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小胶质细胞在暴露于β-淀粉样蛋白后对神经元存活的保护作用

Protective Role of Microglia on Neuronal Survival after Exposure to Amyloid Beta.

作者信息

Lee Sunjun, Choi Won-Seok

机构信息

School of Biological Sciences and Technology, College of Natural Sciences, Chonnam National University, Gwangju, Korea.

出版信息

Chonnam Med J. 2022 Jan;58(1):13-17. doi: 10.4068/cmj.2022.58.1.13. Epub 2022 Jan 25.

Abstract

Alzheimer's disease (AD) is the most common cause of neurodegeneration. It is characterized by deposits of amyloid beta (Aβ) plaques and impaired memory. Microglia are associated with AD. They are activated in the AD brain and AD models. However, the exact role of microglia has not been established. We thus investigated the role of microglia in AD models using a primary culture and an ex-vivo assay. We showed that oligomerized Aβ is toxic to neurons in the primary culture. In the ex-vivo assay, a microglial cell line removed amyloid plaques in the brain of 5XFAD (AD model) mice. To verify if microglia can be protective for the neuron, we co-cultured neurons with primary microglia and treated them with Aβ. The loss of neurons, induced by amyloid toxicity, was attenuated by co-cultured microglia. Taken together, our data suggest that microglia promote neuronal survival by phagocytic clearance of Aβ in AD models.

摘要

阿尔茨海默病(AD)是神经退行性变最常见的病因。其特征是β淀粉样蛋白(Aβ)斑块沉积和记忆受损。小胶质细胞与AD相关。它们在AD大脑和AD模型中被激活。然而,小胶质细胞的确切作用尚未明确。因此,我们使用原代培养和体外试验研究了小胶质细胞在AD模型中的作用。我们发现寡聚化的Aβ对原代培养中的神经元有毒性。在体外试验中,一种小胶质细胞系清除了5XFAD(AD模型)小鼠大脑中的淀粉样斑块。为了验证小胶质细胞是否对神经元有保护作用,我们将神经元与原代小胶质细胞共培养,并用Aβ处理它们。淀粉样毒性诱导的神经元损失被共培养的小胶质细胞减轻。综上所述,我们的数据表明,在AD模型中,小胶质细胞通过吞噬清除Aβ促进神经元存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/116a/8813657/dd7772f7ce64/cmj-58-13-g001.jpg

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