Neuroinflammatory responses in experimental and human stroke lesions

摘要: Neuroinflammation has been suggested as an attractive treatment target in stroke, since it offers a broader therapeutic window comparison to currently established thrombolytic approaches. Inflammatory cells of both the innate and adaptive immune system have identified experimental well human stroke lesions. In animal models, various strategies targeting neuroinflammation shown beneficial effects, however, translation disease so far disappointing. Comparisons numerous findings with until now rather limited data reveal that despite similarities core signature inflammatory reaction, lacks clearly definable temporal spatial sequences lesion maturation can be generalized applied for large patient population. Thus, well-timed models clear succession pathogenic mechanisms, precise stage-dependent patients will difficult achieve. addition, contribution different components quantitatively varies between humans animals even modes ischemia induction models. Finally, lesions develop on basis age-dependent microglia pre-activation, which may major impact further activation functional differentiation these cells. Knowledge about patients, is determined future studies what extent causes co-morbidities result distinct patterns inflammation.