Complement and microglia dependent synapse elimination in brain development.
Complement and microglia dependent synapse elimination in brain development.
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DOI：
10.1002/wsbm.1545
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发表时间：
2022-05
影响因子：
3.1
通讯作者：
中科院分区：
文献类型：
--
作者：
突触消除，也称为突触修剪，是大脑发育过程中神经回路成熟的关键步骤。越来越多的证据表明，先天免疫系统的补体级联在突触消除中起着重要作用。研究表明，发育过程中过剩的突触被补体蛋白调理，随后被表达补体受体的小胶质细胞吞噬。这一过程受多种分子信号的调控，包括影响补体激活的补体抑制剂，以及影响小胶质细胞招募和激活的信号。这些信号可能促进或抑制发育过程中特定突触的移除。补体-小胶质细胞系统也参与了几种发育性脑疾病的发病机制，提示突触修剪机制的失调可能是这些疾病特定回路缺陷的基础。在这里，我们综述了在脑发育过程中补体依赖和小胶质细胞依赖的突触消除的分子和细胞机制的最新证据，并强调了该系统作为发育性脑疾病的治疗靶点的潜力。这篇文章的分类是：神经疾病；分子和细胞生理学；神经疾病；干细胞和发育免疫系统疾病；分子和细胞生理学
Synapse elimination, also known as synaptic pruning, is a critical step in the maturation of neural circuits during brain development. Mounting evidence indicates that the complement cascade of the innate immune system plays an important role in synapse elimination. Studies indicate that excess synapses during development are opsonized by complement proteins and subsequently phagocytosed by microglia which expresses complement receptors. The process is regulated by diverse molecular signals, including complement inhibitors that affect the activation of complement, as well as signals that affect microglial recruitment and activation. These signals may promote or inhibit the removal of specific sets of synapses during development. The complement-microglia system has also been implicated in the pathogenesis of several developmental brain disorders, suggesting that the dysregulation of mechanisms of synapse pruning may underlie the specific circuitry defects in these diseases. Here, we review the latest evidence on the molecular and cellular mechanisms of complement-dependent and microglia-dependent synapse elimination during brain development, and highlight the potential of this system as a therapeutic target for developmental brain disorders. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology Neurological Diseases > Stem Cells and Development Immune System Diseases > Molecular and Cellular Physiology
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影响因子：
4.6
作者：
Chen XS;Reader RH;Hoischen A;Veltman JA;Simpson NH;Francks C;Newbury DF;Fisher SE
通讯作者：
Fisher SE
影响因子：
4.8
作者：
Escudero-Esparza, Astrid;Kalchishkova, Nikolina;Blom, Anna M.
通讯作者：
Blom, Anna M.
影响因子：
25
作者：
Cong, Qifei;Soteros, Breeanne M.;Sia, Gek-Ming
通讯作者：
Sia, Gek-Ming
DOI：
10.1159/000465523
发表时间：
2017-07-01
期刊：
Molecular neuropsychiatry
影响因子：
--
作者：
Fagan, Kiley;Crider, Amanda;Pillai, Anilkumar
通讯作者：
Pillai, Anilkumar
影响因子：
5.3
作者：
Bjartmar, Lisa;Huberman, Andrew D.;Perin, Mark S.
通讯作者：
Perin, Mark S.