2. Academic Validation
  3. Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson's Disease

Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson's Disease

  • Nutrients. 2022 Nov 4;14(21):4678. doi: 10.3390/nu14214678.
Tiantian Li 1 2,  Chuanqi Chu 1 2,  Leilei Yu 1 2,  Qixiao Zhai 1 2,  Shunhe Wang 1 2,  Jianxin Zhao 1 2 3,  Hao Zhang 1 2 3 4,  Wei Chen 1 2 3,  Fengwei Tian 1 2 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
  • 2 School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
  • 3 National Engineering Research Center for Functional Food, Jiangnan University, Wuxi 214122, China.
  • 4 Department of Child Health Care, The Affiliated Wuxi Maternity and Child Health Care Hospital of Nanjing Medical University, Wuxi 214002, China.
PMID: 36364939 DOI: 10.3390/nu14214678
Abstract

There is mounting evidence that the microbiota-gut-brain axis (MGBA) is critical in the pathogenesis and progression of Parkinson's disease (PD), suggesting that probiotic therapy restoring gut microecology may slow down disease progression. In this study, we examined the disease-alleviating effects of Bifidobacterium breve CCFM1067, orally administered for 5 weeks in a PD mouse model. Our study shows that supplementation with the probiotic B. breve CCFM1067 protected dopaminergic neurons and suppressed glial cell hyperactivation and neuroinflammation in PD mice. In addition, the antioxidant capacity of the central nervous system was enhanced and oxidative stress was alleviated. Moreover, B. breve CCFM1067 protected the blood-brain and intestinal barriers from damage in the MPTP-induced mouse model. The results of fecal microbiota analysis showed that B. breve CCFM1067 intervention could act on the MPTP-induced microecological imbalance in the intestinal microbiota, suppressing the number of pathogenic bacteria (Escherichia-Shigella) while increasing the number of beneficial bacteria (Bifidobacterium and Akkermansia) in PD mice. In addition, the increase in short chain fatty acids (acetic and butyric acids) may explain the anti-inflammatory action of B. breve CCFM1067 in the gut or brain of the MPTP-induced PD mouse model. In conclusion, we demonstrated that the probiotic B. breve CCFM1067, which can prevent or treat PD by modulating the gut-brain axis, can be utilized as a possible new oral supplement for PD therapy.

Keywords

Bifidobacterium breve 1067; Parkinson’s disease; microbiota–gut–brain axis.

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