ArticleBiochimica et biophysica acta2011
Analysis of the mitochondrial proteome in multiple sclerosis cortex.
Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.
- A Systematic Review of Tissue and Single Cell Transcriptome/Proteome Studies of the Brain in Multiple Sclerosis.Frontiers in immunology · 2022Pooled it
- Mechanisms of pathophysiology of blood vessels in patients with multiple sclerosis treated with ozone therapy: a systematic review.Acta bio-medica : Atenei Parmensis · 2019Pooled it
- Metabolic and skeletal muscle dysfunctions correlate with fatigue behavior in an animal model of multiple sclerosis.Frontiers in physiology · 2026Article
- Hemoglobin alpha regulates T-lymphocyte activation and mitochondrial function.bioRxiv : the preprint server for biology · 2025Article
- Epigenetic and Mitochondrial Metabolic Dysfunction in Multiple Sclerosis: A Review of Herbal Drug Approaches and Current Clinical Trials.Molecular neurobiology · 2025Review
- Genomic ncRNAs regulating mitochondrial function in neurodegeneration: a neglected clue in the complex etiopathogenesis of multiple sclerosis.Cell & bioscience · 2025Article
- Multiple sclerosis: what have we learned and can we still learn from electron microscopy.Cellular and molecular life sciences : CMLS · 2025Review
- Hemoglobin alpha regulates T-lymphocyte activation and mitochondrial function.Frontiers in immunology · 2025Article
- Fueling neurodegeneration: metabolic insights into microglia functions.Journal of neuroinflammation · 2024Review
- A role for vessel-associated extracellular matrix proteins in multiple sclerosis pathology.Brain pathology (Zurich, Switzerland) · 2024Article
- Axonal response of mitochondria to demyelination and complex IV activity within demyelinated axons in experimental models of multiple sclerosis.Neuropathology and applied neurobiology · 2023Article
- Alterations in Lymphocytic Metabolism-An Emerging Hallmark of MS Pathophysiology?International journal of molecular sciences · 2023Review
- The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS.Frontiers in neuroscience · 2023Review
- Potential biological contributers to the sex difference in multiple sclerosis progression.Frontiers in immunology · 2023Article
- Isolated Mitochondrial Preparations andCurrent neuropharmacology · 2023Review
- Brain proteome-wide association study linking-genes in multiple sclerosis pathogenesis.Annals of clinical and translational neurology · 2023Article
- Histological and Top-Down Proteomic Analyses of the Visual Pathway in the Cuprizone Demyelination Model.Journal of molecular neuroscience : MN · 2022Article
- Proteomics in Multiple Sclerosis: The Perspective of the Clinician.International journal of molecular sciences · 2022Review
- Integrating Lipidomics and Transcriptomics Reveals the Crosstalk Between Oxidative Stress and Neuroinflammation in Central Nervous System Demyelination.Frontiers in aging neuroscience · 2022Article
- Proteomics of Multiple Sclerosis: Inherent Issues in Defining the Pathoetiology and Identifying (Early) Biomarkers.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondrial dysfunction has been proposed to play a role in the neuropathology of multiple sclerosis (MS). Previously, we reported significant alterations in the transcription of nuclear-encoded electron transport chain genes in MS and confirmed translational alterations for components of Complexes I and III that resulted in reductions in their activity. To more thoroughly and efficiently elucidate potential alterations in the expression of mitochondrial and related proteins, we have characterized the mitochondrial proteome in postmortem MS and control cortex using Surface-Enhanced Laser Desorption Ionization Time of Flight Mass Spectrometry (SELDI-TOF-MS). Using principal component analysis (PCA) and hierarchical clustering techniques we were able to analyze the differential patterns of SELDI-TOF spectra to reveal clusters of peaks which distinguished MS from control samples. Four proteins in particular were responsible for distinguishing disease from control. Peptide fingerprint mapping unambiguously identified these differentially expressed proteins. Three proteins identified are involved in respiration including cytochrome c oxidase subunit 5b (COX5b), the brain specific isozyme of creatine kinase, and hemoglobin β-chain. The fourth protein identified was myelin basic protein (MBP). We then investigated whether these alterations were consistent in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS. We found that MBP was similarly altered in EAE but the respiratory proteins were not. These data indicate that while the EAE mouse model may mimic aspects of MS neuropathology which result from inflammatory demyelinating events, there is another distinct mechanism involved in mitochondrial dysfunction in gray matter in MS which is not modeled in EAE.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.