ArticleNeurobiology of disease2010
In toxic demyelination oligodendroglial cell death occurs early and is FAS independent.
Article in Neurobiology of disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 99 citations in OpenAlex.
- Inhibition of Lin-11, Isl-1, and Mec‑3 Kinase (LIMK) Activity Attenuates Astrogliosis and Vascular Remodeling in an Experimental Model of Cuprizone-Induced Demyelination in Mice.ACS pharmacology & translational science · 2026Article
- Loss of oligodendrocyte transcription factor 2 protein expression in metabolically stressed oligodendrocytes.Acta neuropathologica · 2026Article
- Respiratory infection with influenza A virus delays remyelination and alters oligodendrocyte metabolism.iScience · 2024Article
- Oligodendrocyte Maturation Alters the Cell Death Mechanisms That Cause Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Automated analysis of gray matter damage in aged mice reveals impaired remyelination in the cuprizone model.Brain pathology (Zurich, Switzerland) · 2024Article
- How to Use the Cuprizone Model to Study De- and Remyelination.International journal of molecular sciences · 2024Review
- Article
- The Cuprizone Mouse Model: A Comparative Study of Cuprizone Formulations from Different Manufacturers.International journal of molecular sciences · 2023Article
- Abcd1 deficiency accelerates cuprizone-induced oligodendrocyte loss and axonopathy in a demyelinating mouse model of X-linked adrenoleukodystrophy.Acta neuropathologica communications · 2023Article
- Single-cell microglial transcriptomics during demyelination defines a microglial state required for lytic carcass clearance.Molecular neurodegeneration · 2022Article
- Ferulic Acid Ameliorates Cell Injuries, Cognitive and Motor Impairments in Cuprizone-Induced Demyelination Model of Multiple Sclerosis.Cell journal · 2022Article
- Optic Neuritis in Multiple Sclerosis-A Review of Molecular Mechanisms Involved in the Degenerative Process.Current issues in molecular biology · 2022Review
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Oligodendrogenesis and myelination tracing in a CRISPR/Cas9-engineered brain microphysiological system.Frontiers in cellular neuroscience · 2022Article
- Neuroprotective Effects of Telmisartan and Nifedipine Against Cuprizone-Induced Demyelination and Behavioral Dysfunction in Mice: Roles of NF-κB and Nrf2.Inflammation · 2021Article
- Cuprizone-Induced Neurotoxicity in Human Neural Cell Lines Is Mediated by a Reversible Mitochondrial Dysfunction: Relevance for Demyelination Models.Brain sciences · 2021Article
- Effect and Mechanism of Catalpol on Remyelination via Regulation of the NOTCH1 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Diverse Gene Expressions in the Prediction of Cuprizone-Induced Demyelination.Neurotoxicity research · 2020Article
- Differential Susceptibility and Vulnerability of Brain Cells in C57BL/6 Mouse to Mitochondrial Dysfunction Induced by Short-Term Cuprizone Exposure.Frontiers in neuroanatomy · 2020Article
- Supplemental study on 2', 3'-Cyclic Nucleotide 3'-Phosphodiesterase (CNPase) activity in developing rat spinal cord lesions induced by hexachlorophene and cuprizone.The Journal of veterinary medical science · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oligodendroglial cell death is a frequent phenomenon of many neurological diseases, e.g. in demyelinating diseases such as multiple sclerosis (MS). The underlying mechanisms are largely unknown. Here, we demonstrate that in the toxic demyelination cuprizone model, oligodendroglial cell death and downregulation of myelin genes start days after initiation of the cuprizone diet and weeks before demyelination is obvious. In early - but not in later - stages, dying oligodendrocytes express activated caspase 3, suggesting a switch from classical apoptotic pathways to caspase 3-independent mechanisms during the course of the cuprizone diet. The expression level of FAS in the corpus callosum, a cell death receptor crucial for oligodendroglial cell death in experimental autoimmune encephalomyelitis (EAE), correlates with the expression of activated caspase 3 in oligodendrocytes. However, mice lacking FAS in oligodendrocytes are not protected against cuprizone-induced oligodendroglial cell death, showing that FAS is dispensable for oligodendroglial cell death in the cuprizone model.
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