• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

与病理性α-突触核蛋白传递相关的优先小胶质细胞激活。

Preferential microglial activation associated with pathological alpha synuclein transmission.

机构信息

Department of Neurology, Hallym University Sacred Heart Hospital, Hallym University, Anyang, South Korea.

Department of Biomedical Gerontology, Graduate School of Hallym University, Chuncheon, South Korea; Ilsong Institute of Life Science, Hallym University, Anyang, South Korea.

出版信息

J Clin Neurosci. 2020 Nov;81:469-476. doi: 10.1016/j.jocn.2020.09.027. Epub 2020 Nov 2.

DOI:10.1016/j.jocn.2020.09.027
PMID:33222964
Abstract

Self-proliferation of the pathological form of α-synuclein was identified as one of the main pathophysiological presentations of Parkinson's disease (PD) a decade ago. Although inflammation has also been suggested to contribute to PD pathogenesis, it is unclear whether this is associated with the pathological spread of α-synuclein aggregation. Herein, we evaluated two main neuroinflammatory processes in the striatum-microgliosis and astrogliosis-after the injection of preformed fibrils of α-synuclein into the mouse striatum. Thus, our study demonstrated that microgliosis accompanied α-synuclein propagation, while astrogliosis did not. Therefore, we report a preferential association between microglia and the process of α-synuclein proliferation.

摘要

十多年前,研究人员发现病理性α-突触核蛋白的自我增殖是帕金森病 (PD) 的主要病理生理学表现之一。尽管炎症也被认为与 PD 的发病机制有关,但尚不清楚这是否与α-突触核蛋白聚集的病理性传播有关。在此,我们评估了将α-突触核蛋白原纤维注射到小鼠纹状体后纹状体中的两种主要神经炎症过程——小胶质细胞激活和星形胶质细胞增生。因此,我们的研究表明小胶质细胞激活伴随着α-突触核蛋白的传播,而星形胶质细胞增生则没有。因此,我们报告了小胶质细胞与α-突触核蛋白增殖过程之间的优先关联。

相似文献

1
Preferential microglial activation associated with pathological alpha synuclein transmission.与病理性α-突触核蛋白传递相关的优先小胶质细胞激活。
J Clin Neurosci. 2020 Nov;81:469-476. doi: 10.1016/j.jocn.2020.09.027. Epub 2020 Nov 2.
2
Microglial exosomes facilitate α-synuclein transmission in Parkinson's disease.小胶质细胞外泌体促进帕金森病中α-突触核蛋白的传播。
Brain. 2020 May 1;143(5):1476-1497. doi: 10.1093/brain/awaa090.
3
Reactive microglia enhance the transmission of exosomal α-synuclein via toll-like receptor 2.反应性小胶质细胞通过 Toll 样受体 2 增强外泌体 α-突触核蛋白的传递。
Brain. 2021 Aug 17;144(7):2024-2037. doi: 10.1093/brain/awab122.
4
Temporal evolution of microglia and α-synuclein accumulation following foetal grafting in Parkinson's disease.帕金森病胎儿移植后小胶质细胞和α-突触核蛋白积累的时间演变。
Brain. 2019 Jun 1;142(6):1690-1700. doi: 10.1093/brain/awz104.
5
The critical role of Nramp1 in degrading α-synuclein oligomers in microglia under iron overload condition.铁过载条件下Nramp1在小胶质细胞中降解α-突触核蛋白寡聚体的关键作用。
Neurobiol Dis. 2017 Aug;104:61-72. doi: 10.1016/j.nbd.2017.05.001. Epub 2017 May 2.
6
Peripheral inflammation exacerbates α-synuclein toxicity and neuropathology in Parkinson's models.在帕金森病模型中,外周炎症会加剧α-突触核蛋白毒性和神经病理学变化。
Neuropathol Appl Neurobiol. 2021 Feb;47(1):43-60. doi: 10.1111/nan.12644. Epub 2020 Aug 6.
7
miR-let-7a suppresses α-Synuclein-induced microglia inflammation through targeting STAT3 in Parkinson's disease.miR-let-7a 通过靶向 STAT3 抑制帕金森病中 α-Synuclein 诱导的小胶质细胞炎症。
Biochem Biophys Res Commun. 2019 Nov 19;519(4):740-746. doi: 10.1016/j.bbrc.2019.08.140. Epub 2019 Sep 20.
8
Pathological α-synuclein exacerbates the progression of Parkinson's disease through microglial activation.病理性α-突触核蛋白通过小胶质细胞激活加剧帕金森病的进展。
Toxicol Lett. 2017 Jan 4;265:30-37. doi: 10.1016/j.toxlet.2016.11.002. Epub 2016 Nov 16.
9
CXCL12 is involved in α-synuclein-triggered neuroinflammation of Parkinson's disease.CXCL12 参与了帕金森病中 α-突触核蛋白触发的神经炎症。
J Neuroinflammation. 2019 Dec 12;16(1):263. doi: 10.1186/s12974-019-1646-6.
10
Metabotropic glutamate receptor 5 inhibits α-synuclein-induced microglia inflammation to protect from neurotoxicity in Parkinson's disease.代谢型谷氨酸受体 5 抑制 α-突触核蛋白诱导的小胶质细胞炎症,从而保护帕金森病的神经毒性。
J Neuroinflammation. 2021 Jan 18;18(1):23. doi: 10.1186/s12974-021-02079-1.

引用本文的文献

1
Emerging role of microglia in inter-cellular transmission of α-synuclein in Parkinson's disease.小胶质细胞在帕金森病中α-突触核蛋白细胞间传递中的新作用
Front Aging Neurosci. 2024 Oct 9;16:1411104. doi: 10.3389/fnagi.2024.1411104. eCollection 2024.
2
Microglial inhibition alleviates alpha-synuclein propagation and neurodegeneration in Parkinson's disease mouse model.小胶质细胞抑制可减轻帕金森病小鼠模型中α-突触核蛋白的传播和神经退行性变。
NPJ Parkinsons Dis. 2024 Feb 2;10(1):32. doi: 10.1038/s41531-024-00640-2.
3
Evidence of Inflammation in Parkinson's Disease and Its Contribution to Synucleinopathy.
帕金森病中的炎症证据及其对突触核蛋白病的影响
J Mov Disord. 2022 Jan;15(1):1-14. doi: 10.14802/jmd.21078. Epub 2021 Nov 3.
4
Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease.帕金森病中星形胶质细胞和小胶质细胞的神经保护与疾病修饰作用
Antioxidants (Basel). 2022 Jan 17;11(1):170. doi: 10.3390/antiox11010170.
5
Temporal Evolution of Inflammation and Neurodegeneration With Alpha-Synuclein Propagation in Parkinson's Disease Mouse Model.帕金森病小鼠模型中炎症和神经退行性变随α-突触核蛋白传播的时间演变
Front Integr Neurosci. 2021 Oct 5;15:715190. doi: 10.3389/fnint.2021.715190. eCollection 2021.
6
A Summary of Phenotypes Observed in the In Vivo Rodent Alpha-Synuclein Preformed Fibril Model.在体内鼠源α-突触核蛋白原纤维模型中观察到的表型概述。
J Parkinsons Dis. 2021;11(4):1555-1567. doi: 10.3233/JPD-212847.
7
T Cells Limit Accumulation of Aggregate Pathology Following Intrastriatal Injection of α-Synuclein Fibrils.T 细胞限制了 α-突触核蛋白原纤维脑内注射后聚集病理的积累。
J Parkinsons Dis. 2021;11(2):585-603. doi: 10.3233/JPD-202351.