Inflammation, plasticity and real-time imaging after cerebral ischemia

Abstract

With an incidence of approximately 350 in 100,000, stroke is the third leading cause of death and a major cause of disability in industrialized countries. At present, although progress has been made in understanding the molecular pathways that lead to ischemic cell death, the current clinical treatments remain poorly eVective. There is mounting evidence that inXammation plays an important role in cerebral ischemia. Experimentally and clinically, brain response to ischemic injury is associated with an acute and prolonged inXammatory process characterized by the activation of resident glial cells, production of inXammatory cytokines as well as leukocyte and monocyte inWltration in the brain, events that may contribute to ischemic brain injury and aVect brain recovery and plasticity. However, whether the post-ischemic inXammatory response is deleterious or beneWcial to brain recovery is presently a matter of debate and controversies. Here, we summarize the current knowledge on the molecular mechanisms underlying post-ischemic neuronal plasticity and the potential role of inXammation in regenerative processes and functional recovery after stroke. Furthermore, because of the dynamic nature of the brain inXammatory response, we highlight the importance of the development of novel experimental approaches such as real-time imaging. Finally, we discuss the novel transgenic reporter mice models that have allowed us to visualize and to analyze the processes such as neuroinXammation and neuronal repair from the ischemic brains of live animals.

Citicoline Enhances Neuroregenerative Processes After Experimental Stroke in Rats

“…Because microglia is thought to mediate beneficial effects beyond acute ischemic stroke, this finding suggests that other, more powerful mechanisms are also induced by citicoline. 19 Neurogenesis is suggested to play a decisive role in mediating functional recovery after experimental stroke. 20 Within the healthy brain, adult neurogenesis supplies newborn neurons from the subgranular zone to the adjacent dentate gyrus of the hippocampus and from the SVZ to the olfactory bulb (for an in-depth review, see Zhao et al 21 ).…”

“…Только реакция микроглии, окружающей зону поражения, была снижена в группе цитиколина. Поскольку считается, что микроглия опос-редует положительные эффекты за пределами острого ишемического инсульта, этот результат предполагает наличие других, более мощных механизмов, индуцируе-мых цитиколином [19]. Считается, что нейрогенез играет решающую роль в опосредовании функционального восстановления после экспериментального инсульта [20].…”

Changes in Host Blood Factors and Brain Glia Accompanying the Functional Recovery after Systemic Administration of Bone Marrow Stem Cells in Ischemic Stroke Rats

“…That both rMSCs Therefore, we began by sampling blood serum and tracking changes in the expression of 50 circulating inand hMSCs stem cells were equally effective in this regard validates the continued study of xenotransplanted flammatory/immune and/or growth factor/receptors using a custom array. As documented previously (23,51), hMSCs in an MCAO rat as needed for the development of therapies suitable for the treatment of stroke patients.…”

Age-dependent modifications in vascular adhesion molecules and apoptosis after 48-h reperfusion in a rat global cerebral ischemia model

“…Some studies on focal ischemia indicate that 48 h after ischemia, 30 % of cells in the ischemic core appear damaged, but show no signs of death, and 15 % of cells are apparently healthy (Li et al 1998). On the other hand, 48 h after ischemia is considered the limit of the viability for cells in the penumbra area (Meisel et al 2005;Durukan and Tatlisumak 2007;Kadhim et al 2008;Lakhan et al 2009;Kriz and Lalancette-Hebert 2009;Candelario-Jalil 2009). Thus, we chose this time for the study because it seems to be critical in the analysis for both inflammation and cell death.…”