Fibrinogen and Neuroinflammation During Traumatic Brain Injury

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...

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Bibliographic Details
Published in:Molecular neurobiology 2020-11, Vol.57 (11), p.4692-4703
Main Authors: Sulimai, Nurul, Lominadze, David
Format: Article
Language:English
Subjects:
Acute phase proteins
Alzheimer's disease
Astrocytes
Biomedical and Life Sciences
Biomedicine
Cell Biology
Central nervous system
Fibrin
Fibrinogen
Inflammation
Microglia
Multiple sclerosis
Neurobiology
Neurodegenerative diseases
Neurology
Neurosciences
Reviews
Short term memory
Traumatic brain injury
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Summary: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, manifest different reactive states 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.
ISSN:0893-7648
1559-1182
DOI:10.1007/s12035-020-02012-2