The DOI matches its Crossref record; 120 of the 120 references it cites were found in a registry or an index.
The molecular basis of neurodegeneration in multiple sclerosis
Open accessAbstract
Studies aimed to elucidate the pathogenesis of the disease and to find new therapeutic options for multiple sclerosis (MS) patients heavily rely on experimental autoimmune encephalomyelitis (EAE) as a suitable experimental model. This strategy has been highly successful for the inflammatory component of the disease, but had so far little success in the development of neuroprotective therapies, which are also effective in the progressive stage of the disease. Here we discuss opportunities and limitations of EAE models for MS research and provide an overview on the complex mechanisms leading to demyelination and neurodegeneration in this disease. We suggest that the underlying mechanisms involve adaptive and innate immunity. However, mitochondrial injury, resulting in energy failure, is a key element of neurodegeneration in MS and is apparently driven by radical production in activated microglia.
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Cites
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Self-citationAxonal damage in acute multiple sclerosis lesions
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Cited by
Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF
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Self-citationNADPH oxidase in brain injury and neurodegenerative disorders
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Mitochondrial dysfunction contributes to neurodegeneration in multiple sclerosis
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Metadata
- Authors
- Lassmann, H., & van Horssen, J.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2011-08-16
- Volume
- 585
- Issue
- 23
- Pages
- 3715-3723
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2095370244
- Cited by
- 294
- References
- 120
- FWCI
- 18.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.