Human neuroinflammatory and neurodegenerative diseases, whose prevalence keeps rising, are still unsolved pathobiological/therapeutical problems. Among others, recent etiology hypotheses stressed as their main driver a chronic neuroinflammation, which is mediated by innate immunity-related protein oligomers: the inflammasomes. A panoply of exogenous and/or endogenous harmful agents activates inflammasomes’ assembly, signaling, and IL-1β/IL-18 production and neural cells’ pyroptotic death. The underlying concept is that inflammasomes’ chronic activation advances neurodegeneration while their short-lasting operation restores tissue homeostasis. Hence, from a therapeutic standpoint, it is crucial to understand inflammasomes’ regulatory mechanisms. About this, a deluge of recent studies focused on the NLRP3 inflammasome with suggestions that its pharmacologic block would hinder neurodegeneration. Yet hitherto no evidence proves this view. Moreover, known inflammasomes are numerous, and the mechanisms regulating their expression and function may vary with the involved animal species and strains, as well as organs and cells, and the harmful factors triggered as a result. Therefore, while presently leaving out some little-studied inflammasomes, this review focuses on the “other than NLRP3” inflammasomes that participate in neuroinflammation’s complex mechanisms: NLRP1, NLRP2, NLRC4, and AIM2. Although human-specific data about them are relatively scant, we stress that only a holistic view including several human brain inflammasomes and other potential pathogenetic drivers will lead to successful therapies for neuroinflammatory and neurodegenerative diseases.

人类神经炎症和神经退行性疾病的患病率不断上升，仍然是未解决的病理生物学/治疗问题。其中，最近的病因学假设强调慢性神经炎症是其主要驱动因素，这种炎症由先天免疫相关蛋白寡聚体（炎症小体）介导。一整套外源性和/或内源性有害物质激活炎性体的组装、信号传导和 IL-1β/IL-18 产生和神经细胞的焦亡死亡。基本概念是炎症小体的慢性激活会促进神经退行性变，而它们的短暂操作会恢复组织稳态。因此，从治疗的角度来看，了解炎症小体的调节机制至关重要。对这个，最近的大量研究集中在 NLRP3 炎症小体上，并暗示其药理学阻滞会阻碍神经退行性变。然而迄今为止没有证据证明这种观点。此外，已知炎症小体众多，调节其表达和功能的机制可能因所涉及的动物物种和品系以及器官和细胞以及由此引发的有害因素而异。因此，虽然目前忽略了一些研究较少的炎症小体，但本综述侧重于参与神经炎症复杂机制的“NLRP3 以外的”炎症小体：NLRP1、NLRP2、NLRC4 和 AIM2。尽管关于它们的人类特定数据相对较少，