Yoshiyama Y, Arai K, Hattori T
Department of Neurology, School of Medicine, Chiba University, Japan.
Neuroreport. 2001 Aug 28;12(12):2641-5. doi: 10.1097/00001756-200108280-00011.
Inflammatory and immune responses are known to be involved in the pathogenesis of Alzheimer's disease (AD). NF-kappaB is a major transcription factor that plays a central role in the inflammatory and immune responses and is regulated by I-kappaB through an autoregulatory feedback system. Southwestern immunohistochemistry and immunohistochemistry in our study demonstrated activated NF-kappaB in AD brains. However, there was also activated expression of I-kappaB in a distribution that corresponded to the neurofibrillary pathology of AD. These observations indicate that disruption of the autoregulatory mechanism of NF-kappaB in brain regions with neurofibrillary pathology may play a role in the pathogenesis of AD.
已知炎症和免疫反应参与阿尔茨海默病（AD）的发病机制。核因子κB（NF-κB）是一种主要的转录因子，在炎症和免疫反应中起核心作用，并通过自身调节反馈系统由I-κB调节。我们研究中的蛋白质印迹免疫组化和免疫组化显示AD脑中有活化的NF-κB。然而，I-κB也有活化表达，其分布与AD的神经原纤维病理相对应。这些观察结果表明，在有神经原纤维病理的脑区中，NF-κB自身调节机制的破坏可能在AD的发病机制中起作用。
