March 3, 2026Open Access

TLR4/NF-κB signaling-mediated neuroinflammation is associated with gut microbiota dysbiosis in a mouse model of Parkinson’s disease

Key Points

Neuroinflammation correlates significantly with gut microbiota dysbiosis in a mouse model of Parkinson's disease.
Key findings reveal a deep connection between TLR4/NF-κB signaling and gut microbiota disturbances when triggered by rotenone.
Assessment of the microbiota-gut-brain axis shows how inflammatory signaling pathways affect neurological health.
Therapeutic implications suggest targeting TLR4/NF-κB pathways to potentially alleviate Parkinson's disease symptoms.

Abstract

This study demonstrates a key role of the TLR4/NF-κB signaling pathway in the microbiota-gut-brain axis of a rotenone-induced PD mouse model, where gut microbiota dysbiosis exhibits a significant correlation with inflammation induced by TLR4/NF-κB activation.

TLR4/NF-κB signaling-mediated neuroinflammation is associated with gut microbiota dysbiosis in a mouse model of Parkinson’s disease

Key Points

Abstract

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