• 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

健康和患病大脑中神经胶质细胞对突触数量的调控

Glial Control of Synapse Number in Healthy and Diseased Brain.

作者信息

Lee Eunbeol, Chung Won-Suk

机构信息

Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea.

出版信息

Front Cell Neurosci. 2019 Feb 13;13:42. doi: 10.3389/fncel.2019.00042. eCollection 2019.

DOI:10.3389/fncel.2019.00042
PMID:30814931
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6381066/
Abstract

Glial cells are emerging as crucial players that mediate development and homeostasis of the central nervous system (CNS). In particular, glial cells are closely associated with synapses, and control synapse formation, function, plasticity, and elimination during the stages of development and adulthood. Importantly, it is now increasingly evident that abnormal glial function can be an active inducer of the initiation and progression of various neurodegenerative diseases. Here, we discuss recent developments on the physiological roles of glial cells in the brain, and propose that synapse loss, which is a common characteristic of several neurodegenerative diseases, can be initiated by mis-regulation of normal glial function.

摘要

神经胶质细胞正逐渐成为介导中枢神经系统(CNS)发育和稳态的关键角色。特别是,神经胶质细胞与突触密切相关,并在发育和成年阶段控制突触的形成、功能、可塑性和消除。重要的是,现在越来越明显的是,神经胶质细胞功能异常可能是各种神经退行性疾病发生和进展的主动诱导因素。在这里,我们讨论了神经胶质细胞在大脑中生理作用的最新进展,并提出突触丧失作为几种神经退行性疾病的共同特征,可能是由正常神经胶质细胞功能的调节异常引发的。

相似文献

1
Glial Control of Synapse Number in Healthy and Diseased Brain.健康和患病大脑中神经胶质细胞对突触数量的调控
Front Cell Neurosci. 2019 Feb 13;13:42. doi: 10.3389/fncel.2019.00042. eCollection 2019.
2
Astrocyte-dependent circuit remodeling by synapse phagocytosis.星形胶质细胞依赖性突触吞噬作用的回路重塑。
Curr Opin Neurobiol. 2023 Aug;81:102732. doi: 10.1016/j.conb.2023.102732. Epub 2023 May 27.
3
Phagocytic Roles of Glial Cells in Healthy and Diseased Brains.神经胶质细胞在健康和患病大脑中的吞噬作用
Biomol Ther (Seoul). 2018 Jul 1;26(4):350-357. doi: 10.4062/biomolther.2017.133.
4
Insight into the role of phosphatidylserine in complement-mediated synapse loss in Alzheimer's disease.深入了解磷脂酰丝氨酸在阿尔茨海默病补体介导的突触丧失中的作用。
Fac Rev. 2021 Feb 24;10:19. doi: 10.12703/r/10-19. eCollection 2021.
5
Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer's Disease.神经元和神经胶质细胞在发育、衰老和阿尔茨海默病过程中介导补体介导的突触消除中的作用。
Mediators Inflamm. 2018 Nov 11;2018:2530414. doi: 10.1155/2018/2530414. eCollection 2018.
6
Roles of Glial Cells in Sculpting Inhibitory Synapses and Neural Circuits.神经胶质细胞在塑造抑制性突触和神经回路中的作用。
Front Mol Neurosci. 2017 Nov 13;10:381. doi: 10.3389/fnmol.2017.00381. eCollection 2017.
7
Techniques and Methods of Animal Brain Surgery: Perfusion, Brain Removal, and Histological Techniques动物脑外科手术技术与方法:灌注、脑切除及组织学技术
8
The Role of Glial Cells and Synapse Loss in Mouse Models of Alzheimer's Disease.神经胶质细胞和突触丧失在阿尔茨海默病小鼠模型中的作用
Front Cell Neurosci. 2018 Dec 11;12:473. doi: 10.3389/fncel.2018.00473. eCollection 2018.
9
Microglia and synapse interactions: fine tuning neural circuits and candidate molecules.小胶质细胞与突触相互作用:神经回路的精细调节及候选分子。
Front Cell Neurosci. 2013 May 15;7:70. doi: 10.3389/fncel.2013.00070. eCollection 2013.
10
Glia: guardians, gluttons, or guides for the maintenance of neuronal connectivity?神经胶质细胞:神经元连接维持的守护者、吞噬者还是引导者?
Ann N Y Acad Sci. 2015 Sep;1351(1):1-10. doi: 10.1111/nyas.12711. Epub 2015 Mar 9.

引用本文的文献

1
Synergistic effects of the Aβ/fibrinogen complex on synaptotoxicity, neuroinflammation, and blood-brain barrier damage in Alzheimer's disease models.Aβ/纤维蛋白原复合物对阿尔茨海默病模型中突触毒性、神经炎症和血脑屏障损伤的协同作用。
Alzheimers Dement. 2025 May;21(5):e70119. doi: 10.1002/alz.70119.
2
An In Vitro Assay to Measure Astrocyte-Dependent Synaptic Phagocytosis in Health and Major Depressive Disorder.一种用于测量健康和重度抑郁症中星形胶质细胞依赖性突触吞噬作用的体外检测方法。
Methods Mol Biol. 2025;2896:191-201. doi: 10.1007/978-1-0716-4366-2_14.
3
Repetitive concussions promote microglia-mediated engulfment of presynaptic excitatory input associated with cognitive dysfunction.

