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阿尔茨海默病小鼠模型中淀粉样β吞噬能力的定量评估。

Quantitative assessment of amyloid-beta phagocytic capacity in an Alzheimer's disease mouse model.

机构信息

Division of Life Science, State Key Laboratory of Molecular Neuroscience, Molecular Neuroscience Center, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.

Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China.

出版信息

STAR Protoc. 2021 Jan 13;2(1):100265. doi: 10.1016/j.xpro.2020.100265. eCollection 2021 Mar 19.

DOI:10.1016/j.xpro.2020.100265
PMID:33490981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7811161/
Abstract

Alzheimer's disease is characterized by the deposition of extracellular amyloid-beta (Aβ) plaques. While microglial phagocytosis is a major mechanism through which Aβ is cleared, there is no method for quantitatively assessing Aβ phagocytic capacity of microglia . Here, we present a flow cytometry-based method for investigating the Aβ phagocytic capacity of microglia . This method enables the direct comparison of Aβ phagocytic capacity between different microglial subpopulations as well as the direct isolation of Aβ phagocytic microglia for downstream applications. For complete details on the use and execution of this protocol, please refer to Lau et al. (2020).

摘要

阿尔茨海默病的特征是细胞外淀粉样蛋白-β(Aβ)斑块的沉积。虽然小胶质细胞吞噬是清除 Aβ 的主要机制,但目前还没有定量评估小胶质细胞 Aβ吞噬能力的方法。在这里,我们提出了一种基于流式细胞术的方法来研究小胶质细胞的 Aβ吞噬能力。该方法能够直接比较不同小胶质细胞亚群之间的 Aβ吞噬能力,并且能够直接分离 Aβ吞噬小胶质细胞用于下游应用。有关该方案的使用和执行的完整详细信息,请参考 Lau 等人(2020 年)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/ead8c5ea249a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/72962ca2179c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/b974f97a899b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/718b9ab5a59a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/94feb8432d4f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/dff9436dc0e7/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/ead8c5ea249a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/72962ca2179c/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/b974f97a899b/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/718b9ab5a59a/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/94feb8432d4f/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/dff9436dc0e7/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d308/7811161/ead8c5ea249a/gr5.jpg

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Cell Rep. 2020 Apr 21;31(3):107530. doi: 10.1016/j.celrep.2020.107530.
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IL-33 ameliorates Alzheimer's disease-like pathology and cognitive decline.白细胞介素-33可改善阿尔茨海默病样病理及认知功能衰退。
Proc Natl Acad Sci U S A. 2016 May 10;113(19):E2705-13. doi: 10.1073/pnas.1604032113. Epub 2016 Apr 18.
Extracellular vesicles from human-induced pluripotent stem cell-derived neural stem cells alleviate proinflammatory cascades within disease-associated microglia in Alzheimer's disease.
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J Extracell Vesicles. 2024 Nov;13(11):e12519. doi: 10.1002/jev2.12519.
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Modulation of Alzheimer's disease brain pathology in mice by gut bacterial depletion: the role of IL-17a.肠道细菌耗竭对小鼠阿尔茨海默病脑病理的调节作用:IL-17a 的作用。
Gut Microbes. 2024 Jan-Dec;16(1):2363014. doi: 10.1080/19490976.2024.2363014. Epub 2024 Jun 21.
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Nat Aging. 2023 Oct;3(10):1219-1236. doi: 10.1038/s43587-023-00491-1. Epub 2023 Sep 21.
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