CAJ | 학술논문

阿尔茨海默病(Alzheimer's disease，AD)的发病机制涉及到很多方面，新近研究表明G蛋白信号转导途径异常在AD的发病中起着重要作用。AD患者脑中信号转导活性明显增强，且信号转导缺陷的位点出现在“受体-G蛋白界面”，研究表明G蛋白耦联受体激酶(GRKs)功能缺陷，主要是GRK5，与AD的发生联系密切。
아이자해묵병(Alzheimer's disease，AD)적발병궤제섭급도흔다방면，신근연구표명G단백신호전도도경이상재AD적발병중기착중요작용。AD환자뇌중신호전도활성명현증강，차신호전도결함적위점출현재“수체-G단백계면”，연구표명G단백우련수체격매(GRKs)공능결함，주요시GRK5，여AD적발생련계밀절。
The pathogenesis of Alzheimer's disease (AD) involves many aspects. Recent studies have shown that the G-protein signal transduction deficits play important roles in the pathogenesis of AD. The signal transduction activity in AD brain is significantly enhanced, and the site of the signal transduction defects is at the“receptor-G pro-tein interface”. Studies have indicated that the G protein-coupled receptor kinases (GRKs) functional deficiency, pri-marily GRK5, plays a significant role in AD pathogenesis.