The X11 proteins, Abeta production and Alzheimer's disease.
The X11 proteins, Abeta production and Alzheimer's disease.
复制标题
X11 蛋白、Abeta 产生和阿尔茨海默病。
作者：
Christopher C. J. Miller;D. McLoughlin;K. Lau;Maria E. Tennant;B. Rogelj
脑内淀粉样β蛋白(Abeta)在神经炎斑块中的沉积是阿尔茨海默病的标志性病理。现在人们普遍认为，这种病理的发展是阿尔茨海默病发病机制的核心。因此，抑制Abeta沉积或一旦形成Abeta沉积就代表了阿尔茨海默病的治疗靶点。Abeta来自一种前体，即淀粉样前体蛋白(APP)，APP与X11家族的适配器蛋白结合。几个实验室的研究现在表明，X11pha和X11beta(两个神经元的X11)抑制APP的处理和Abeta的产生。具体是如何实现这一点尚不清楚，但最近发现了其他X11结合伙伴的研究开始揭示潜在的机制。
Cerebral deposition of amyloid-beta peptide (Abeta) within neuritic plaques is a hallmark pathology of Alzheimer's disease. It is now generally believed that the development of this pathology is central to the pathogenesis of Alzheimer's disease. As such, inhibiting Abeta deposition or removing Abeta deposits once they are formed represent therapeutic targets for Alzheimer's disease. Abeta is derived from a precursor, the amyloid precursor protein (APP), and APP binds to the X11 family of adaptor proteins. Studies from several laboratories have now shown that X11alpha and X11beta (the two neuronal X11s) inhibit APP processing and Abeta production. Exactly how this is achieved is not yet known but recent studies in which other X11 binding partners have been identified are beginning to reveal potential mechanisms.