摘要
阿尔茨海默病(Alzheimer’s disease,AD)是一种以进行性认知功能减退为特征的神经退行性疾病。发病的确切机制尚未完全清楚。目前认为胰岛素抵抗与胰岛素信号系统受损是加速AD发病的危险因素,胰岛素降解酶(insulin-degrading enzyme,IDE)在糖代谢异常促使AD发病的过程中发挥重要的作用。除调节β淀粉样蛋白降解和清除之外,还可能通过调节tau蛋白磷酸化水平,协同载脂蛋白Eε4(ApoEε4)及影响胰岛素信号传导等参与AD的发病机制。本文就IDE生物学特性及在AD发病机制中的作用作一综述。
Alzheimer＇s disease （AD） is a neurodegenerative diseases characterized by progressive cognitive function impaired. The pathogenesis of AD is still not understood. At present, it is considered that insulin resistance and imPaired insulin signaling system accelerate the risk of onset for AD. The link between abnormal glucose metabolism and AD is insulin-degrading enzyme （IDE）, which plays a major role in the pathogenesis of AD. In addition to the regulation of β-amyloid clearance and degradation, IDE take part in the pathogenesis of AD also by regulating the phosphorylation of tau protein, apolipoprotein -Eε4 （ApoEε4） and the effects of insulin signaling. The biological characteristics of IDE and its role in the. pathogenesis of AD are reviewed here.
出处
《生命科学》
CSCD
北大核心
2009年第1期126-130,共5页
Chinese Bulletin of Life Sciences
