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The Neurotoxicant, Cuprizone, as a Model to Study Demyelination and Remyelination in the Central Nervous System
Open accessAbstract
Myelin of the adult CNS is vulnerable to a variety of metabolic, toxic, and autoimmune insults. That remyelination can ensue, following demyelinating insult, has been well demonstrated. Details of the process of remyelination are, however difficult to ascertain since in most experimental models of demyelination/remyelination the severity, localization of lesion site, or time course of the pathophysiology is variable from animal to animal. In contrast, an experimental model in which massive demyelination can be reproducibly induced in large areas of mouse brain is exposure to the copper chelator, cuprizone, in the diet. We review work from several laboratories over the past 3 decades, with emphasis on our own recent studies, which suggest an overall picture of cellular events involved in demyelination/remyelination. When 8 week old C57BL/6 mice are fed 0.2% cuprizone in the diet, mature olidgodendroglia are specifically insulted (cannot fulfill the metabolic demand of support of vast amounts of myelin) and go through apoptosis.This is closely followed by recruitment of microglia and phagoctytosis of myelin. Studies of myelin gene expression, coordinated with morphological studies, indicate that even in the face of continued metabolic challenge, oligodendroglial progenitor cells proliferate and invade demyelinated areas. If the cuprizone challenge is terminated, an almost complete remyelination takes place in a matter of weeks. Communication between different cell types by soluble factors may be inferred. This material is presented in the context of a model compatible with present data—and which can be tested more rigorously with the cuprizone model. The reproducibility of the model indicates that it may allow for testing of manipulations (e.g. available knockouts or transgenics on the common genetic background, or pharmacological treatments) which may accelerate or repress the process of demyelination and or remyelination.
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“The C57BL/6 mice showed a dramatic loss of myelin staining at this time point (Fig. 1b), which is consistent with previous reports [5].”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Upon treatment with cuprizone, mice typically exhibit profound demyelination in the corpus callosum, the cortex and the superior cerebellar peduncles [4, 5].”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Most investigators use the standard C57BL/6 mouse strain in the cuprizone model to study the different molecular components involved in the complex pathogenic processes leading to corpus callosum demyelination [5].”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“In the corpus callosum, apoptosis of oligodendrocytes is observed, together with recruitment of microglia/macrophages, astrocytes and oligodendrocyte progenitor cells (OPCs) [5, 6].”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“In contrast, the continuous exposure of C57BL/6 mice to cuprizone results in a pattern of two cycles of demyelination and remyelination, followed by chronic demyelination from which animals do not recover 36, 39.”
From SJL Mice Exposed to Cuprizone Intoxication Reveal Strain and Gender Pattern Differences in Demyelination (2009) · cites this paper as [39]
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“In addition, C57BL/6 mice experience a spontaneous partial remyelination after 6 weeks and then continue to demyelinate further when exposed continuously to cuprizone 36, 39.”
From SJL Mice Exposed to Cuprizone Intoxication Reveal Strain and Gender Pattern Differences in Demyelination (2009) · cites this paper as [39]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Thus, unlike microglia and astrocytes in C57BL/6 mice that respond vigorously to demyelination 2, 23, 39, these cell types in SJL mice have a guarded response at midline and in the lateral region, which correlates with subdued demyelination.”
From SJL Mice Exposed to Cuprizone Intoxication Reveal Strain and Gender Pattern Differences in Demyelination (2009) · cites this paper as [39]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cuprizone toxicity produces profound demyelination in the white and grey matter of the brain that mirrors sites of MS pathology [46].”
From Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination (2022) · cites this paper as [46]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Other features common to both cuprizone-induced and type 3 MS lesions are mitochondrial stress, selective loss of myelin-associated glycoprotein (MAG), lesions with indistinct borders that are not perivascular, pronounced glial activation, and lymphocyte infiltration [43, 46, 65, 69–71].”
From Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination (2022) · cites this paper as [46]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“The histopathological hallmark of the cuprizone model as standardized by Hiremath is oligodendrocyte death and subsequent demyelination in the corpus callosum, superior cerebellar peduncles, hippocampus [42, 46–54] and several other areas of the mouse brain (reviewed in [20]).”
From Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination (2022) · cites this paper as [46]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Microglial activation and axonal loss positively correlate with demyelination and the reproducible lesion localization – primarily in the corpus callosum [186], cerebellar peduncle [186], hippocampus [187], and cortex [184, 185, 188] – mirrors the topographical specificity of MS pathology, including subpial cortical demyelination seen in PMS patients.”
