Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 262, Issue 1-2, Pages 128-131Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2013.06.012
Keywords
Cuprizone; Copper chelation; Mitochondrial toxicity; Demyelination; Selective vulnerability; Multiple sclerosis
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Funding
- Veterans Administration
- NMSS
- Serono Foundation
- Hungarian Neuroimaging Foundation
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Cuprizone is a copper-chelating mitochondrial toxin that causes oligodendrocyte apoptosis and demyelination preferentially in the corpus callosum (CC) and the superior cerebellar peduncles, but not in the spinal cord (SC) of C57BL/6 mice. Here we aimed to determine the activities of copper-containing enzymes in correlation with the distribution of demyelination during exposure to cuprizone. The study revealed mitochondrial complex IV and superoxide dismutase activity alterations in both the pathology-affected CC and the non-affected SC. This observation raises the possibility that regionally different subcellular molecular interactions lead to the selective oligodendrocyte loss induced by the nonselective mitochondrial toxin, cuprizone. (C) 2013 Elsevier B.V. All rights reserved.
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