Summary
Ischemic brain lesions result in chronic neuroinflammation which is insufficiently resolved. We identified a subpopulation of chronically activated microglia (ChrAMs) after stroke, which are distinct from acutely reactive as well as other previously described microglia identities. Manipulation of microglial activation was able to modulate neuronal function and recovery but also affected multiple other cell populations. Hence, the goal of this project is to identify the cellular interactions of microglia during post-stroke recovery by defining the cellular interaction partners, mechanisms of interaction and the impact of microglia on multicellular network function.
