Lactobacillus plantarum PS128 alleviates neurodegenerative progression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse models of Parkinson’s disease

Liao, Jian; Cheng, Yun Fang; You, Shu Ting; Kuo, Wen Chun; Huang, Chi Wei; Chiou, Jen Jie; Hsu, Ching–Sheng; Hsieh-Li, Hsiu Mei; Wang, Sabrina; Tsai, Yao‐Chou

doi:10.1016/j.bbi.2020.07.036

Cited by 102 publications

(141 citation statements)

References 122 publications

Supporting

Mentioning

134

Contrasting

Order By: Relevance

“…Additionally, some studies have confirmed the presence of Lewy bodies in the enteric nervous system (Keshavarzian et al, 2015). Liao et al had shown that oral Lactobacillus plantarum PS128 attenuates oxidative stress and neuroinflammation in the nigra-striatum pathway induced by MPTP and inhibits the increase of Enterobacteriaceae and lipopolysaccharide and peptidoglycan biosynthesis-related microbial modules induced by MPTP (Liao et al, 2020). Pu et al (2019) confirmed that antibiotic-induced microbiome depletion can significantly improve the decrease of dopamine transporter (DAT) immunoreactivity in the striatum and TH immunoreactivity in the SN.…”

Section: Discussionmentioning

confidence: 96%

Fisetin Regulates Gut Microbiota and Exerts Neuroprotective Effect on Mouse Model of Parkinson’s Disease

et al. 2020

View full text Add to dashboard Cite

Previous studies have reported the anti-oxidant, anti-inflammatory, and anti-cancer effects of fisetin. However, the therapeutic efficacy of fisetin in Parkinson’s disease (PD) is unclear. In this study, we demonstrated that fisetin could markedly alleviate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurodegeneration in mice. To confirm the reported correlation between gut microbiota and PD, the bacterial DNA in the fresh feces of mice from each group was subjected to 16S rRNA (V3 and V4 regions) sequencing. The results revealed that fisetin changed the number, diversity, and distribution of gut microbiota in MPTP-induced mice model of PD. The alpha and beta diversity analyses showed that the fisetin intervented MPTP group gut microbiota exhibited a significantly higher abundance of Lachnospiraceae and a significantly lower abundance of uncultured_bacterium_g_Escherichia-Shigella and uncultured_bacterium_g_Bacillus than the MPTP group gut microbiota. These findings indicated that fisetin exerts a neuroprotective effect on neurodegeneration by altering the composition and diversity of gut microbiota. Thus, fisetin could be a potential novel therapeutic for PD.

show abstract

Section: Discussionmentioning

confidence: 96%

Fisetin Regulates Gut Microbiota and Exerts Neuroprotective Effect on Mouse Model of Parkinson’s Disease

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In addition, several studies have suggested that MPO inhibitors can be therapeutic in neurodegenerative diseases (35)(36)(37)(38). It has been reported that PS128 intervention not only significantly improves motor impairment but can also restore the survival of dopaminergic neurons in the substantia nigra and striatum of PD-model mice (18). The immune system plays an important role in the pathophysiology of PD (39).…”

Section: Discussionmentioning

confidence: 99%

“…In comparison with healthy subjects, hyperactivation of microglial cells and induction of microglia-derived cytokines were found in the patients with PD ( 40 – 42 ). Notably, administration of PS128 ameliorated neuroinflammation, increased antioxidant activity, and enhanced levels of neurotrophic factor in PD-model mice ( 18 ).…”

Section: Discussionmentioning

confidence: 99%

“…Oral administration of PS128 also modulated peripheral serotonin levels in rats ( 16 ), suggesting an interaction between PS128 and serotonin-producing EECs, which account for ~90% of the body's serotonin levels ( 17 ). Furthermore, PS128 ingestion alleviated motor deficits, nigrostriatal dopaminergic neuronal cell death, and striatal dopamine reduction in a PD mouse model ( 18 ), thus providing an insight into the use of PS128 as a potential treatment or add-on treatment alternative for patients with PD.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Add-On Effect of Lactobacillus plantarum PS128 in Patients With Parkinson's Disease: A Pilot Study

Lu¹,

Chang²,

Weng

et al. 2021

Front. Nutr.

