Wlds-Mediated Protection of Dopaminergic Fibers in an Animal Model of Parkinson Disease
Open accessAbstract
Parkinson disease (PD) is characterized by the progressive degeneration of substantia nigra dopaminergic neurons projecting to the striatum. Since the deficit in striatal dopamine is the main cause of PD symptoms, it appears critical to preserve axon terminals. Significant axon protection from peripheral nerve Wallerian degeneration is observed in Wlds mice, a phenotype conferred by a spontaneous dominant mutation. To assess any Wlds-mediated rescue of dopamine fibers in a PD model, the nigrostriatal pathway of Wlds mice was lesioned with 6-hydroxydopamine (6-OHDA), a catecholaminergic neurotoxin. Following 6-OHDA injection in the medial forebrain bundle, Wlds mice showed remarkable dopamine fiber protection in the striatum. Drug-induced rotational behavior confirmed the nigrostriatal fiber ability to release dopamine, although revealing an abnormal neurotransmitter control presumably due to disrupted axonal transport. Following 6-OHDA injection in the midstriatum, only a protection trend was observed. Strikingly, no protection of Wlds nigral dopaminergic cell bodies was obtained following either nigrostriatal lesion. Besides showing subtle differences in the degeneration process between subcellular compartments, the reported Wlds-mediated protection of the dopamine axon terminals in an animal model of PD may lead to the understanding of mechanisms underlying axon loss and to the development of new therapeutic approaches.
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In the CNS, WldS protects nigrostriatal axons from degeneration in a model of Parkinson's disease, reduces the number of axonal spheroids in mice with gracile axonal dystrophy, and protects axons from neuronal degeneration induced by toxic insults.
“In the CNS, Wld S has been shown to protect nigrostriatal axons from degeneration in a model of Parkinson's disease, to reduce the number of axonal spheroids in mice with gracile axonal dystrophy, and to protect axons from neuronal degeneration induced by toxic insults (85)(86)(87).”
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References 29 · Cited by 142
Research works printed but not linked: 9
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- Authors
- Sajadi, A., Schneider, B. L., & Aebischer, P.
- Affiliations
- École Polytechnique Fédérale de Lausanne (CH)
- Corresponding author
- Aebischer, Patrick
- ORCID
- Schneider, Bernard L
- Venue
- Current Biology
- Publisher
- Elsevier BV
- Published
- 2004-02
- Volume
- 14
- Issue
- 4
- Pages
- 326-330
- ISSN
- 0960-9822 (ISSN-L)
- OpenAlex
- W2021312591
- Cited by
- 142
- References
- 29
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 5 · 2020: 8 · 2019: 9 · 2018: 5 · 2017: 2 · 2016: 5 · 2015: 5 · 2014: 11 · 2013: 7 · 2012: 5
- FWCI
- 6.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Current Biology (publishedVersion)
- PubMed (publishedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- École Polytechnique Fédérale de Lausanne
- 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, Wallerian degeneration, nigrostriatal pathway, 6-hydroxydopamine lesion, striatum, substantia nigra, dopamine release, axonal transport, axonal loss, rotational behavior
- MeSH terms
- Amphetamine, Animals, Cell Survival, Disease Models, Animal, Dopamine, Immunohistochemistry, Mice, Mutant Strains, Motor Activity, Nerve Tissue Proteins, Parkinson Disease, Substantia Nigra, Wallerian Degeneration, Oxidopamine, Presynaptic Terminals, Mice
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