD 的神经原纤维病理学相对应。这些观察结果表明，具有神经原纤维病理学的大脑区域中 NF-κB 的自动调节机制的破坏可能在 AD 的发病机制中发挥作用。
Inflammatory and immune responses are known to be involved in the pathogenesis of Alzheimer's disease (AD). NF-κB is a major transcription factor that plays a central role in the inflammatory and immune responses and is regulated by I-κB through an autoregulatory feedback system. Southwestern immunohistochemistry and immunochistochemistry in our study demonstrated activated NF-κB in AD brains. However, there was also activated expression of I-κB in a distribution that corresponded to the neurofibrillary pathology of AD. These observations indicate that disruption of the autoregulatory mechanism of NF-κB in brain regions with neurofibrillary pathology may play a role in the pathogenesis of AD.