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Updated: May 4, 2026
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
NLRP3 Inflammasome in Vascular Dementia: Regulatory Mechanisms, Functions, and Therapeutic Implications: A
Yujia Lu1,2, Lin Cheng2,3, Yinyi Xiong2,4
1Department of Pathology, Clinical Medical School of Jiujiang University, Jiujiang, Jiangxi, China.
Background:
Vascular dementia, the second most common type of dementia globally after Alzheimer's disease, is associated with neuroinflammation. Activation of the NLRP3 inflammasome, an important pattern recognition receptor in human innate immunity, plays a key role in the pathogenesis of vascular dementia.
Results:
The NLRP3 inflammasome pathway destroys neuronal cells primarily through the production of IL-18 and IL-1β. Moreover, it exacerbates vascular dementia by producing IL-18, IL-1β, and the N-terminal fragment of GSDMD, which also contributes to neuronal cell death. Thus, blocking the NLRP3 inflammasome pathway presents a new therapeutic strategy for treating vascular dementia, thereby delaying or curing the disease more effectively and mitigating adverse effects.
Conclusions:
This review explores the role and mechanisms of the NLRP3 inflammasome in vascular dementia, summarizing current research and therapeutic strategies. Investigating the activation of the NLRP3 inflammasome can reveal the pathogenesis of vascular dementia from a new perspective and propose innovative preventive and treatment strategies.
