Rebeck G William, LaDu Mary Jo, Estus Steven, Bu Guojun, Weeber Edwin J
Department of Neuroscience, Georgetown University, Washington, DC, USA.
Mol Neurodegener. 2006 Oct 24;1:15. doi: 10.1186/1750-1326-1-15.
More than a decade has passed since apolipoprotein E4 (APOE-epsilon4) was identified as a primary risk factor for Alzheimer 's disease (AD), yet researchers are even now struggling to understand how the apolipoprotein system integrates into the puzzle of AD etiology. The specific pathological actions of apoE4, methods of modulating apolipoprotein E4-associated risk, and possible roles of apoE in normal synaptic function are still being debated. These critical questions will never be fully answered without a complete understanding of the life cycle of the apolipoprotein receptors that mediate the uptake, signaling, and degradation of apoE. The present review will focus on apoE receptors as modulators of apoE actions and, in particular, explore the functions of soluble apoE receptors, a field almost entirely overlooked until now.
自从载脂蛋白E4（APOE-ε4）被确定为阿尔茨海默病（AD）的主要危险因素以来，已经过去了十多年，但即便到现在，研究人员仍在努力理解载脂蛋白系统是如何融入AD病因这个谜题之中的。载脂蛋白E4的具体病理作用、调节与载脂蛋白E4相关风险的方法以及载脂蛋白E在正常突触功能中的可能作用仍在争论之中。如果不能完全理解介导载脂蛋白E摄取、信号传导和降解的载脂蛋白受体的生命周期，这些关键问题将永远无法得到充分解答。本综述将聚焦于作为载脂蛋白E作用调节剂的载脂蛋白E受体，尤其会探讨可溶性载脂蛋白E受体的功能，这一领域至今几乎完全被忽视。
