Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases, and it is characterised by progressive deterioration in cognitive and memory abilities, which can severely influence the elderly population’s daily living abilities. Although researchers have made great efforts in the field of AD, there are still no well-established strategies to prevent and treat this disease. Therefore, better clarification of the molecular mechanisms associated with the onset and progression of AD is critical to provide a theoretical basis for the establishment of novel preventive and therapeutic strategies. Currently, it is generally believed that neuroinflammation plays a key role in the pathogenesis of AD. Inflammasome, a multiprotein complex, is involved in the innate immune system, and it can mediate inflammatory responses and pyroptosis, which lead to neurodegeneration. Among the various types of inflammasomes, the NLRP3 inflammasome is the most characterised in neurodegenerative diseases, especially in AD. The activation of the NLRP3 inflammasome causes the generation of caspase-1-mediated interleukin (IL)-1β and IL-18 in microglia cells, where neuroinflammation is involved in the development and progression of AD. Thus, the NLRP3 inflammasome is likely to be a crucial therapeutic molecular target for AD via regulating neuroinflammation. In this review, we summarise the current knowledge on the role and regulatory mechanisms of the NLRP3 inflammasome in the pathogenic mechanisms of AD. We also focus on a series of potential therapeutic treatments targeting NLRP3 inflammasome for AD. Further clarification of the regulatory mechanisms of the NLRP3 inflammasome in AD may provide more useful clues to develop novel AD treatment strategies.

阿尔茨海默氏病（AD）是最常见的神经退行性疾病之一，其特征是认知和记忆能力逐步下降，这可能严重影响老年人的日常生活能力。尽管研究人员在AD领域做出了巨大的努力，但仍没有完善的策略来预防和治疗这种疾病。因此，更好地阐明与AD的发生和发展有关的分子机制对于为建立新的预防和治疗策略提供理论基础至关重要。当前，通常认为神经炎症在AD的发病机理中起关键作用。炎性小体是一种多蛋白复合物，与先天免疫系统有关，它可以介导炎症反应和细胞凋亡，导致神经变性。在各种类型的炎性小体中，NLRP3炎性小体在神经退行性疾病中，尤其是在AD中最具特征。NLRP3炎性体的激活导致小胶质细胞中caspase-1介导的白介素（IL）-1β和IL-18的产生，其中神经炎症与AD的发生和发展有关。因此，通过调节神经炎症，NLRP3炎性小体可能是AD的关键治疗分子靶标。在这篇综述中，我们总结了有关NLRP3炎性小体在AD的致病机制中的作用和调控机制的最新知识。我们还专注于针对AD的NLRP3炎性小体的一系列潜在治疗方法。