小胶质细胞对β淀粉样蛋白暴露后神经元存活的保护作用。

Chonnam Medical Journal Pub Date : 2022-01-01 Epub Date: 2022-01-25 DOI:10.4068/cmj.2022.58.1.13
Sunjun Lee, Won-Seok Choi
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摘要

阿尔茨海默病(AD)是神经变性最常见的原因。其特征是β淀粉样蛋白(Aβ)斑块沉积和记忆受损。小胶质细胞与阿尔茨海默病有关。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确定。因此,我们通过原代培养和离体实验研究了小胶质细胞在AD模型中的作用。我们发现,在原代培养中,寡聚的Aβ对神经元具有毒性。在离体实验中,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具有保护作用,我们将神经元与原代小胶质细胞共培养,并用Aβ处理。由淀粉样蛋白毒性引起的神经元损失,通过共培养的小胶质细胞可以减轻。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来促进神经元的存活。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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

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.

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