Neuroprotection after Transient Global Cerebral Ischemia in Wld s Mutant Mice
Abstract
The Wld s mouse mutant demonstrates a remarkable phenotype of delayed axonal and synaptic degeneration after nerve lesion. In this study, the authors tested the hypothesis that expression of Wld protein is neuroprotective in an in vivo mouse model of global cerebral ischemia. This model is associated with selective neuronal degeneration in specific brain regions such as the caudate nucleus and CA2 hippocampal pyramidal cell layer. The extent of neuronal damage was quantified in Wld s compared to wild-type mice after an identical episode of global cerebral ischemia. The results demonstrated a significant and marked reduction in the extent of neuronal damage in Wld s as compared to wild-type C57Bl/6 mice. In the caudate nucleus, Wld expression significantly reduced the percentage of ischemic neuronal damage after global ischemia (Wld s , 27.7 ± 16.8%; wild-type mice, 58.7 ± 32.3%; P = 0.036). Similarly, in the CA2 pyramidal cell layer, there was a significant reduction of neuronal damage in the Wld s mice as compared to wild-type mice after ischemia (Wld s , 17.7 ± 23.0%; wild-type mice, 41.9 ± 28.0%; P < 0.023). Thus, these results clearly demonstrate that the Wld gene confers substantial neuroprotection after cerebral ischemia, and suggest a new role to that previously described for Wld s .
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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).”
Cites
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Increased Nuclear NAD Biosynthesis and SIRT1 Activation Prevent Axonal Degeneration
Araki, T., Sasaki, Y., & Milbrandt, J. (2004) · Science · doi:10.1126/science.1098014 · Cited by 1,060 · see citing works
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Coleman, M. (2005) · Nature reviews. Neuroscience · doi:10.1038/nrn1788 · Cited by 819 · see citing works
Nmnat delays axonal degeneration caused by mitochondrial and oxidative stress
Press, C., & Milbrandt, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0525-08.2008 · Cited by 137 · see citing works
“…axonal degeneration resulting from damage caused by mechanical, genetic, or chemical injury (Gillingwater and Ribchester, 2001; Wang et al., 2001a,b; Ferri et al., 2003; Samsam et al., 2003; Araki et al., 2004; Gillingwater et al., 2004; Mi et al., 2005; Sasaki et al., 2006; Zhai et al., 2006).”
BackgroundLjungberg, M. C., Ali, Y. O., Zhu, J., Wu, C.-S., Oka, K., Zhai, R. G., & Lu, H.-C. (2012) · Human Molecular Genetics · doi:10.1093/hmg/ddr492 · Cited by 107 · see citing works
- Authors
- Gillingwater, T. H., Haley, J. E., Ribchester, R. R., & Horsburgh, K.
- Affiliations
- University of Edinburgh (GB)
- Corresponding author
- Gillingwater, Thomas H.
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2004-01
- Volume
- 24
- Issue
- 1
- Pages
- 62-66
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- OpenAlex
- W2133648237
- Cited by
- 68
- References
- 1
- Citations by year
- 2023: 2 · 2020: 4 · 2019: 2 · 2018: 1 · 2016: 1 · 2015: 4 · 2014: 2 · 2013: 4 · 2012: 4
- FWCI
- 3.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- neuroprotection, transient global cerebral ischemia, neurodegeneration, caudate nucleus, axonal degeneration, synaptic degeneration, ischemic neuronal injury
- MeSH terms
- Animals, Caudate Nucleus, Brain Ischemia, Hippocampus, Immunohistochemistry, Mice, Inbred C57BL, Nerve Tissue Proteins, Neurons, Carotid Stenosis, Muscle, Skeletal, Mice
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