Targeted complement inhibition salvages stressed neurons and inhibits neuroinflammation after stroke in mice.

ABSTRACT: Ischemic stroke results from the interruption of blood flow to the brain resulting in long-term motor and cognitive neurological deficits, and it is a leading cause of death and disability. Current interventions focus on the restoration of blood flow to limit neuronal death, but these treatments have a therapeutic window of only a few hours and do not address post-stroke cerebral inflammation. The complement system, a component of the innate immune system, is activated by natural immunoglobulin M (IgM) antibodies that recognize neoepitopes expressed in the brain after ischemic stroke. We took advantage of this recognition system to inhibit complement activation locally in the ischemic area in mice. A single chain antibody recognizing a post-ischemic neoepitope linked to a complement inhibi

SUBMITTER: Alawieh A 

PROVIDER: S-EPMC6689196 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature