ReviewNeuropsychiatric disease and treatment2026
Exosomes Regulate the NLRP3/Caspase-1/IL-1β Signaling Pathway in Parkinson's Disease: Mechanisms of Neuroinflammation Modulation and α-Synuclein Propagation.
Review in Neuropsychiatric disease and treatment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Parkinson's disease (PD) is a progressive neurodegenerative disorder, with neuroinflammation as core pathological drivers. The NLRP3/Caspase-1/IL-1β signaling pathway acts as a pivotal mediator of PD-related neuroinflammation, while exosome serves as key regulatory mediators of this pathway. This review systematically synthesizes the molecular mechanisms underlying exosome-mediated modulation of the NLRP3/Caspase-1/IL-1β axis in PD. Methods: We screened PubMed and Embase databases from January 2010 to January 2025 to search for published studies. The search keywords used are as follows: ["Parkinsonl" or "PD"], ["exosome"], ["NLRP3" or "inflammation"], ["acupuncture" or "electroacupuncture"]. Studies on human/animal models were included, and articles that did not meet the requirements were excluded. Results: Exosomes exert dual regulatory effects on the NLRP3/Caspase-1/IL-1β axis, with functional divergence determined by their cellular origin. From a pro-inflammatory perspective, exosomes derived from microglia and neurons are enriched in NLRP3, ASC, α-syn oligomers, and pro-IL-1β. After endocytosis by target dopaminergic neurons or surrounding microglia, these exosomes trigger mitochondrial ROS overproduction and intracellular K⁺ efflux-two critical signals for NLRP3 inflammasome activation. This leads to the assembly of the NLRP3-ASC-Caspase-1 complex, subsequent cleavage of pro-IL-1β/pro-IL-18 into mature cytokines, and exacerbation of dopaminergic neuronal pyroptosis. Notably, α-syn oligomers carried by these exosomes also enhance fibril formation in recipient cells, further amplifying NLRP3 activation and α-syn propagation; for example, microglial exosomes from MPTP-induced PD mice show 2-3-fold higher NLRP3 expression compared to wild-type controls. Conclusion: The exosome-NLRP3/Caspase-1/IL-1β axis mediates PD pathology. Targeting this axis holds promise for PD, and future research ought to optimize its clinical translation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.