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

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...

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Bibliographic Details
Published in:Journal of neuroimmunology 2013-09, Vol.262 (1), p.66-71
Main Authors: Fiebiger, Sebastian M, Bros, Helena, Grobosch, Thomas, Janssen, Antonia, Chanvillard, Coralie, Paul, Friedemann, Dörr, Jan, Millward, Jason M, Infante-Duarte, Carmen
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Antioxidants - administration & dosage
Antioxidants - pharmacology
Chronic Disease
Disease Models, Animal
EAE
Encephalomyelitis, Autoimmune, Experimental - chemically induced
Encephalomyelitis, Autoimmune, Experimental - drug therapy
Encephalomyelitis, Autoimmune, Experimental - pathology
Female
Hippocampus - cytology
Hippocampus - drug effects
Hippocampus - pathology
Idebenone
Inflammation
Inflammation - drug therapy
Mice
Mice, Inbred C57BL
Multiple sclerosis
Neurology
Neurons - cytology
Neurons - drug effects
Neurons - pathology
Oxidative stress
Severity of Illness Index
Ubiquinone - administration & dosage
Ubiquinone - analogs & derivatives
Ubiquinone - cerebrospinal fluid
Ubiquinone - pharmacology
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Summary: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.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2013.07.002