Mechanism of NLRP3 inflammasome activation and its role in Alzheimer’s disease

Xiaoying Gao, Xiaoxia Zhang, Yaxuan Sun, Xueling Dai
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引用次数: 0

Abstract

Alzheimer’s disease (AD) is a common neurological disease in the elderly, and the major manifestations are cognitive dysfunction, neuronal loss, and neuropathic lesions in the brain. In the process of AD pathogenesis, the inflammatory response plays an indispensable role. The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) inflammasome containing NOD, leucine-rich repeat (LRR), and pyran domains is a multi-molecular complex that can detect dangerous signals related to neurological diseases. The assembly of NLRP3 inflammasome promotes the maturation of interleukin-1beta (IL-1β) and IL-18 mediated by caspase-1 in microglia, which leads to neuroinflammation and finally contributes to the occurrence and development of AD. This review aimed to clarify the structure and activating mechanism of NLRP3 inflammasome and its key role in the pathogenesis of AD, summarize the latest findings on the suppression of NLRP3 inflammasome activation for the treatment of AD, as well as indicate that targeting regulation of NLRP3 inflammasome assembly may be a potential strategy for the treatment of AD, providing a theoretical basis for the research of AD.
NLRP3炎性体激活机制及其在阿尔茨海默病中的作用
阿尔茨海默病(AD)是老年人常见的神经系统疾病,主要表现为认知功能障碍、神经元丧失和大脑神经病变。在AD的发病过程中,炎症反应起着不可或缺的作用。核苷酸结合寡聚结构域(NOD)样受体家族pyrin结构域包含3(NLRP3)炎症小体包含NOD、富含亮氨酸重复序列(LRR)和吡喃结构域是一种可以检测与神经疾病相关的危险信号的多分子复合物。NLRP3炎症小体的组装促进了小胶质细胞中由胱天蛋白酶-1介导的白细胞介素-1β(IL-1β)和IL-18的成熟,从而导致神经炎症,最终参与AD的发生和发展,总结了抑制NLRP3炎症小体激活治疗AD的最新发现,并指出靶向调节NLRP3炎性小体组装可能是治疗AD的一种潜在策略,为AD的研究提供了理论依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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