Background The brain's initial innate response to stroke is primarily mediated by microglia,
the resident macrophage of the CNS. However, as early as 4 h after stroke, the blood–brain …

Neuroinflammation has been suggested as an attractive treatment target in stroke, since it
offers a broader therapeutic window in comparison to currently established thrombolytic …

Ischemic stroke generates an immune response that contributes to neuronal loss as well as
tissue repair. This is a complex process involving a range of cell types and effector …

Inflammatory mechanisms, involving granulocytes, T‐cells, B‐cells, macrophages and
activated microglia, have been suggested to play a pathogenic role in experimental models …

Inflammation and immune mechanisms are crucially involved in the pathophysiology of the
development, acute damage cascades, and chronic course after ischemic stroke …

Inflammation has been implicated as a secondary injury mechanism following ischemia and
stroke. A variety of experimental models, including thromboembolic stroke, focal and global …

Recent works in the area of stroke and brain ischemia has demonstrated the significance of
the inflammatory response accompanying necrotic brain injury. Acutely, this response …

Stroke is a frequent cause of long-term disability and death worldwide. Ischemic stroke is
more commonly encountered compared to hemorrhagic stroke, and leads to tissue death by …

Ischemic stroke is one of the leading health issues and the major cause of permanent
disability in adults worldwide. Energy depletion and hypoxia occurring after ischemic stroke …

Stroke causes neuronal cell death and destruction of neuronal circuits in the brain and
spinal cord. Injury to the brain tissue induces sterile inflammation triggered by the …