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J Neuroimmunol. 2013 Sep 15;262(1-2):66-71. doi: 10.1016/j.jneuroim.2013.07.002. Epub 2013 Jul 18.

The antioxidant idebenone fails to prevent or attenuate chronic experimental autoimmune encephalomyelitis in the mouse.

Author information

1
Institute for Medical Immunology, Charité-Universitätmedizin Berlin, Augustenburger Platz 1, 13353 Berlin, Germany.

Abstract

Oxidative stress and mitochondrial dysfunction appear to contribute to neurodegenerative processes during multiple sclerosis (MS). Thus, antioxidants may represent a therapeutic option for MS. The antioxidant idebenone was proven to be beneficial in Friedreich's ataxia and Leber's hereditary optic neuropathy, two disorders caused by mitochondrial alterations. Here we showed that idebenone protected neuronal HT22 cells from glutamate-induced death in vitro. However, in experimental autoimmune encephalomyelitis, idebenone failed to affect disease incidence or onset when applied preventively, or to reduce disease severity when applied therapeutically. Histopathological examination of CNS from idebenone treated mice showed no improvement in inflammation, demyelination, or axonal damage. Thus, we hypothesize that idebenone treatment will likely not benefit patients with MS.

KEYWORDS:

EAE; Idebenone; Inflammation; Multiple sclerosis; Oxidative stress

PMID:
23871488
DOI:
10.1016/j.jneuroim.2013.07.002
[Indexed for MEDLINE]

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