.png){kind=icon}
返回
COVID, complement, and the brain
.png){kind=icon}
OA
AI
DOI：10.3389/fimmu.2023.1216457.png)
.png){kind=icon}
.png){kind=icon}
分享.png){kind=icon}
收藏
摘要
En 中文
The brains of COVID-19 patients are affected by the SARS-CoV-2 virus, and these effects may contribute to several COVID-19 sequelae, including cognitive dysfunction (termed long COVID by some researchers). Recent advances concerning the role of neuroinflammation and the consequences for brain function are reviewed in this manuscript. Studies have shown that respiratory SARS-CoV-2 infection in mice and humans is associated with selective microglial reactivity in the white matter, persistently impaired hippocampal neurogenesis, a decrease in the number of oligodendrocytes, and myelin loss. Brain MRI studies have revealed a greater reduction in grey matter thickness in the orbitofrontal cortex and parahippocampal gyrus, associated with a greater reduction in global brain size, in those with SARS-CoV-2 and a greater cognitive decline. COVID-19 can directly infect endothelial cells of the brain, potentially promoting clot formation and stroke; complement C3 seems to play a major role in this process. As compared to controls, the brain tissue of patients who died from COVID-19 have shown a significant increase in the extravasation of fibrinogen, indicating leakage in the blood-brain barrier; furthermore, recent studies have documented the presence of IgG, IgM, C1q, C4d, and C5b-9 deposits in the brain tissue of COVID-19 patients. These data suggest an activation of the classical complement pathway and an immune-mediated injury to the endothelial cells. These findings implicate both the classical and alternative complement pathways, and they indicate that C3b and the C5b-9 terminal complement complex (membrane attack complex, MAC) are acting in concert with neuroinflammatory and immune factors to contribute to the neurological sequelae seen in patients with COVID.
Keyword:
COVID
brain
complement system
C5b-9
endothelial cells
cognitive dysfunction
AI总结
对已上传原文的论文进行重点信息的提取，主要内容包括：简要概述、研究摘要、背景介绍、关键亮点、图文解析、展望与总结。
期刊
IF:
5.9
论文数:
5.0W
被引数:
22.7W
机构
引用论文
Complement component C3 mediates inflammatory injury following focal cerebral ischemia.png)
CIRCULATION RESEARCHOAAI
CIRCULATION RESEARCHIF16.2
OAAI分享收藏Membrane attack by complement: the assembly and biology of terminal complement complexes补体的膜攻击: 末端补体复合物的组装和生物学IMMUNOLOGIC RESEARCHOAAI
IMMUNOLOGIC RESEARCHIF3.1
OAAI分享收藏Cerebral hypoperfusion in post-COVID-19 cognitively impaired subjects revealed by arterial spin labeling MRISCIENTIFIC REPORTSOAAI
SCIENTIFIC REPORTSIF3.9
OAAI分享收藏SARS-CoV-2 Spike protein induces TLR4-mediated long-term cognitive dysfunction recapitulating post-COVID-19 syndrome in miceSARS-CoV-2纤突蛋白诱导TLR4-mediated长期认知功能障碍重述小鼠post-COVID-19综合征CELL REPORTSOAAI
CELL REPORTSIF6.9
OAAI分享收藏
查看更多内容