Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice

@article{Stahel2008AbsenceOT,
  title={Absence of the complement regulatory molecule CD59a leads to exacerbated neuropathology after traumatic brain injury in mice},
  author={Philip F. Stahel and Michael Flierl and B. Paul Morgan and Ivonne Persigehl and Christiane Stoll and Claudia Conrad and Basel M Touban and Wade R. Smith and Kathryn M Beauchamp and Oliver I. Schmidt and Wolfgang Ertel and Iris Leinhase},
  journal={Journal of Neuroinflammation},
  year={2008},
  volume={6},
  pages={2 - 2}
}
Complement represents a crucial mediator of neuroinflammation and neurodegeneration after traumatic brain injury. The role of the terminal complement activation pathway, leading to generation of the membrane attack complex (MAC), has not been thoroughly investigated. CD59 is the major regulator of MAC formation and represents an essential protector from homologous cell injury after complement activation in the injured brain. Mice deleted in the Cd59a gene (CD59a-/-) and wild-type littermates (n… CONTINUE READING
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