Epilepsy remains a major health concern as anti-seizure medications frequently fail, and there is currently no treatment to stop or prevent epileptogenesis, the process underlying the onset and progression of epilepsy. The identification of the pathological processes underlying epileptogenesis is instrumental to the development of drugs that may prevent the generation of seizures or control pharmaco-resistant seizures, which affect about 30% of patients. mTOR signalling and neuroinflammation have been recognized as critical pathways that are activated in brain cells in epilepsy. They represent a potential node of biological convergence in structural epilepsies with either a genetic or an acquired aetiology. Interventional studies in animal models and clinical studies give strong support to the involvement of each pathway in epilepsy. In this Review, we focus on available knowledge about the pathophysiological features of mTOR signalling and the neuroinflammatory brain response, and their interactions, in epilepsy. We discuss mitigation strategies for each pathway that display therapeutic effects in experimental and clinical epilepsy. A deeper understanding of these interconnected molecular cascades could enhance our strategies for managing epilepsy. This could pave the way for new treatments to fill the gaps in the development of preventative or disease-modifying drugs, thus overcoming the limitations of current symptomatic medications.

癫痫仍然是一个主要的健康问题，因为抗癫痫药物经常失效，并且目前没有治疗方法可以阻止或预防癫痫发生，即癫痫发作和进展的过程。癫痫发生的病理过程的识别有助于开发可预防癫痫发作或控制耐药性癫痫发作的药物，这种癫痫影响约 30% 的患者。 mTOR 信号传导和神经炎症已被认为是癫痫脑细胞激活的关键途径。它们代表了具有遗传或后天病因的结构性癫痫的生物趋同的潜在节点。动物模型和临床研究的介入研究有力地支持了癫痫各通路的参与。在这篇综述中，我们重点关注关于癫痫中 mTOR 信号传导和神经炎症脑反应及其相互作用的病理生理学特征的现有知识。我们讨论了在实验和临床癫痫中显示出治疗效果的每种途径的缓解策略。对这些相互关联的分子级联的更深入了解可以增强我们治疗癫痫的策略。这可能为新疗法铺平道路，以填补预防或疾病缓解药物开发的空白，从而克服当前对症药物的局限性。