ArticleDialogues in clinical neuroscience2018
An emerging role of dysfunctional axon-oligodendrocyte coupling in neurodegenerative diseases.
Article in Dialogues in clinical neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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
42 citing papers in PubMed, 48 citations in OpenAlex.
- An Exploratory Phase IIa Study of the PPAR delta/gamma Agonist T3D-959 Assessing Metabolic and Cognitive Function in Subjects with Mild to Moderate Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2020Trial
- Lactate as a metabolic-epigenetic hub in neurological disorders.Metabolic brain disease · 2026Review
- Oligodendrocyte dysfunction contributes to motor deficits and Purkinje cell axonopathy in spinocerebellar ataxia type 1.The Journal of clinical investigation · 2026Article
- Mutant SOD1 expressed by oligodendrocytes aggregates in myelinic nanochannels and accelerates disease progression in familial ALS mice.bioRxiv : the preprint server for biology · 2026Article
- Multimodal MRI Reveals Cerebral and Vascular Amyloid-Driven Myeloarchitectural Disorganization in a Mouse Model of Alzheimer's Disease.NMR in biomedicine · 2026Article
- Enhancing oligodendrocytes generation and myelin renewal by vitamin C mitigate Parkinson-relevant phenotypes in a murine model of Parkinson's disease.Frontiers in cellular neuroscience · 2026Article
- Identifying transcriptomic signatures that mediate the causal effect of genotype on Alzheimer's disease.Frontiers in neuroscience · 2026Article
- NF-κB RelA regulates temporal oligodendrocyte differentiation in the postnatal brains.Frontiers in cellular neuroscience · 2025Article
- An Overview of Oligodendrocyte Metabolism.Advances in neurobiology · 2025Review
- Relationship between Alzheimer's Disease and Type 2 Diabetes: Critical Review On Cellular and Molecular Common Pathogenic Mechanisms.Current Alzheimer research · 2025Review
- Del Río Hortega's insights into oligodendrocytes: recent advances in subtype characterization and functional roles in axonal support and disease.Frontiers in neuroanatomy · 2025Review
- Oligodendrocytes and myelination: pioneering new frontiers in cognitive neuroscience.Frontiers in neuroscience · 2025Review
- Extracellular Vesicle-Mediated Neuron-Glia Communications in the Central Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- Bioenergetics of Axon Integrity and Its Regulation by Oligodendrocytes and Schwann Cells.Molecular neurobiology · 2024Review
- Distinctive whole-brain cell types predict tissue damage patterns in thirteen neurodegenerative conditions.eLife · 2024Article
- Oligodendrocyte-axon metabolic coupling is mediated by extracellular KNature neuroscience · 2024Article
- Longitudinal single-cell transcriptional dynamics throughout neurodegeneration in SCA1.Neuron · 2024Article
- Advances of Genome Editing with CRISPR/Cas9 in Neurodegeneration: The Right Path towards Therapy.Biomedicines · 2023Review
- CaNeural regeneration research · 2023Article
- Alterations of Oligodendrocyte and Myelin Energy Metabolism in Multiple Sclerosis.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelin is made by highly specialized glial cells and enables fast axonal impulse propagation. Recent studies show that oligodendrocytes in the central nervous system are, in addition to myelination, required for the integrity and survival of axons, independent of the presence or absence of myelin itself. The underlying mechanism of this support is given by glycolytic oligodendrocytes which provide axons with energy-rich metabolites. These findings represent a paradigm shift for the physiological function of axon-associated glia, and open the intriguing possibility that oligodendrocytes are important contributors to neurodegenerative diseases in which myelinated axons are lost, such as in Alzheimer disease, amyotrophic lateral sclerosis, and multiple system atrophy. Understanding the role of axon-oligodendrocyte coupling in neurodegenerative diseases may pave the way for the development of metabolism-based therapeutic approaches.
Indexed as
Identifiers
30936768PMC6436955W2922954538What 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.