Evidence map›Paper›PMID 24055980›Full record

ArticleBiochimica et biophysica acta2013

MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.

Peizhong Mao, Maria Manczak, Ulziibat P Shirendeb, P Hemachandra Reddy

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

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  14. Integrated elemental analysis supports targeting copper perturbations as a therapeutic strategy in multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
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4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Peizhong MaoNeurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA; Department of Physiology and Pharmacology, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USA.
Maria Manczak
Ulziibat P Shirendeb
P Hemachandra Reddy
Oregon National Primate Research Center · US

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI FRUH, KLAUS J · 1985 to 2011
$140.8M
Dynamin-Related Protein 1 and Mitochondrial Fragmentation in Alzheimer's DiseaseR01AG042178 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2012 to 2016
$2.0M
Abeta Toxicity, ROS and Mitochondrial Dysfunction in Aging/Alzheimer's DiseaseR01AG028072 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI REDDY, P. HEMACHANDRA · 2007 to 2011
$1.5M
REPRODUCTIVE STEROIDS AND EXPERIMENTAL STROKEK01RR000163 · NCRR · OREGON HEALTH AND SCIENCE UNIVERSITY · PI MURPHY, STEPHANIE J · 2000 to 2004
$479k
NCRR NIH HHS K01 RR000163NCRR NIH HHS P51 RR000163NCRR NIH HHS RR000163NIA NIH HHS AG028072NIA NIH HHS AG042178NIA NIH HHS R01 AG028072NIA NIH HHS R01 AG042178
6 · The paper itself

Abstract

Oxidative stress and mitochondrial dysfunction are involved in the progression and pathogenesis of multiple sclerosis (MS). MitoQ is a mitochondria-targeted antioxidant that has a neuroprotective role in several mitochondrial and neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Here we sought to determine the possible effects of a systematic administration of MitoQ as a therapy, using an experimental autoimmune encephalomyelitis (EAE) mouse model. We studied the beneficial effects of MitoQ in EAE mice that mimic MS like symptoms by treating EAE mice with MitoQ and pretreated C57BL6 mice with MitoQ plus EAE induction. We found that pretreatment and treatment of EAE mice with MitoQ reduced neurological disabilities associated with EAE. We also found that both pretreatment and treatment of the EAE mice with MitoQ significantly suppressed inflammatory markers of EAE, including the inhibition of inflammatory cytokines and chemokines. MitoQ treatments reduced neuronal cell loss in the spinal cord, a factor underlying motor disability in EAE mice. The neuroprotective role of MitoQ was confirmed by a neuron-glia co-culture system designed to mimic the mechanism of MS and EAE in vitro. We found that axonal inflammation and oxidative stress are associated with impaired behavioral functions in the EAE mouse model and that treatment with MitoQ can exert protective effects on neurons and reduce axonal inflammation and oxidative stress. These protective effects are likely via multiple mechanisms, including the attenuation of the robust immune response. These results suggest that MitoQ may be a new candidate for the treatment of MS.

Indexed as

AnimalsAntioxidantsBiomarkersBlotting, WesternCoculture TechniquesCytokinesDisease ProgressionEncephalomyelitis, Autoimmune, ExperimentalImmunoenzyme TechniquesInflammationMaleMiceMice, Inbred C57BLMitochondriaMultiple SclerosisNeuronsAntioxidantsBiomarkersCytokinesmitoquinoneOrganophosphorus CompoundsRNA, MessengerUbiquinoneInflammationMitochondrial dysfunctionMitochondria-targeted antioxidantMultiple sclerosisNeuronOxidative stress

Identifiers

PMID24055980
PMCPMC3830526
OpenAlexW1970908751

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.