The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis
Open accessAbstract
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Rosen, D. R., Siddique, T., Patterson, D., Figlewicz, D. A., Sapp, P., Hentati, A., Donaldson, D., Goto, J., O'Regan, J. P., Deng, H.-X., et al. (1993) · Nature · doi:10.1038/362059a0 · Cited by 7,062
Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis
Neumann, M., Sampathu, D. M., Kwong, L. K., Truax, A. C., Micsenyi, M. C., Chou, T. T., Bruce, J., Schuck, T., Grossman, M., Clark, C. M., et al. (2006) · Science · doi:10.1126/science.1134108 · Cited by 6,576
DeJesus-Hernandez, M., Mackenzie, I. R., Boeve, B. F., Boxer, A. L., Baker, M., Rutherford, N. J., Nicholson, A. M., Finch, N. A., Flynn, H., Adamson, J., et al. (2011) · Neuron · doi:10.1016/j.neuron.2011.09.011 · Cited by 4,936 · cited 1×
“Mutations in superoxide dismutase 1 (SOD1) and hex- anucleotide repeats in C9orf72 are the most prevalent (Rosen et al., 1993; DeJesus-Hernandez et al., 2011).”
BackgroundTDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis
Sreedharan, J., Blair, I. P., Tripathi, V. B., Hu, X., Vance, C., Rogelj, B., Ackerley, S., Durnall, J. C., Williams, K. L., Buratti, E., et al. (2008) · Science · doi:10.1126/science.1154584 · Cited by 2,630
Oligodendroglia metabolically support axons and contribute to neurodegeneration
Lee, Y., Morrison, B. M., Li, Y., Lengacher, S., Farah, M. H., Hoffman, P. N., Liu, Y., Tsingalia, A., Jin, L., Zhang, P.-W., et al. (2012) · Nature · doi:10.1038/nature11314 · Cited by 1,664
Myelination and support of axonal integrity by glia
Nave, K.-A. (2010) · Nature · doi:10.1038/nature09614 · Cited by 1,062
Non–cell autonomous toxicity in neurodegenerative disorders: ALS and beyond
Ilieva, H., Polymenidou, M., & Cleveland, D. W. (2009) · Journal of Cell Biology · doi:10.1083/jcb.200908164 · Cited by 1,008
Zawadzka, M., Rivers, L. E., Fancy, S. P. J., Zhao, C., Tripathi, R., Jamen, F., Young, K., Goncharevich, A., Pohl, H., Rizzi, M., et al. (2010) · Cell stem cell · doi:10.1016/j.stem.2010.04.002 · Cited by 650
Self-citationRegulation of Oligodendrocyte Development and Myelination by Glucose and Lactate
Rinholm, J. E., Hamilton, N. B., Kessaris, N., Richardson, W. D., Bergersen, L. H., & Attwell, D. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.3516-10.2011 · Cited by 383
Self-citation
Cited by
Stages of pTDP‐43 pathology in amyotrophic lateral sclerosis
Brettschneider, J., Del Tredici, K., Toledo, J. B., Robinson, J. L., Irwin, D. J., Grossman, M., Suh, E., Van Deerlin, V. M., Wood, E. M., Baek, Y., et al. (2013) · Annals of Neurology · doi:10.1002/ana.23937 · Cited by 1,065
Myelination of the Nervous System: Mechanisms and Functions
Nave, K.-A., & Werner, H. B. (2014) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-100913-013101 · Cited by 983
The changing scene of amyotrophic lateral sclerosis
Robberecht, W., & Philips, T. (2013) · Nature Reviews Neuroscience · doi:10.1038/nrn3430 · Cited by 957
Self-citationThe role of myelin and oligodendrocytes in axonal energy metabolism
Saab, A. S., Tzvetanova, I. D., & Nave, K.-A. (2013) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2013.09.008 · Cited by 324
Dynamics and Mechanisms of CNS Myelination
Bercury, K. K., & Macklin, W. B. (2015) · Developmental Cell · doi:10.1016/j.devcel.2015.01.016 · Cited by 320
Metadata
- Authors
- Philips, T., Bento-Abreu, A., Nonneman, A., Haeck, W., Staats, K., Geelen, V., Hersmus, N., Küsters, B., Van Den Bosch, L., Van Damme, P., Richardson, W. D., & Robberecht, W.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-01-31
- Volume
- 136
- Issue
- 2
- Pages
- 471-482
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2114080032
- Cited by
- 260
- References
- 9
- FWCI
- 11.97
- Type
- journal article
- Language
- en
- Open access
- bronze
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 ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis. https://app.cochat.ai/papers/10.1093/brain/aws339
- The paper
- Philips, T., Bento-Abreu, A., Nonneman, A., Haeck, W., Staats, K., Geelen, V., Hersmus, N., Küsters, B., Van Den Bosch, L., Van Damme, P., Richardson, W. D., & Robberecht, W. (2013). Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis. Brain. https://doi.org/10.1093/brain/aws339
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
