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Akkermansia muciniphila Akk11 Supplementation Attenuates MPTP-Induced Neurodegeneration by Inhibiting Microglial
Wei Wang1, Shijie Shi2,3, Mingyu Su2,4
1The Second Clinical Medical School, Xuzhou Medical University, Xuzhou, China.
Abstract:
The gut dysbiosis is associated with the progression of Parkinson's disease (PD). Probiotics have been demonstrated to impact disease progression via the gut-brain axis. This study aims to investigate the therapeutic potential of Akkermansia Muciniphila Akk11 (Akk11) in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. Our results indicated that Akk11 administration significantly improved the MPTP-induced behavioral abnormalities, reduced the loss of dopaminergic neurons, microglia activation, reversed the production of inflammatory cytokines, and colonic damage. Mechanistic studies showed that Akk11 administration suppressed inflammatory responses by inhibiting microglial NLRP3 inflammasome activation. In summary, Akk11 alleviated MPTP-induced motor deficits and neural damage by inhibiting microglial NLRP3 inflammasome. These findings suggest that Akk11 supplementation has therapeutic potential in treating PD through the gut-brain axis.
Insights
Akkermansia Muciniphila Akk11 (Akk11) probiotic supplementation improved Parkinson's disease symptoms in mice. Akk11 reduced neural damage and inflammation by targeting the gut-brain axis.
Area of Science:
- Neuroscience
- Microbiology
- Immunology
Background:
- Gut dysbiosis is linked to Parkinson's disease (PD) progression.
- The gut-brain axis plays a role in PD pathogenesis.
- Probiotics show potential for modulating PD via the gut-brain axis.
Purpose of the Study:
- To evaluate the therapeutic efficacy of Akkermansia Muciniphila Akk11 (Akk11) in a mouse model of Parkinson's disease.
- To investigate the underlying mechanisms of Akk11's action in PD.
Main Methods:
- Utilized a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease mouse model.
- Administered Akk11 and assessed behavioral changes, dopaminergic neuron survival, microglial activation, inflammatory cytokine production, and colonic damage.
- Investigated the impact of Akk11 on microglial NLRP3 inflammasome activation.
Main Results:
- Akk11 administration significantly ameliorated MPTP-induced behavioral deficits.
- Akk11 treatment reduced dopaminergic neuron loss, microglial activation, and inflammatory cytokine levels.
- Akk11 suppressed colonic damage and inhibited microglial NLRP3 inflammasome activation, thereby reducing inflammation.
Conclusions:
- Akk11 demonstrates significant therapeutic potential for Parkinson's disease.
- Akk11 alleviates motor deficits and neuroinflammation in PD models by inhibiting the microglial NLRP3 inflammasome.
- Targeting the gut-brain axis with Akk11 offers a promising therapeutic strategy for PD.
