β‐Asarone Attenuates Neuroinflammation of Alzheimer's Disease by Activating Autophagy and Suppressing NLRP3 Inflammasome Assembly

Feb 4, 2026CNS neuroscience & therapeutics

β-Asarone may reduce Alzheimer's brain inflammation by boosting cell cleanup and blocking inflammasome formation

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Abstract

β-Asarone administration improved cognitive performance in 3×Tg-AD mice over 8 weeks.

Enhanced cognitive abilities were observed in 3×Tg-AD mice treated with β-asarone.
Treatment resulted in reduced microglial cell death caused by amyloid-beta (Aβ).
Accumulation of Aβ and phosphorylated Tau was decreased, supporting neuronal survival.
In both hippocampal tissue and BV-2 cell models, β-asarone led to lower levels of neuroinflammatory markers.
The treatment also modulated proteins related to autophagy while suppressing components of the NLRP3 inflammasome.
An autophagy inhibitor counteracted the effects of β-asarone on NLRP3 activation.

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AIM: Alzheimer's Disease (AD) is a neurodegenerative condition with poorly understood mechanisms and few effective treatments. β-asarone has shown potential in AD management, though its molecular actions require further clarification. This study investigates the mechanisms through which β-asarone exerts its effects using both animal and cellular models.

METHODS: In vivo, the 3×Tg-AD mice were administered β-asarone for 8 weeks. Learning and memory abilities were assessed via the Morris water maze and step-down tests. Histomorphological examination, immunofluorescence, immunohistochemistry, ELISA, transmission electron microscopy, and Western blotting were employed to detect pathological changes, neuroinflammation, and protein expression of relevant signaling pathway molecules. In vitro, Aβ was used to culture BV-2 cells to mimic the brain microenvironment in Alzheimer's disease; changes in neuroinflammation, autophagy, and NLRP3 inflammasome-related proteins were observed after treatment with β-asarone.

RESULTS: The administration of β-asarone resulted in enhanced cognitive performance in 3×Tg-AD mice, alongside a reduction in microglial apoptosis induced by Aβ. Additionally, β-asarone diminished the accumulation of Aβ and phosphorylated Tau, ultimately supporting neuronal survival. In both the hippocampal tissue and BV-2 cell models, treatment with β-asarone led to a downregulation of neuroinflammatory markers and modulation of autophagy-related proteins (Beclin-1, P62, ATG5, LC3-II/I), while concurrently suppressing components of the NLRP3 inflammasome (NLRP3, ASC, Caspase-1, cleaved Caspase-1). Notably, the autophagy inhibitor 3-MA counteracted the inhibitory effects of β-asarone on NLRP3 activation.

CONCLUSION: β-Asarone attenuates AD-related neuroinflammation by activating autophagy to inhibit NLRP3 inflammasome assembly.

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β‐Asarone Attenuates Neuroinflammation of Alzheimer's Disease by Activating Autophagy and Suppressing NLRP3 Inflammasome Assembly

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