Fibrinogen and Neuroinflammation During Traumatic Brain Injury.

Fibrinogen and Neuroinflammation During Traumatic Brain Injury.
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创伤性脑损伤期间的纤维蛋白原和神经炎症。

DOI:
10.1007/s12035-020-02012-2
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发表时间:
2020-11
影响因子:
5.1
通讯作者:
Lominadze D
Lominadze D
中科院分区:
医学2区
文献类型:
--
作者:
Sulimai N;Lominadze D

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许多神经退行性疾病如阿尔茨海默病(AD)、多发性硬化和创伤性脑损伤(TBI)与全身性炎症相关。炎症本身导致血液中纤维蛋白原(Fg)含量增加,称为高纤维蛋白原血症(HFg)。纤维蛋白原不仅被认为是一种急性时相蛋白和炎症标志物,而且已被证明可以引起炎症反应。纤维蛋白沉积与神经炎性疾病如AD和TBI的记忆力下降有关。在最常见的TBI形式,轻度至中度TBI期间,短期记忆减少。在轻度至中度TBI患者的大脑中发现了fib沉积物。绝大多数文献强调纤维蛋白激活的小胶质细胞作为神经炎症通路中的介质的作用。然而,最近的发现,星形胶质细胞,其中构成约30%的细胞在哺乳动物中枢神经系统(CNS),保证进一步调查的致病作用HFg星形胶质细胞介导的神经炎症。我们前期的研究表明,沉积在血管-星形胶质细胞界面的纤维蛋白原激活星形胶质细胞。然而,很少有人知道Fg如何直接影响星形胶质细胞和神经元。在这篇综述中,我们总结了研究表明,纤维蛋白原对不同类型的细胞在血管神经元单位的影响。我们还将讨论HFg在TBI期间诱导神经炎症的可能机制。
Many neurodegenerative diseases such as Alzheimer’s disease (AD), multiple sclerosis, and traumatic brain injury (TBI) are associated with systemic inflammation. Inflammation itself results in increased blood content of fibrinogen (Fg), called hyperfibrinogenemia (HFg). Fg is not only considered an acute phase protein and a marker of inflammation, but has been shown that it can cause inflammatory responses. Fibrin deposits have been associated with memory reduction in neuroinflammatory diseases such as AD and TBI. Reduction in short-term memory has been seen during the most common form of TBI, mild-to-moderate TBI. Fibrin deposits have been found in brains of patients with mild-to-moderate TBI. The vast majority of the literature emphasizes the role of fibrin-activated microglia as the mediator in the neuroinflammation pathway. However, the recent discovery that astrocytes, which constitute approximately 30% of the cells in the mammalian central nervous system (CNS), warrants further investigations in the causative role of HFg in astrocyte-mediated neuroinflammation. Our previous study showed that Fg deposited in the vasculo-astrocyte interface activated astrocytes. However, little is known of how Fg directly affects astrocytes and neurons. In this review, we summarize studies that show the effect of Fg on different types of cells in the vasculo-neuronal unit. We will also discuss the possible mechanism of HFg-induced neuroinflammation during TBI.
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