The DOI matches its Crossref record; 116 of the 119 references it cites were found in a registry or an index.
Can the brain be protected through exercise? Lessons from an animal model of parkinsonism☆
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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“exercise increases levels of neurotrophic factors that have been shown to be neuroprotective, to enhance cell and neuron growth, and to engender synaptic plasticity”
From Enrichment Effects on Adult Cognitive Development: Can the Functional Capacity of Older Adults Be Preserved and Enhanced? (2008) · cites this paper as Smith & Zigmond, 2003
Citations
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Hertzog, C., Kramer, A. F., Wilson, R. S., & Lindenberger, U. (2008) · Psychological Science in the Public Interest · doi:10.1111/j.1539-6053.2009.01034.x · Cited by 1,495
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Exercise, cognition, and the aging brain
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Metadata
- 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 › 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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