The role of complement in stroke therapy.
Cerebral ischemia and reperfusion initiate an inflammatory process which results in secondary neuronal damage. Immunomodulatory agents represent a promising means of salavaging viable tissue following stroke. The complement cascade is a potent mediator of inflammation which is activated following cerebral ischemia. Complement is deposited on apoptotic neurons which likely leads to injury in adjacent viable cells. Studies suggest that blocking the complement cascade during the early phases of infarct evolution may result in decreased penumbral tissue infarction and limit the extent of brain injury. Additionally, other elements of the complement cascade may play a critical role in cell survival. In this paper, we review the role of the complement cascade in neuronal damage following ischemic injury and emphasize possible therapeutic targets.
Komotar
Ricardo J
RJ
Department of Neurological Surgery, Columbia University, New York, NY 10032, USA.
Kim
Grace H
GH
Otten
Marc L
ML
Hassid
Benjamin
B
Mocco
J
J
Sughrue
Michael E
ME
Starke
Robert M
RM
Mack
William J
WJ
Ducruet
Andrew F
AF
Merkow
Maxwell B
MB
Garrett
Matthew C
MC
Connolly
E Sander
ES
D002545:Brain Ischemia / Q000503:physiopathology; D003165:Complement System Proteins / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D009474:Neurons / Q000473:pathology; D015427:Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology; D020521:Stroke / Q000188:drug therapy*
D003165:Complement System Proteins