Chronic inflammasome activation in post-stroke recovery

在我们的合作项目中，我们想了解炎性小体激活如何参与中风后的慢性神经炎症。在我们第一个资助期的研究结果的基础上，我们现在想解决导致慢性炎性小体激活的机制，并分析炎性小体激活对长距离神经元连接的影响。具体来说，我们将分析功能失调的脂质代谢作为大脑免疫和非免疫细胞中炎性小体激活的原因。我们将着重于脑卒中后皮质脊髓束的重组，以研究炎性小体激活对神经元可塑性的作用。

In our collaborative project, we want to understand how inflammasome activation is involved in chronic neuroinflammation after stroke. Expanding on our findings from the first funding period, we want to address now the mechanisms which lead contributing to chronic inflammasome activation and analyze the impact of inflammasome activation on long-range neuronal connectivity. Specifically, we will analyze dysfunctional lipid metabolism as a cause of inflammasome activation in immune and non-immune cells of the brain. We will focus on reorganization of the corticospinal tract after stroke to study the role of inflammasome activation on neuronal plasticity.