Polymannuronic acid prebiotic plus Lacticaseibacillus rhamnosus GG probiotic as a novel synbiotic promoted their separate neuroprotection against Parkinson’s disease

Liu, Xin; Du, Zhong Rui; Wang, Xiong; Sun, Xiang Rong; Zhao, Qing; Zhao, Fang; Wong, Wing Tak; Wong, Ka Hing; Dong, Xiaoli

doi:10.1016/j.foodres.2022.111067

Cited by 42 publications

(42 citation statements)

References 44 publications

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“…The α- and β-diversity data indicated that the microbial community of B. breve CCFM1067 was comparable to that of the control group ( Figure 4 ). According to previous studies, MPTP induction may increase the occurrence of certain pathogenic bacteria and significantly impair the antioxidant and anti-inflammatory capabilities of the body [ 7 , 65 ], corroborating our findings. According to our research, MPTP intervention drastically changed the intestinal microbiota of PD mice ( Figure 5 ), increasing Bacteroides , Escherichia-Shigella , and Dubosiella , and decreasing Akkermansia ( Figure 5 ), which is consistent with the findings of previous studies [ 47 , 66 , 67 ].…”

Section: Discussionsupporting

confidence: 92%

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

Chu

et al. 2022

Nutrients

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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.

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Section: Discussionsupporting

confidence: 92%

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

Chu

et al. 2022

Nutrients

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“…Recently, Liu et al found that polymannuronic acid plus L. rhamnosus GG as a novel synbiotic promoted their individual neuroprotection against PD, which could therefore be one of the ideal oral agents for PD therapy (174). An RCT found that the consumption of a fermented milk containing multiple probiotic strains and prebiotic fiber was superior to placebo in improving constipation in patients with PD (156).…”

Section: Probiotics Psychobiotics Prebiotics Synbiotics and Postbioticsmentioning

confidence: 99%

Gut Microbiota: A Novel Therapeutic Target for Parkinson’s Disease

Zhu

Liu

et al. 2022

Front. Immunol.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease characterized by motor dysfunction. Growing evidence has demonstrated that gut dysbiosis is involved in the occurrence, development and progression of PD. Numerous clinical trials have identified the characteristics of the changed gut microbiota profiles, and preclinical studies in PD animal models have indicated that gut dysbiosis can influence the progression and onset of PD via increasing intestinal permeability, aggravating neuroinflammation, aggregating abnormal levels of α-synuclein fibrils, increasing oxidative stress, and decreasing neurotransmitter production. The gut microbiota can be considered promising diagnostic and therapeutic targets for PD, which can be regulated by probiotics, psychobiotics, prebiotics, synbiotics, postbiotics, fecal microbiota transplantation, diet modifications, and Chinese medicine. This review summarizes the recent studies in PD-associated gut microbiota profiles and functions, the potential roles, and mechanisms of gut microbiota in PD, and gut microbiota-targeted interventions for PD. Deciphering the underlying roles and mechanisms of the PD-associated gut microbiota will help interpret the pathogenesis of PD from new perspectives and elucidate novel therapeutic strategies for PD.

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“…Recently, it has been reported that in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice, fecal microbiota transplantation successfully reduced motor deficits and dopaminergic neuronal damage [ 10 ]; moreover, the probiotic strain Lactobacillus plantarum PS128 alleviated the neurodegenerative progression and neurobehavioral impairment of PD [ 17 ]. Recent studies in animal models have demonstrated that the modulation of gut microbiota by probiotic or post-biotic treatments could ameliorate motor symptoms, alleviating the neurodegeneration and counteracting the neurobehavioral impairment of PD [ 17 , 18 ]. Gut microbiota alteration in PD patients, as well as animal models, has been associated with a reduction in those bacteria producing short-chain fatty acids (SCFAs) [ 17 , 19 , 20 , 21 , 22 , 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

Dual-Hit Model of Parkinson’s Disease: Impact of Dysbiosis on 6-Hydroxydopamine-Insulted Mice—Neuroprotective and Anti-Inflammatory Effects of Butyrate

Avagliano

Coretti

Lama

et al. 2022

IJMS

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Recent evidence highlights Parkinson’s disease (PD) initiation in the gut as the prodromal phase of neurodegeneration. Gut impairment due to microbial dysbiosis could affect PD pathogenesis and progression. Here, we propose a two-hit model of PD through ceftriaxone (CFX)-induced dysbiosis and gut inflammation before the 6-hydroxydopamine (6-OHDA) intrastriatal injection to mimic dysfunctional gut-associated mechanisms preceding PD onset. Therefore, we showed that dysbiosis and gut damage amplified PD progression, worsening motor deficits induced by 6-OHDA up to 14 days post intrastriatal injection. This effect was accompanied by a significant increase in neuronal dopaminergic loss (reduced tyrosine hydroxylase expression and increased Bcl-2/Bax ratio). Notably, CFX pretreatment also enhanced systemic and colon inflammation of dual-hit subjected mice. The exacerbated inflammatory response ran in tandem with a worsening of colonic architecture and gut microbiota perturbation. Finally, we demonstrated the beneficial effect of post-biotic sodium butyrate in limiting at once motor deficits, neuroinflammation, and colon damage and re-shaping microbiota composition in this novel dual-hit model of PD. Taken together, the bidirectional communication of the microbiota–gut–brain axis and the recapitulation of PD prodromal/pathogenic features make this new paradigm a useful tool for testing or repurposing new multi-target compounds in the treatment of PD.

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Polymannuronic acid prebiotic plus Lacticaseibacillus rhamnosus GG probiotic as a novel synbiotic promoted their separate neuroprotection against Parkinson’s disease

Cited by 42 publications

References 44 publications

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

Gut Microbiota: A Novel Therapeutic Target for Parkinson’s Disease

Dual-Hit Model of Parkinson’s Disease: Impact of Dysbiosis on 6-Hydroxydopamine-Insulted Mice—Neuroprotective and Anti-Inflammatory Effects of Butyrate

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