Self Cite

View full text Add to dashboard Cite

Background:Lactobacillus plantarum PS128 (PS128) is a specific probiotic, known as a psychobiotic, which has been demonstrated to alleviate motor deficits and inhibit neurodegenerative processes in Parkinson's disease (PD)-model mice. We hypothesize that it may also be beneficial to patients with PD based on the possible mechanism via the microbiome-gut-brain axis.Methods: This is an open-label, single-arm, baseline-controlled trial. The eligible participants were scheduled to take 60 billion colony-forming units of PS128 once per night for 12 weeks. Clinical assessments were conducted using the Unified Parkinson's Disease Rating Scale (UPDRS), modified Hoehn and Yahr scale, and change in patient “ON-OFF” diary recording as primary outcome measures. The non-motor symptoms questionnaire, Beck depression inventory-II, patient assessment of constipation symptom, 39-item Parkinson's Disease Questionnaire (PDQ-39), and Patient Global Impression of Change (PGI-C) were assessed as secondary outcome measures.Results: Twenty-five eligible patients (32% women) completed the study. The mean age was 61.84 ± 5.74 years (range, 52–72), mean disease duration was 10.12 ± 2.3 years (range, 5–14), and levodopa equivalent daily dosage was 1063.4 ± 209.5 mg/daily (range, 675–1,560). All patients remained on the same dosage of anti-parkinsonian and other drugs throughout the study. After 12 weeks of PS128 supplementation, the UPDRS motor scores improved significantly in both the OFF and ON states (p = 0.004 and p = 0.007, respectively). In addition, PS128 intervention significantly improved the duration of the ON period and OFF period as well as PDQ-39 values. However, no obvious effect of PS128 on non-motor symptoms of patients with PD was observed. Notably, the PGI-C scores improved in 17 patients (68%). PS128 intervention was also found to significantly reduce plasma myeloperoxidase and urine creatinine levels.Conclusion: The present study demonstrated that PS128 supplementation for 12 weeks with constant anti-parkinsonian medication improved the UPDRS motor score and quality of life of PD patients. We suggest that PS128 could serve as a therapeutic adjuvant for the treatment of PD. In the future, placebo-controlled studies are needed to further support the efficacy of PS128 supplementation.Clinical Trial Registration:https://clinicaltrials.gov/, identifier: NCT04389762.

show abstract

“…Recent studies (Ellett et al, 2016;Poirier et al, 2016;Lai et al, 2018;Sun et al, 2018;Zhou et al, 2019;Dong et al, 2020;Liao et al, 2020) have observed changes of GM composition, GM metabolites of short chain fatty acids (SCFAs), and/or enteric dopaminergic neurons in these three classical MPTP mice models. The detailed information is summarized and shown in Supplementary Table 1.…”

Section: Introductionmentioning

confidence: 99%

Colonic Dopaminergic Neurons Changed Reversely With Those in the Midbrain via Gut Microbiota-Mediated Autophagy in a Chronic Parkinson’s Disease Mice Model

Liu

Wang

et al. 2021

Front. Aging Neurosci.

View full text Add to dashboard Cite

The role of gut-brain axis in the pathogenesis of Parkinson’s disease (PD) have become a research hotspot, appropriate animal model to study gut-brain axis in PD is yet to be confirmed. Our study employed a classical PD mice model achieved by chronic MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) injection to study concurrent changes of dopaminergic neurons in the midbrain and the colon of mice. Our results showed such a PD model exhibited apparent locomotor deficits but not gastrointestinal dysfunction. Tyrosine hydroxylase expressions and dopamine content reduced greatly in the substantia nigra pars compacta (SNpc) or striatum, but increased in the colon of PD mice. Mechanism investigation indicated autophagy activity and apoptosis were stimulated in the SNpc, but inhibited in the colon of PD mice. Interplay of gut microbiota (GM) and autophagy in response to chronic MPTP injection led to GM dysbiosis and defective autophagy in mice colon. Meanwhile, fecal short chain fatty acids (SCFAs), acetate and propionate in particular, declined greatly in PD mice, which could be attributed to the decreased bacteria abundance of phylum Bacteroidetes, but increased abundance of phylum Firmicutes. GM dysbiosis derived fecal SCFAs might be one of the mediators of downregulated autophagy in the colon of PD mice. In conclusion, colonic dopaminergic neurons changed in the opposition direction with those in the midbrain via GM dysbiosis-mediated autophagy inhibition followed by suppressed apoptosis in response to chronic MPTP injection. Such a chronic PD mice model might not be an ideal model to study role of gut-brain axis in PD progression.

show abstract

Lactobacillus plantarum PS128 alleviates neurodegenerative progression in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse models of Parkinson’s disease

Cited by 102 publications

References 122 publications

Fisetin Regulates Gut Microbiota and Exerts Neuroprotective Effect on Mouse Model of Parkinson’s Disease

Fisetin Regulates Gut Microbiota and Exerts Neuroprotective Effect on Mouse Model of Parkinson’s Disease

The Add-On Effect of Lactobacillus plantarum PS128 in Patients With Parkinson's Disease: A Pilot Study

Colonic Dopaminergic Neurons Changed Reversely With Those in the Midbrain via Gut Microbiota-Mediated Autophagy in a Chronic Parkinson’s Disease Mice Model

Contact Info

Product

Resources

About