The role of complement in stroke therapy
Document Type
Article
Abstract
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.
Medical Subject Headings
Brain Ischemia (physiopathology); Complement System Proteins (therapeutic use); Humans; Inflammation (drug therapy); Neurons (pathology); Reperfusion Injury (drug therapy, physiopathology); Stroke (drug therapy)
Publication Date
1-1-2008
Publication Title
Advances in experimental medicine and biology
ISSN
0065-2598
Volume
632
First Page
23
Last Page
33
PubMed ID
19025111
Recommended Citation
Komotar, Ricardo J.; Kim, Grace H.; Otten, Marc L.; Hassid, Benjamin; Mocco, J; Sughrue, Michael E.; Starke, Robert M.; Mack, William J.; Ducruet, Andrew F.; Merkow, Maxwell B.; Garrett, Matthew C.; and Connolly, E Sander, "The role of complement in stroke therapy" (2008). Translational Neuroscience. 2047.
https://scholar.barrowneuro.org/neurobiology/2047