The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Familial amyotrophic lateral sclerosis
Abstract
The increasing complexity of the pathways implicated in the pathogenesis of familial amyotrophic lateral sclerosis (ALS) has stimulated intensive research in many directions. Genetic analysis of familial ALS has yielded six loci and one disease gene (SOD1), initially suggesting a role for free radicals in the disease process, although the mechanisms through which the mutant exerts toxicity and results in selective motor neuron death remain uncertain. Numerous studies have focused on structural elements of the affected cell, emphasizing the role of neurofilaments and peripherin and their functional disruption in disease. Other topics examined include cellular homeostasis of copper and calcium, particularly in the context of oxidative stress and the processes of protein aggregation, glutamate excitotoxicity, and apoptosis. It has become evident that there is considerable interplay between these mechanisms and, as the role of each is established, a common picture may emerge, enabling the development of more targeted therapies. This study discusses the main areas of investigation and reviews the findings. © 2002 John Wiley & Sons, Inc. Muscle Nerve 25: 135–159, 2002 DOI 10.1002/mus.10000
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Rosen, D. R., Siddique, T., Patterson, D., Figlewicz, D. A., Sapp, P., Hentati, A., Donaldson, D., Goto, J., O'Regan, J. P., Deng, H.-X., et al. (1993) · Nature · doi:10.1038/362059a0 · Cited by 7,062
Self-citationDilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase
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Toxic DNA damage by hydrogen peroxide through the Fenton reaction in vivo and in vitro
Imlay, J. A., Chin, S. M., & Linn, S. (1988) · Science · doi:10.1126/science.2834821 · Cited by 1,555 · cited 1×
“Another possibility was that overactive mutant SOD might produce excessive hydrogen peroxide, which may be rapidly converted to the more toxic hydroxyl radical in the presence of ferrous ions.(91,120) A dominant negative effect means that not only would the mutant be dysfunctional, but it could also impair the activit…”
BackgroundBruijn, L. I., Becher, M. W., Lee, M. K., Anderson, K. L., Jenkins, N. A., Copeland, N. G., Sisodia, S. S., Rothstein, J. D., Borchelt, D. R., Price, D. L., et al. (1997) · Neuron · doi:10.1016/s0896-6273(00)80272-x · Cited by 1,341
Oxidative damage to mitochondrial DNA shows marked age-dependent increases in human brain
Mecocci, P., MacGarvey, U., Kaufman, A. E., Koontz, D., Shoffner, J. M., Wallace, D. C., & Beal, M. F. (1993) · Annals of Neurology · doi:10.1002/ana.410340416 · Cited by 757 · cited 1×
“Evidence indicates that there is an age-related accumulation in oxidative damage to DNA, particularly mitochondrial DNA, in the brain.(149) The oxidative stress theory is attractive as the explanation of ALS, because it allows for cumulative damage in a late-onset, progressive disease and places the major target for d…”
BackgroundNeurodegenerative disorders: the role of peroxynitrite
Torreilles, F., Salman-Tabcheh, S., Guérin, M.-C., & Torreilles, J. (1999) · Brain Research Reviews · doi:10.1016/s0165-0173(99)00014-4 · Cited by 430
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Cited by
Converging Mechanisms in ALS and FTD: Disrupted RNA and Protein Homeostasis
Ling, S.-C., Polymenidou, M., & Cleveland, D. W. (2013) · Neuron · doi:10.1016/j.neuron.2013.07.033 · Cited by 1,811
Reactive oxygen species in health and disease
Alfadda, A. A., & Sallam, R. M. (2012) · Journal of Biomedicine and Biotechnology · doi:10.1155/2012/936486 · Cited by 824
Snowden, J. S., Rollinson, S., Thompson, J. C., Harris, J. M., Stopford, C. L., Richardson, A. M. T., Jones, M., Gerhard, A., Davidson, Y. S., Robinson, A., et al. (2012) · Brain · doi:10.1093/brain/awr355 · Cited by 523
VEGF: once regarded as a specific angiogenic factor, now implicated in neuroprotection
Storkebaum, E., Lambrechts, D., & Carmeliet, P. (2004) · BioEssays · doi:10.1002/bies.20092 · Cited by 507
Oxidative stress in ALS: A mechanism of neurodegeneration and a therapeutic target
Barber, S. C., Mead, R. J., & Shaw, P. J. (2006) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2006.03.008 · Cited by 474
Metadata
- Authors
- Hand, C. K., & Rouleau, G. A.
- Venue
- Muscle & Nerve
- Publisher
- Wiley
- Published
- 2002-02
- Volume
- 25
- Issue
- 2
- Pages
- 135-159
- ISSN
- 0148-639X (ISSN-L)
- 1097-4598
- OpenAlex
- W1967542752
- Cited by
- 235
- References
- 7
- FWCI
- 18.84
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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