Cited by 209Parkinson's Disease Mechanisms and TreatmentsNerve injury and regenerationNuclear Receptors and Signaling

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

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

DOI 10.1016/j.expneurol.2003.08.017

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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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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)
DOI: 10.1016/j.expneurol.2003.08.017
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
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
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 › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › 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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Can the brain be protected through exercise? Lessons from an animal model of parkinsonism☆

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