Cited by 210Parkinson's Disease Mechanisms and TreatmentsNerve injury and regenerationNuclear Receptors and Signaling

Can the brain be protected through exercise? Lessons from an animal model of parkinsonism☆

Smith, Amanda D, Zigmond, Michael J·2003·Experimental Neurology

Abstract

Evidence suggests that following injury the brain has the capacity for self-repair and that this can be promoted through a variety of experiences including motor activity. In their article, Döbrössy and Dunnett have provided further evidence that this is the case in an animal model in which an excitotoxin is applied to the neostriatum. Under standard conditions, such a toxin would cause considerable damage to the GABAergic cells of this region and produce behavioral deficits. This model has been used to explore certain aspects of Huntington's disease, which also involves the loss of these neurons. However, Döbrössy and Dunnett show that the damage can be reduced by prior motor training. We have been exploring the neuroprotective effects of motor exercise in a different model, one involving 6-hydroxydopamine, which normally destroys dopamine neurons. Our results indicate that forced exercise can reduce the vulnerability of dopamine neurons to 6-hydroxydopamine. The results further suggest that this protection is due in part to an increase in the availability of the trophic factor GDNF, which can in turn stimulate certain signaling cascades, including one that activates ERK. Our results, together with those of Döbrössy and Dunnett and others, raise the possibility that exercise will protect against a variety of neurodegenerative conditions.

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Crossref · 10.1016/j.expneurol.2003.08.017

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Authors
Smith, A. D., & Zigmond, M. J.
Affiliations
University of Pittsburgh (US)
Corresponding author
Zigmond, Michael J
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
2003-11
Volume
184
Issue
1
Pages
31-39
ISSN
0014-4886 (ISSN-L)
OpenAlex
W2065546153
Cited by
209
References
119
Citations by year
2026: 3 · 2025: 4 · 2024: 2 · 2023: 2 · 2022: 7 · 2021: 4 · 2020: 6 · 2019: 6 · 2018: 5 · 2017: 10 · 2016: 4 · 2015: 8 · 2014: 6 · 2013: 18 · 2012: 10
FWCI
1.29
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Michael J. Fox Foundation for Parkinson's Research
  • National Institutes of Health (5r01ns039267-05, 5r21ns043701-02)
  • National Institute of Mental Health (MH-29670)
  • National Institute of Neurological Disorders and Stroke (NS 19608, NS39267, NS43701)
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
physical activity, neuroprotection, parkinsonism, 6-hydroxydopamine, dopaminergic neurons, glial cell line-derived neurotrophic factor, ERK signaling, motor training, excitotoxicity, neostriatum, neurodegeneration
MeSH terms
Animals, Physical Exertion, Humans, Nerve Growth Factors, Synaptic Transmission, Parkinson Disease, Secondary, Physical Conditioning, Animal, Sympatholytics, Oxidopamine, Glial Cell Line-Derived Neurotrophic Factor

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