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Cited by 39Parkinson's Disease Mechanisms and TreatmentsNerve injury and regenerationNuclear Receptors and Signaling

Neuroplasticity and Neuroprotective Effect of Treadmill Training in the Chronic Mouse Model of Parkinson’s Disease

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Palasz, Ewelina, Niewiadomski, Wiktor, Gasiorowska, Anna, Mietelska-Porowska, Anna, Niewiadomska, Grazyna·2019·Neural Plasticity
DOI 10.1155/2019/8215017PMC PMC6470436
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Abstract

Physical training confers protection to dopaminergic neurons in rodent models of parkinsonism produced by neurotoxins. The sparing effect of physical training on dopaminergic neurons can be tested with training applied during chronic MPTP treatment, while the neurorestorative effect when training is applied after completing such treatment. In this study, the effect of the onset of training respective to chronic MPTP treatment was specifically addressed. Three groups of mice were injected with 10 doses of MPTP (12.5 mg/kg/injection) over 5 weeks. The first group remained sedentary; the second one underwent early onset training, which started 1 week before commencing MPTP treatment, continued throughout 5 weeks of treatment and 4 weeks thereafter; the third group underwent late-onset training of the same length and intensity as the former group, except that it started immediately after the end of MPTP treatment. Two groups served as controls: a saline-injected group that remained sedentary and saline-injected group, which underwent the same training as the early and late-onset training groups. Both early and late-onset physical training saved almost all nigral and VTA dopaminergic neurons, prevented inflammatory response, and increased the BDNF and GDNF levels to a similar extent. From these results one may conclude that early and late-onset training schedules were equipotent in their neuroprotective effect and that the mechanism of neuroprotection was similar. The sparing effect of early onset training may be satisfactorily explained by assuming that the increased level of BDNF and GDNF prevented the degeneration of dopaminergic neurons. To explain a similar number of dopaminergic neurons detected at the end of the early and late-onset training, one should additionally assume that the former training schedule induced neurogenesis. Results of this study support the view that physical activity may be neuroprotective even at a more advanced stage of PD and justify starting physical activity at any point of the disease.

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  • Long-term endurance training increases TrkB receptor expression in structures involved in extrapyramidal movement regulation, i.e., the ST and midbrain.

    “Animal studies have shown that long-term endurance training increased both TrkB receptor and TH expression in structures involved in extrapyramidal movement regulation, i.e., in the ST and midbrain [128,129,179,183,184,185].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [179]

  • Long-term endurance training increases TH expression in structures involved in extrapyramidal movement regulation, i.e., the ST and midbrain.

    “Animal studies have shown that long-term endurance training increased both TrkB receptor and TH expression in structures involved in extrapyramidal movement regulation, i.e., in the ST and midbrain [128,129,179,183,184,185].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [179]

  • Training increases BDNF expression in the hippocampus, cerebral cortex, ST, brainstem, and spinal cord.

    “Under the influence of the training process, increased BDNF expression in the hippocampus, cerebral cortex, ST, brainstem, and spinal cord was observed [131,174,179,181,182].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [179]

  • Physical training protects DA neurons in the SNpc against inflammatory insult.

    “Physical training protects DA neurons in the SNpc against inflammatory insult [179].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [179]

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Research works printed but not linked: 1

  1. [35]Paxinos G. Franklin K. The Mouse Brain in Stereotaxic Coordinates 2013 Academic Press, Elsevier

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Authors
Palasz, E., Niewiadomski, W., Gasiorowska, A., Mietelska-Porowska, A., & Niewiadomska, G.
Affiliations
  • Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland
  • Mossakowski Medical Research Institute, Polish Academy of Sciences (PL)
ORCID
Venue
Neural Plasticity
Publisher
Wiley
Published
2019-04-03
Volume
2019
Pages
1-14
ISSN
  • 1687-5443 (ISSN-L)
  • 2090-5904
DOI
10.1155/2019/8215017
PMC
PMC6470436
OpenAlex
W2934552985
Cited by
39
References
71
Citations by year
2026: 3 · 2025: 9 · 2024: 3 · 2023: 6 · 2022: 6 · 2021: 5 · 2020: 5 · 2019: 2
FWCI
3.05
Type
journal article
Language
en
Open access
Licence
Locations
  • Neural Plasticity (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Nencki Institute of Experimental Biology (UMO-2014/15/B/NZ4/05041)
  • TauRx Therapeutics/WisTa Laboratories Ltd., Singapore (UMO-2014/15/B/NZ4/05041)
  • Narodowe Centrum Nauki (UMO-2014/15/B/NZ4/05041)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
Parkinson's disease, treadmill training, physical activity, neuroprotection, MPTP-induced neurotoxicity, dopaminergic neurons, substantia nigra, ventral tegmental area, brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, neuroinflammation, neurogenesis, neuroplasticity
MeSH terms
Animals, Astrocytes, Chronic Disease, Disease Models, Animal, Exercise Therapy, Male, Mice, Inbred C57BL, Neuronal Plasticity, Parkinson Disease, Ventral Tegmental Area, Microglia, Parkinsonian Disorders, Dopaminergic Neurons, Pars Compacta

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