ArticleAutoimmune diseases2011
Mitochondria as crucial players in demyelinated axons: lessons from neuropathology and experimental demyelination.
Article in Autoimmune diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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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.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
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- Decreased mitochondrial activity in the demyelinating cerebellum of progressive multiple sclerosis and chronic EAE contributes to Purkinje cell loss.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The complexities of investigating mitochondria dynamics in multiple sclerosis and mouse models of MS.Frontiers in neuroscience · 2023Review
- Melatonin and multiple sclerosis: antioxidant, anti-inflammatory and immunomodulator mechanism of action.Inflammopharmacology · 2022Review
- Newly Identified Deficiencies in the Multiple Sclerosis Central Nervous System and Their Impact on the Remyelination Failure.Biomedicines · 2022Review
- IFN-β rescues neurodegeneration by regulating mitochondrial fission via STAT5, PGAM5, and Drp1.The EMBO journal · 2021Article
- Brain atrophy in multiple sclerosis: mechanisms, clinical relevance and treatment options.Auto- immunity highlights · 2019Review
- Distinctive functional deficiencies in axonal conduction associated with two forms of cerebral white matter injury.CNS neuroscience & therapeutics · 2019Article
- Melatonin and Multiple Sclerosis: From Plausible Neuropharmacological Mechanisms of Action to Experimental and Clinical Evidence.Clinical drug investigation · 2019Review
- Combined effects of rat Schwann cells and 17β-estradiol in a spinal cord injury model.Metabolic brain disease · 2018Article
- Cerebrospinal fluid lactate is associated with multiple sclerosis disease progression.Journal of neuroinflammation · 2016Article
- Cell type-specific Nrf2 expression in multiple sclerosis lesions.Acta neuropathologica · 2015Article
- Nuclear export inhibitors avert progression in preclinical models of inflammatory demyelination.Nature neuroscience · 2015Article
- Protective effects of melatonin against mitochondrial injury in a mouse model of multiple sclerosis.Experimental brain research · 2014Article
- Aging-related changes of optic nerve of Wistar albino rats.Age (Dordrecht, Netherlands) · 2014Article
- Is a hypothetical melanoma-like neuromelanin the underlying factor essential for the aetiopathogenesis and clinical manifestations of multiple sclerosis?BMC neurology · 2013Article
- Paradigms in multiple sclerosis: time for a change, time for a unifying concept.Inflammopharmacology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are the most efficient producers of energy in the form of ATP. Energy demands of axons, placed at relatively great distances from the neuronal cell body, are met by mitochondria, which when functionally compromised, produce reactive oxygen species (ROS) in excess. Axons are made metabolically efficient by myelination, which enables saltatory conduction. The importance of mitochondria for maintaining the structural integrity of myelinated axons is illustrated by neuroaxonal degeneration in primary mitochondrial disorders. When demyelinated, the compartmentalisation of ion channels along axons is disrupted. The redistribution of electrogenic machinery is thought to increase the energy demand of demyelinated axons. We review related studies that focus on mitochondria within unmyelinated, demyelinated and dysmyelinated axons in the central nervous system. Based on neuropathological observations we propose the increase in mitochondrial presence within demyelinated axons as an adaptive process to the increased energy need. An increased presence of mitochondria would also increase the capacity to produce deleterious agents such as ROS when functionally compromised. Given the lack of direct evidence of a beneficial or harmful effect of mitochondrial changes, the precise role of increased mitochondrial presence within axons due to demyelination needs to be further explored in experimental demyelination in-vivo and in-vitro.
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.