The role of complement in stroke therapy

Ricardo J. Komotar, Grace H. Kim, Marc L. Otten, Benjamin Hassid, J. Mocco, Michael E. Sughrue, Robert M. Starke, William J. MacK, Andrew F. Ducruet, Maxwell B. Merkow, Matthew C. Garrett, E. Sander Connolly

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


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.

Original languageEnglish
Pages (from-to)23-33
Number of pages11
JournalAdvances in Experimental Medicine and Biology
StatePublished - Dec 1 2008
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)


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