Department of Pharmaceutics, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
ACS Chem Neurosci. 2020 Dec 16;11(24):4060-4072. doi: 10.1021/acschemneuro.0c00637. Epub 2020 Nov 29.
Apolipoprotein J (ApoJ), or clusterin, is one of the main apolipoproteins in the brain. It is synthesized and released from astrocytes in a healthy brain, and its expression increases in neurodegenerative disorders. Genetic evidence has suggested an association between ApoJ polymorphism and the risk of Alzheimer's disease (AD)-it is now considered the third main genetic risk factor for late-onset AD. However, the role of ApoJ overexpression in the state of disorder, toxicity, or protection is not yet clear. Since ApoJ plays different roles in AD, we review the function of ApoJ using different cell signaling pathways in AD and outline its paradoxical roles in AD. ApoJ helps in amyloid-beta (Aβ) clearance. Vice versa, ApoJ gene knock-out causes fibrillary Aβ reduction and prevents Aβ-induced neuron cell death. Understanding ApoJ, through various cellular signaling pathways, creates a new perspective on AD's cellular principles. The overall message is that ApoJ can be a valuable tool in controlling AD.
载脂蛋白 J(ApoJ),亦称簇集素,是大脑中主要的载脂蛋白之一。在健康的大脑中,它由星形胶质细胞合成并释放,其表达在神经退行性疾病中增加。遗传证据表明 ApoJ 多态性与阿尔茨海默病(AD)的风险之间存在关联-它现在被认为是晚发性 AD 的第三个主要遗传风险因素。然而,ApoJ 过表达在紊乱、毒性或保护状态下的作用尚不清楚。由于 ApoJ 在 AD 中发挥不同的作用,我们使用 AD 中的不同细胞信号通路来综述 ApoJ 的功能,并概述其在 AD 中的矛盾作用。ApoJ 有助于清除淀粉样β(Aβ)。反之,ApoJ 基因敲除会导致纤维状 Aβ减少,并防止 Aβ诱导的神经元细胞死亡。通过各种细胞信号通路了解 ApoJ,为 AD 的细胞原理提供了新的视角。总的来说,ApoJ 可以成为控制 AD 的一种有价值的工具。