ArticleNeurotoxicity research2013
The yeast product Milmed enhances the effect of physical exercise on motor performance and dopamine neurochemistry recovery in MPTP-lesioned mice.
Article in Neurotoxicity research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- The Probiotic Yeast, Milmed, Promotes Autophagy and Antioxidant Pathways in BV-2 Microglia Cells andAntioxidants (Basel, Switzerland) · 2025Article
- Milmed Yeast Alters the LPS-Induced M1 Microglia Cells to Form M2 Anti-Inflammatory Phenotype.Biomedicines · 2022Article
- Effect of treadmill exercise on catalepsy and the expression of the BDNF gene in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine -induced Parkinson in maleIranian journal of basic medical sciences · 2020Article
- Impact of Plant-Derived Flavonoids on Neurodegenerative Diseases.Neurotoxicity research · 2016Review
- Neurotoxin mechanisms and processes relevant to Parkinson's disease: an update.Neurotoxicity research · 2015Article
- Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both clinical and laboratory studies have demonstrated that different types of physical exercise may alleviate Parkinsonism yet evidence for complete restoration of motor function and biomarker integrity are difficult to identify. MPTP (1 × 30 mg/kg, s.c., 4 groups) or saline (vehicle 1 × 5 ml/kg, s.c., 1 group) were administered in a single dose regime over three consecutive weeks on Fridays. Three MPTP groups were given four 30-min periods/week (Mondays to Thursdays), of these two groups, MPTP + Exer + M(i) and MPTP + Exer + M(ii); the former were introduced to exercise and Milmed (oral injection) on the week following the 1st MPTP injection and the latter on the Monday prior to the 1st injection of MPTP onwards. One MPTP group, MPTP + Exer, was given access to exercise (running wheels) from the week following the 1st MPTP injection onwards. The fourth MPTP group, MPTP-NoEx, and the Vehicle group were only given access to exercise on a single day each week (Wednesdays, exercise test) from the week following the 1st MPTP injection onwards. The exercise/exercise + Milmed regime was maintained for a further 9 weeks. It was observed that exercise by itself ameliorated MPTP-induced deficits regarding motor function and dopamine loss only partially whereas in the groups combining exercise with twice weekly dosages of Milmed the MPTP-induced deficits were abolished by the 10th week of the intervention. The three main conclusions that were drawn from correlational analyses of individual mice were: (i) that DA integrity was observed to be a direct function of ability to express running exercise in a treadmill wheel-running arrangement, and (ii) that DA integrity was observed to be a direct function of the capacity for motor performance as measured by spontaneous motor activity and subthreshold L-Dopa (5 mg/kg) induced activity in the motor activity test chambers, and (iii) that the extent to which running exercise in a running wheel was predictive of later motor performance in the activity test chambers was highly convincing.
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