Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis
Open accessAbstract
Oligodendrocytes associate with axons to establish myelin and provide metabolic support to neurons. In the spinal cord of amyotrophic lateral sclerosis (ALS) mice, oligodendrocytes downregulate transporters that transfer glycolytic substrates to neurons and oligodendrocyte progenitors (NG2(+) cells) exhibit enhanced proliferation and differentiation, although the cause of these changes in oligodendroglia is unknown. We found extensive degeneration of gray matter oligodendrocytes in the spinal cord of SOD1 (G93A) ALS mice prior to disease onset. Although new oligodendrocytes were formed, they failed to mature, resulting in progressive demyelination. Oligodendrocyte dysfunction was also prevalent in human ALS, as gray matter demyelination and reactive changes in NG2(+) cells were observed in motor cortex and spinal cord of ALS patients. Selective removal of mutant SOD1 from oligodendroglia substantially delayed disease onset and prolonged survival in ALS mice, suggesting that ALS-linked genes enhance the vulnerability of motor neurons and accelerate disease by directly impairing the function of oligodendrocytes.
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6-OHDA causes dopamine containing nerve terminals to degenerate, which leads to oligodendrocyte precursor cell infiltration.
“6-OHDA causes dopamine containing nerve terminals to degenerate, which leads to oligodendrocyte precursor cell infiltration.24,25”
From Characterization of a novel adeno-associated viral vector with preferential oligodendrocyte tropism (2016) · cites this paper as [25]
The Results section on degeneration of early-born oligodendrocytes examines motor-neuron loss after ricin injection, not dopamine-terminal degeneration after 6-OHDA. Our copy reports no 6-OHDA experiment or finding that loss of dopamine-containing terminals causes oligodendrocyte precursor infiltration (searched: 6-OHDA, 6-hydroxydopamine, dopaminergic axons, NG2 cells). (LLM, conf=0.76)
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- Authors
- Kang, S. H., Li, Y., Fukaya, M., Lorenzini, I., Cleveland, D. W., Ostrow, L. W., Rothstein, J. D., & Bergles, D. E.
- Affiliations
- Johns Hopkins University (US)
- Kitasato University (JP)
- University of California San Diego (US)
- Corresponding author
- Rothstein, Jeffrey D
- Bergles, Dwight E
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2013-03-31
- Volume
- 16
- Issue
- 5
- Pages
- 571-579
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3637847
- OpenAlex
- W2166043619
- Cited by
- 599
- References
- 54
- Citations by year
- 2026: 33 · 2025: 39 · 2024: 42 · 2023: 39 · 2022: 51 · 2021: 62 · 2020: 62 · 2019: 38 · 2018: 45 · 2017: 47 · 2016: 39 · 2015: 44 · 2014: 30 · 2013: 26
- FWCI
- 29.43
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Emory University
- Johns Hopkins University
- Wellcome Trust (089701)
- Japan Society for the Promotion of Science (23700416)
- National Eye Institute (T32EY017203)
- National Institute of Neurological Disorders and Stroke (NS051509, NS 27036, NS 33958, R37NS027036, R01NS051509, R01NS033958, R01NS027036)
- Robert Packard Center for ALS Research, Johns Hopkins University
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- amyotrophic lateral sclerosis, oligodendrocytes, demyelination, gray matter degeneration, SOD1 G93A mice, mutant SOD1, oligodendrocyte precursor cells, myelination, motor neurons, disease onset, motor cortex
- MeSH terms
- Amyotrophic Lateral Sclerosis, Animals, Animals, Newborn, Cells, Cultured, Disease Models, Animal, Humans, Functional Laterality, Mice, Transgenic, Motor Cortex, Myelin Sheath, Nerve Degeneration, Nerve Fibers, Myelinated, Nerve Tissue Proteins, Oligodendroglia, Regeneration, Spinal Cord, Survival Analysis, Receptor, Platelet-Derived Growth Factor alpha, Cell Proliferation, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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