Stroke creates a complex interplay of multiple signaing pathways including excitotoxicity, ionic imbalance, inflammation, oxidative stress and apoptosis. There are very few treatments that have been shown to be beneficial in acute stroke. Recent findings have provided insights into the pathophysiology and mechanisms of ischemic stroke, complementing the traditional glutamate hypothesis: the molecular interaction between PSD95 and GluN2B has been identified as a culprit in stroke-mediated excitotoxicity, leading to the discovery of NA-1, a peptide that disrupts that interaction, as a potent neuroprotective agent for the treatment of acute stroke. In this review we describe its signaling cascade, the target of its therapeutic intervention and its translation from bench to clinical trial.

中文翻译：

---

NA-1的发现和开发，用于治疗急性缺血性中风。

中风产生多种信号通路的复杂相互作用，包括兴奋性毒性，离子失衡，炎症，氧化应激和细胞凋亡。很少有疗法被证明对急性中风有益。最近的发现提供了对缺血性中风的病理生理学和机制的见解，补充了传统的谷氨酸假说：PSD95和GluN2B之间的分子相互作用已被确定为中风介导的兴奋性毒性的元凶，从而导致了肽NA-1的发现。作为治疗急性中风的有效神经保护剂，可破坏这种相互作用。在这篇综述中，我们描述了其信号传导级联，其​​治疗干预的目标及其从实验台到临床试验的翻译。