ArticleBrain : a journal of neurology2013
Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis.
Article in Brain : a journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers, 1 of them a synthesis that pooled it.
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Who cites it
164 citing papers in PubMed, 1 synthesis or guideline pooled it, 247 citations in OpenAlex.
- Histaminergic transmission slows progression of amyotrophic lateral sclerosis.Journal of cachexia, sarcopenia and muscle · 2019Pooled it
- Combined rituximab and magnesium acetyl taurate therapy attenuates neurodegeneration via ERK/c-JNK/P38MAPK signaling modulation in methylmercury-induced amyotrophic lateral sclerosis-like neurotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Rapid Generation of Functional Oligodendrocytes From Human Induced Pluripotent Stem Cells Through Small Molecule Guided Differentiation.Journal of neuroscience research · 2026Article
- Revisiting oligodendrocytes in amyotrophic lateral sclerosis using human multicellular stem cell models.Trends in cell biology · 2026Review
- Review
- Single-nucleus multiome shows motor neuron glutamate overactivation in amyotrophic lateral sclerosis.Brain : a journal of neurology · 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
- MYC-driven gliosis impairs neuron-glia communication in amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- Caffeic Acid Phenethyl Ester Enhanced the Klotho/SIRT1/Nrf2/HO-1 Axis to Protect Against Methylmercury-Induced ALS-Like Neurodegeneration.Molecular neurobiology · 2026Article
- Neuronal TDP-43 regulates myelin formation via neurexin 1 mRNA stabilization.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Glial Cells as Key Mediators in the Pathophysiology of Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Review
- Article
- A single-cell, long-read, isoform-resolved case-control study of FTD reveals cell-type-specific and broad splicing dysregulation in human brain.Cell reports · 2025Article
- Autophagy Dysfunction and Neurodegeneration: Where Does It Go Wrong?Journal of molecular biology · 2025Review
- Meta-Analysis of Gene Expression in Bulk-Processed Post-Mortem Spinal Cord from ALS Patients and Normal Controls.NeuroSci · 2025Article
- One gene, many phenotypes: the role of KIF5A in neurodegenerative and neurodevelopmental diseases.Cell communication and signaling : CCS · 2025Review
- SRSF10 regulates oligodendrocyte differentiation during mouse central nervous system development by modulating pre-mRNA splicing.Nucleic acids research · 2025Article
- Modulation of OPC Mitochondrial Function by Inhibiting USP30 Promotes Their Differentiation.Glia · 2025Article
- Stem cell extracellular vesicles: a new dawn for anti-inflammatory treatment of neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
104 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Oligodendrocytes are well known targets for immune-mediated and infectious diseases, and have been suggested to play a role in neurodegeneration. Here, we report the involvement of oligodendrocytes and their progenitor cells in the ventral grey matter of the spinal cord in amyotrophic lateral sclerosis, a neurodegenerative disease of motor neurons. Degenerative changes in oligodendrocytes were abundantly present in human patients with amyotrophic lateral sclerosis and in an amyotrophic lateral sclerosis mouse model. In the mouse model, morphological changes in grey matter oligodendrocytes became apparent before disease onset, increasingly so during disease progression, and oligodendrocytes ultimately died. This loss was compensated by increased proliferation and differentiation of oligodendrocyte precursor cells. However, these newly differentiated oligodendrocytes were dysfunctional as suggested by their reduced myelin basic protein and monocarboxylate transporter 1 expression. Mutant superoxide dismutase 1 was found to directly affect monocarboxylate transporter 1 protein expression. Our data suggest that oligodendroglial dysfunction may be a contributor to motor neuron degeneration in amyotrophic lateral sclerosis.
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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.