本文引用的文献

1
Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer's Disease.补体 C3aR 失活可减轻 Tau 病理学并逆转 Tau 病模型和阿尔茨海默病中失调的免疫网络。
Neuron. 2018 Dec 19;100(6):1337-1353.e5. doi: 10.1016/j.neuron.2018.10.031. Epub 2018 Nov 8.
2
Pentraxin 3 regulates synaptic function by inducing AMPA receptor clustering via ECM remodeling and β1-integrin.五聚素 3 通过 ECM 重塑和β1 整合素诱导 AMPA 受体聚集来调节突触功能。
EMBO J. 2019 Jan 3;38(1). doi: 10.15252/embj.201899529. Epub 2018 Nov 5.
3
Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies.
重复性脑震荡会促进小胶质细胞介导的对与认知功能障碍相关的突触前兴奋性输入的吞噬作用。
Commun Biol. 2025 Feb 28;8(1):335. doi: 10.1038/s42003-025-07729-1.
4
RIPK1 inhibition mitigates neuroinflammation and rescues depressive-like behaviors in a mouse model of LPS-induced depression.RIPK1 抑制减轻了脂多糖诱导的抑郁小鼠模型的神经炎症并挽救了抑郁样行为。
Cell Commun Signal. 2024 Sep 2;22(1):427. doi: 10.1186/s12964-024-01796-3.
5
Neuron-Astrocyte Interactions: A Human Perspective.神经元-星形胶质细胞相互作用:人类视角。
Adv Neurobiol. 2024;39:69-93. doi: 10.1007/978-3-031-64839-7_4.
6
Alzheimer's disease: from early pathogenesis to novel therapeutic approaches.阿尔茨海默病:从早期发病机制到新的治疗方法。
Metab Brain Dis. 2024 Aug;39(6):1231-1254. doi: 10.1007/s11011-024-01389-6. Epub 2024 Jul 24.
7
Advancing stroke recovery: unlocking the potential of cellular dynamics in stroke recovery.推进中风康复:释放中风康复中细胞动力学的潜力。
Cell Death Discov. 2024 Jul 11;10(1):321. doi: 10.1038/s41420-024-02049-5.
8
Early Inhibition of Phosphodiesterase 4B (PDE4B) Instills Cognitive Resilience in APPswe/PS1dE9 Mice.早期抑制磷酸二酯酶 4B(PDE4B)可增强 APPswe/PS1dE9 小鼠的认知弹性。
Cells. 2024 Jun 8;13(12):1000. doi: 10.3390/cells13121000.
9
Brain stars take the lead during critical periods of early postnatal brain development: relevance of astrocytes in health and mental disorders.脑星在出生后早期大脑发育的关键时期起主导作用:星形胶质细胞在健康和精神障碍中的相关性。
Mol Psychiatry. 2024 Sep;29(9):2821-2833. doi: 10.1038/s41380-024-02534-4. Epub 2024 Mar 29.
10
Retinal-glia ischemia and inflammation induced by chronic stress: The SABPA study.慢性应激诱导的视网膜-神经胶质细胞缺血与炎症:SABPA研究
Brain Behav Immun Health. 2019 Dec 17;2:100027. doi: 10.1016/j.bbih.2019.100027. eCollection 2020 Feb.
tau 病中的突触蛋白组变化及 C1q 抗体对 tau 诱导的突触丢失的挽救作用。
Neuron. 2018 Dec 19;100(6):1322-1336.e7. doi: 10.1016/j.neuron.2018.10.014. Epub 2018 Nov 1.
4
Astrocyte-Secreted Chordin-like 1 Drives Synapse Maturation and Limits Plasticity by Increasing Synaptic GluA2 AMPA Receptors.星形细胞分泌的 Chordin-like 1 通过增加突触 GluA2 AMPA 受体促进突触成熟并限制可塑性。
Neuron. 2018 Dec 5;100(5):1116-1132.e13. doi: 10.1016/j.neuron.2018.09.043. Epub 2018 Oct 18.
5
Block of A1 astrocyte conversion by microglia is neuroprotective in models of Parkinson's disease.小胶质细胞诱导 A1 型星形胶质细胞转化对帕金森病模型具有神经保护作用。
Nat Med. 2018 Jul;24(7):931-938. doi: 10.1038/s41591-018-0051-5. Epub 2018 Jun 11.
6
The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity.小胶质细胞先天免疫受体 TREM2 对于突触消除和正常大脑连接是必需的。
Immunity. 2018 May 15;48(5):979-991.e8. doi: 10.1016/j.immuni.2018.04.016. Epub 2018 May 8.
7
TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function.TREM2 是 β-淀粉样蛋白的受体,可介导小胶质细胞的功能。
Neuron. 2018 Mar 7;97(5):1023-1031.e7. doi: 10.1016/j.neuron.2018.01.031.
8
Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy.在TDP-43蛋白病小鼠模型中,小胶质细胞介导的与肌萎缩侧索硬化症相关的运动神经元变性恢复。
Nat Neurosci. 2018 Mar;21(3):329-340. doi: 10.1038/s41593-018-0083-7. Epub 2018 Feb 20.
9
Astrocyte-derived interleukin-33 promotes microglial synapse engulfment and neural circuit development.星形胶质细胞衍生的白细胞介素-33促进小胶质细胞的突触吞噬和神经回路发育。
Science. 2018 Mar 16;359(6381):1269-1273. doi: 10.1126/science.aal3589. Epub 2018 Feb 1.
10
Glia-to-neuron transfer of miRNAs via extracellular vesicles: a new mechanism underlying inflammation-induced synaptic alterations.通过细胞外囊泡进行的微小 RNA 从神经胶质到神经元的转移:炎症诱导的突触改变的一个新机制。
Acta Neuropathol. 2018 Apr;135(4):529-550. doi: 10.1007/s00401-017-1803-x. Epub 2018 Jan 4.