Contribution of Fibrinogen to Inflammation and Neuronal Density in Human Traumatic Brain Injury

Area of Science:

• Neuroscience
• Neuropathology
• Trauma Research

Background:

• Traumatic brain injury (TBI) is a major cause of death and disability with no specific treatments.
• Blood-brain barrier disruption and fibrinogen deposition occur in TBI, but their role in neuropathology is unclear.
• Fibrinogen activates microglia/macrophages, potentially linking it to neuroinflammation and injury.

Purpose of the Study:

• To investigate the association between fibrinogen deposition and neuropathology in human TBI.
• To determine if fibrinogen contributes to neuroinflammation and neuronal/axonal injury following TBI.

Main Methods:

• Human TBI cases (survival: 12h to 13 years) and controls were analyzed.
• Tissue sections (frontal lobe, temporal lobe, corpus callosum, cingulate gyrus, brainstem) were examined.
• Assessed plasma protein deposition (fibrinogen, IgG), microglial/macrophage activation (CD68, Iba-1), neuronal density, and axonal injury (βAPP).

Main Results:

• Acute TBI showed significantly increased parenchymal fibrinogen and IgG deposition compared to controls and long-term survivors.
• Fibrinogen, not IgG, correlated with increased microglial/macrophage activation and reduced neuronal density.
• Perivascular fibrinogen was linked to microglial clustering and axonal βAPP accumulation.

Conclusions:

• Fibrinogen deposition is significantly elevated in acute TBI.
• Fibrinogen is associated with neuroinflammation and neuronal loss in TBI.
• Further research is needed to explore the causal role of fibrinogen in TBI neuropathology.