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

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☆

Smith, Amanda D, Zigmond, Michael J·2003·Experimental Neurology
DOI 10.1016/j.expneurol.2003.08.017
Open this paper in CoChat — free account

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.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.expneurol.2003.08.017

Cites

116 of 116 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Show all 119 references

3 of the 119 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Hirsch, 2000, Nigrostriatal system plasticity in Parkinson's disease, Ann. Neurol., 47, S115
  2. Szekely, 1982, Adjunctive treatment in Parkinson's disease, Rehabil. Lit., 43, 72

Cited by

Sorted by citations

Items 101–200 of 209

Related

See all

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)
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review