Neher Jonas J, Neniskyte Urte, Brown Guy C
Department of Biochemistry, University of Cambridge Cambridge, UK.
Front Pharmacol. 2012 Feb 28;3:27. doi: 10.3389/fphar.2012.00027. eCollection 2012.
Microglial phagocytosis of dead or dying neurons can be beneficial by preventing the release of damaging and/or pro-inflammatory intracellular components. However, there is now evidence that under certain conditions, such as inflammation, microglia can also phagocytose viable neurons, thus executing their death. Such phagocytic cell death may result from exposure of phosphatidylserine (PS) or other eat-me signals on otherwise viable neurons as a result of physiological activation or sub-toxic insult, and neuronal phagocytosis by activated microglia. In this review, we discuss the mechanisms of phagocytic cell death and its potential roles in Alzheimer's Disease, Parkinson's Disease, and Frontotemporal Dementia.
小胶质细胞对死亡或濒死神经元的吞噬作用通过阻止有害和/或促炎细胞内成分的释放可能是有益的。然而,现在有证据表明,在某些条件下,如炎症时,小胶质细胞也可以吞噬存活的神经元,从而导致其死亡。这种吞噬性细胞死亡可能是由于生理激活或亚毒性损伤导致原本存活的神经元上暴露磷脂酰丝氨酸(PS)或其他“吃我”信号,以及活化的小胶质细胞对神经元的吞噬作用所致。在这篇综述中,我们讨论了吞噬性细胞死亡的机制及其在阿尔茨海默病、帕金森病和额颞叶痴呆中的潜在作用。