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Iron in multiple sclerosis: roles in neurodegeneration and repair

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Author
Stephenson, Erin
Nathoo, Nabeela
Mahjoub, Yasamin
Dunn, Jeffery F.
Yong, V. Wee
Accessioned
2017-03-17T22:54:53Z
Available
2017-03-17T22:54:53Z
Issued
2014-07-08
Subject
multiple sclerosis
Neurology
Iron
Type
journal article
Metadata
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Abstract
MRI and histological studies have shown global alterations in iron levels in the brains of patients with multiple sclerosis (MS), including increases in the iron stored by macrophages and microglia. Excessive free iron can be toxic, and accumulation of iron in MS has generally been thought to be detrimental. However, iron maintains the integrity of oligodendrocytes and myelin, and facilitates their regeneration following injury. The extracellular matrix, a key regulator of remyelination, might also modulate iron levels. This Review highlights key histological and MRI studies that have investigated changes in iron distribution associated with MS. Potential sources of iron, as well as iron regulatory proteins and the detrimental roles of excessive iron within the CNS, are also discussed, with emphasis on the importance of iron within cells for oxidative metabolism, proliferation and differentiation of oligodendrocytes, and myelination. In light of the beneficial and detrimental properties of iron within the CNS, we present considerations for treatments that target iron in MS. Such treatments must balance trophic and toxic properties of iron, by providing sufficient iron levels for remyelination and repair while avoiding excesses that might overwhelm homeostatic mechanisms and contribute to damage.
Grantingagency
Canadian Institutes of Health Research; Multiple Sclerosis Society of Canada; Alberta Innovates–Health Solutions CRIO Team programme
Refereed
Yes
Citation
Stephenson, E. et al. Nat. Rev. Neurol. 10, 459–468 (2014); published online 8 July 2014; doi:10.1038/nrneurol.2014.118
Corporate
University of Calgary
Department
Neuroscience
Faculty
Medicine
Institution
University of Calgary
Publisher
Nature Publishing Group
Doi
http://dx.doi.org/10.1038/nrneurol.2014.118
http://dx.doi.org/10.11575/PRISM/33509
Uri
http://hdl.handle.net/1880/51880
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