Inflammasomes are molecular scaffolds that are activated by damage-associated and pathogen-associated molecular patterns and form a key element of innate immune responses. Consequently, the involvement of inflammasomes in several diseases that are characterized by inflammatory processes, such as multiple sclerosis, is widely appreciated. However, many other neurological conditions, including Alzheimer disease, Parkinson disease, amyotrophic lateral sclerosis, stroke, epilepsy, traumatic brain injury, sepsis-associated encephalopathy and neurological sequelae of COVID-19, all involve persistent inflammation in the brain, and increasing evidence suggests that inflammasome activation contributes to disease progression in these conditions. Understanding the biology and mechanisms of inflammasome activation is, therefore, crucial for the development of inflammasome-targeted therapies for neurological conditions. In this Review, we present the current evidence for and understanding of inflammasome activation in neurological diseases and discuss current and potential interventional strategies that target inflammasome activation to mitigate its pathological consequences.

炎症小体是由损伤相关和病原体相关分子模式激活的分子支架，形成先天免疫反应的关键要素。因此，人们广泛认识到炎症小体参与多种以炎症过程为特征的疾病，例如多发性硬化症。然而，许多其他神经系统疾病，包括阿尔茨海默病、帕金森病、肌萎缩侧索硬化症、中风、癫痫、创伤性脑损伤、脓毒症相关脑病和 COVID-19 的神经系统后遗症，都与大脑中的持续炎症有关，并且越来越多的证据表明炎症小体激活有助于这些情况下的疾病进展。因此，了解炎症小体激活的生物学和机制对于开发针对神经系统疾病的炎症小体靶向疗法至关重要。在这篇综述中，我们提出了神经系统疾病中炎症小体激活的当前证据和理解，并讨论了针对炎症小体激活以减轻其病理后果的当前和潜在的干预策略。