Neuroglia in stroke

Stroke, ischemic or hemorrhagic, triggers a complex and coordinated glial response, which, to a large extent, defines the progression and outcome of this focal damage of the nervous tissue. Massive cell death in the infarction core results in a release of damage-associated molecular patterns, which, together with blood-borne factors entering the brain through either ruptured vessels or through compromised blood-brain barrier, trigger reactive gliosis. Microglia are the first to migrate toward the lesion, proliferate, and phagocytose cellular debris in and around the infarct core. Reactive astrogliosis occurs around the margins of the infarct core and is characterized by astrocytic proliferation, morphologic remodeling with loss of territorial domain segregation, and transcriptional reprogramming into wound repair astrocytes that form a periinfarct border that protects the healthy tissue and assists postlesional regeneration.