From Insights and challenges on animal models for progressive multiple sclerosis (2026) · cites this paper as [186]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Remyelination is very robust in the cuprizone model and starts directly after demyelination is complete, irrespective if cuprizone is further fed or not (Matsushima and Morell, 2001; Hiremath et al., 2008; Gudi et al., 2009).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Matsushima and Morell, 2001
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In the citing paper
“Depletion of microglia likewise prevented the loss of oligodendrocytes (OLs) in the CC that normally results from CUP treatment (Matsushima & Morell, 2001).”
From Activated microglia drive demyelination via CSF1R signaling (2021) · cites this paper as Matsushima & Morell, 2001
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The cuprizone model involves administration of the toxin cuprizone to induce oligodendrocyte apoptosis [4, 5].”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [5]
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In the citing paper
“Here, we explored the effect of antibody-mediated TREM2 activation on microglia in a well-established toxin-induced model of demyelination in the CNS resulting from exposure to the copper chelator cuprizone (CPZ) in the diet [31].”
From TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis (2020) · cites this paper as [31]
The cited source says what the claim attributes to it.
In the citing paper
“These events lead to OPC recruitment, differentiation into mature OLs, and then remyelination which is almost complete within few weeks from toxin withdrawal [31].”
From TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis (2020) · cites this paper as [31]
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In the citing paper
“It may suggest that NODDI could be sensitive biomarkers to probe the different stages of white matter pathology between acute demyelination and chronic demyelination (Matsushima and Morell 2001).”
From Neurite orientation dispersion and density imaging of mouse brain microstructure (2019) · cites this paper as Matsushima and Morell 2001
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Historically these cells are not linked to demyelination following cuprizone treatment because the loss of the V(D)J recombination activation gene-1 (RAG-1), which is critical for B- and T- lymphocyte generation [269], does not alter demyelination and T-cell accumulation in the corpus callosum [46, 270].”
From Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination (2022) · cites this paper as [46]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Demyelination peaks between 4.5 and 5 weeks of cuprizone exposure in the CC and between 5 and 6 weeks in the cortex and hippocampus (Hiremath et al., 1998; Matsushima and Morell, 2001; Skripuletz et al., 2008; Gudi et al., 2009; Koutsoudaki et al., 2009).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Matsushima and Morell, 2001
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Strong astrogliosis comprising hypertrophy and hyperplasia of astrocytes occurs as a response to cuprizone treatment in different white and gray matter structures for instance the CC (Matsushima and Morell, 2001; Gudi et al., 2009), hippocampus, (Koutsoudaki et al., 2009; Norkute et al., 2009), cerebellum, cortex (Skripuletz et al., 2008), and basal ganglia (Pott et al., 2009).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Matsushima and Morell, 2001
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Astrogliosis is an additional pathological hallmark of CUP treatment (Matsushima & Morell, 2001).”
From Activated microglia drive demyelination via CSF1R signaling (2021) · cites this paper as Matsushima & Morell, 2001
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Citations
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Metadata
- Authors
- Matsushima, G. K., & Morell, P.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Matsushima, Glenn K.
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2001-01
- Volume
- 11
- Issue
- 1
- Pages
- 107-116
- ISSN
- 1015-6305 (ISSN-L)
- 1750-3639
- PMC
- PMC8098267
- OpenAlex
- W2100904149
- Cited by
- 984
- References
- 45
- Citations by year
- 2026: 31 · 2025: 38 · 2024: 42 · 2023: 50 · 2022: 58 · 2021: 48 · 2020: 55 · 2019: 75 · 2018: 59 · 2017: 65 · 2016: 39 · 2015: 58 · 2014: 39 · 2013: 53 · 2012: 40
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ns011615-29, 5r01ns037815-05, 5r29ns035372-05)
- National Institute of Neurological Disorders and Stroke (NS37815, NS-11615, NS-35372)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cuprizone, demyelination, remyelination, oligodendrocyte apoptosis, microglia, myelin phagocytosis, oligodendrocyte precursor cells, myelin gene expression, C57BL/6 mice, copper chelators
- MeSH terms
- Animals, Central Nervous System, Chelating Agents, Cuprizone, Demyelinating Diseases, Mice, Inbred C57BL, Myelin Sheath, Oligodendroglia, Microglia, Models, Animal, Mice
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