Mediation of coagulation factors to limit neuroinflammation post-ischaemic stroke

Stroke is a global leading cause of death and disability. Despite this, there is currently no treatment to limit inflammatory events which has been shown to enhance brain injury after stroke. In this project, we hypothesise interrupting interactions between coagulation factors (thrombin/fibrin) and brain-resident immune cells (microglia) will limit cerebral thrombo-inflammation and associated tissue injury to improve stroke outcome. To test this, we will use an internationally recognised preclinical model of ischaemic stroke and state-of- the-art in vivo brain imaging to examine the molecular mechanisms underlying coagulation factor- microglial interactions. Better understanding of the interactions in the brain post- stroke will lead to novel therapeutic targets and new treatment options.