NLRP3 炎性小体在阿尔茨海默病发病机制和治疗中的作用。
The NLRP3 Inflammasome in the Pathogenesis and Treatment of Alzheimer's Disease.
机构信息
Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.
Krembil Research Institute, Toronto, ON, Canada.
出版信息
J Alzheimers Dis. 2021;84(2):579-598. doi: 10.3233/JAD-210660.
Alzheimer's disease (AD) is the most common form of dementia. Although AD is one of the most socioeconomically devastating diseases confronting humanity, no "curative" disease modifying drug has been identified. Recent decades have witnessed repeated failures of drug trials and have called into question the utility of the amyloid hypothesis approach to AD therapeutics design. Accordingly, new neurochemical processes are being evaluated and explored as sources of alternative druggable targets. Among these newly identified targets, neuroinflammation is emerging as a front-runner, and within the realm of neuroinflammation, the inflammasome, particularly the NLRP3 complex, is garnering focussed attention. This review summarizes current data and approaches to understanding the role of the NLRP3 inflammasome in neuroinflammation and AD, and systematically identifies and evaluates multiple targets within the NLRP3 inflammasome cascade as putative drug targets.
阿尔茨海默病（AD）是最常见的痴呆症形式。尽管 AD 是人类面临的最具社会经济破坏性的疾病之一，但尚未发现“治愈”疾病的药物。近几十年来，药物试验一再失败，这使得人们对淀粉样蛋白假说在 AD 治疗设计中的应用产生了质疑。因此，人们正在评估和探索新的神经化学过程，以寻找新的可药物治疗靶点。在这些新发现的靶点中，神经炎症正在成为一个领跑者，在神经炎症领域，炎症小体，特别是 NLRP3 复合物，正在引起人们的关注。这篇综述总结了目前关于 NLRP3 炎症小体在神经炎症和 AD 中的作用的研究数据和方法，并系统地确定和评估了 NLRP3 炎症小体级联反应中的多个靶点作为潜在的药物靶点。
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