Role of CD59a in Brain Injury After Trauma
Author Information
Author(s): Philip F Stahel, Michael A Flierl, B Paul Morgan, Ivonne Persigehl, Christiane Stoll, Claudia Conrad, Basel M Touban, Wade R Smith, Kathryn Beauchamp, Oliver I Schmidt, Wolfgang Ertel, Iris Leinhase
Primary Institution: Department of Orthopedic Surgery, Denver Health Medical Center, University of Colorado School of Medicine
Hypothesis
CD59a-/- mice would be more susceptible to complement-mediated secondary brain injury than wild-type littermates in a standardized model of closed head injury.
Conclusion
CD59a-/- mice showed significantly worse neurological outcomes and increased neuronal cell death after traumatic brain injury compared to wild-type mice.
Supporting Evidence
- CD59a-/- mice had a significantly impaired neurological outcome within 7 days after trauma.
- NSE serum levels were significantly elevated in CD59a-/- mice at 4 h and 24 h after trauma.
- Increased neuronal cell death and brain tissue destruction was detected in CD59a-/- mice within 24 hours to 7 days after head trauma.
Takeaway
Mice without the CD59a gene get hurt more badly in the brain after an injury than normal mice.
Methodology
Mice were subjected to focal closed head injury, and neurological impairment was assessed using a standardized Neurological Severity Score (NSS) and serum levels of neuron-specific enolase (NSE).
Potential Biases
The study used male mice exclusively, which may limit the generalizability of the findings.
Limitations
The study was conducted in a mouse model, which may not fully replicate human brain injury responses.
Participant Demographics
Mice were of age 10–12 weeks, weighing 28–32 g, and male gender exclusively.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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