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 4 weeks of cuprizone treatment.
“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]
The opening passage (section and page unavailable) describes massive cuprizone-induced demyelination in mouse brain and specifically discusses C57BL/6 mice fed cuprizone. It does not establish that a dramatic loss of myelin staining occurs at four weeks, so the cited report supports the general finding but not that time point or staining observation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredUpon treatment with cuprizone, mice typically exhibit profound demyelination in the corpus callosum, the cortex and the superior cerebellar peduncles.
“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]
The opening passage in our copy (section and page not labeled) says cuprizone reproducibly induces massive demyelination in large areas of mouse brain. The references include a study titled “Demyelination of the superior cerebellar peduncle in the mouse induced by cuprizone,” but no passage in our copy establishes that profound demyelination typically occurs in all three named regions; the corpus callosum and cortex are not identified. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMost investigators use the standard C57BL/6 mouse strain in the cuprizone model to study molecular components of corpus callosum demyelination.
“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]
The opening summary (page not supplied) describes cuprizone-induced demyelination in C57BL/6 mice and studies of myelin gene expression and cellular events. It does not establish that most investigators use this strain or specify the corpus callosum as the site studied. (LLM, conf=0.82)
Experimental — accuracy not yet measuredIn the corpus callosum, cuprizone treatment induces apoptosis of oligodendrocytes together with recruitment of microglia/macrophages, astrocytes and OPCs.
“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]
The main-text passage supplied in our copy (no page label) says that cuprizone-fed mice undergo mature oligodendrocyte apoptosis, followed by microglial recruitment, and that oligodendrocyte progenitors proliferate and invade demyelinated areas. It does not specify the corpus callosum or say that astrocytes are recruited; the reference-list mentions of astrocytes do not establish that part of the claim. (LLM, conf=0.85)
Experimental — accuracy not yet measuredContinuous exposure of C57BL/6 mice to cuprizone results in two cycles of demyelination and remyelination, followed by chronic demyelination from which animals do not recover.
“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]
The paper’s summary passage describes cuprizone-induced demyelination in C57BL/6 mice and oligodendroglial progenitor activity despite continued exposure. It does not describe two cycles of demyelination and remyelination or establish that the animals cannot recover; it instead reports almost complete remyelination when cuprizone is withdrawn. The indexed passages provide no page number for this passage. (LLM, conf=0.82)
Experimental — accuracy not yet measured
C57BL/6 mice experience a spontaneous partial remyelination after 6 weeks and then continue to demyelinate further when exposed continuously to cuprizone.
“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]
The opening passage (section and page not supplied) describes cuprizone-induced demyelination in C57BL/6 mice and progenitor-cell activity despite continued exposure. It does not say that partial remyelination occurs after six weeks or that further demyelination follows; it describes almost complete remyelination after cuprizone is stopped. (LLM, conf=0.82)
Experimental — accuracy not yet measuredUnlike microglia and astrocytes in C57BL/6 mice that respond vigorously to demyelination, these cell types in SJL mice have a guarded response at midline and in the lateral region, which correlates with subdued demyelination.
“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]
The introductory overview (page not provided) says that cuprizone-induced injury in C57BL/6 mice is closely followed by microglial recruitment and myelin phagocytosis. It does not establish a vigorous astrocyte response in those mice. The citation follows the C57BL/6 clause; the subsequent observation about SJL mice is the citing authors’ comparison, not a finding attributed to this source. (LLM, conf=0.83)
Experimental — accuracy not yet measuredCuprizone toxicity produces profound demyelination in the white and grey matter of the brain that mirrors sites of MS pathology.
“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]
The paper’s opening passage says dietary cuprizone reproducibly induces massive demyelination in large areas of mouse brain. The available passages do not specify demyelination in both white and grey matter or say that its sites mirror MS pathology (searched: white and grey matter; MS lesion distribution). (LLM, conf=0.84)
Experimental — accuracy not yet measuredFeatures common to both cuprizone-induced and type 3 MS lesions include mitochondrial stress, selective loss of myelin-associated glycoprotein (MAG), lesions with indistinct borders that are not perivascular, pronounced glial activation, and lymphocyte infiltration.
“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]
The unpaginated overview of the cuprizone model reports metabolic challenge to oligodendroglia and recruitment of microglia, supporting part of the description of cuprizone lesions. It does not compare those lesions with type 3 MS lesions or establish the claimed selective MAG loss, indistinct nonperivascular borders, or lymphocyte infiltration. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe histopathological hallmark of the cuprizone model as standardized by Hiremath is oligodendrocyte death and subsequent demyelination in the corpus callosum, superior cerebellar peduncles, hippocampus, and several other areas of the mouse brain.
“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]
The paper’s opening summary (p. 107) says that cuprizone causes mature oligodendroglia to undergo apoptosis and induces demyelination across large areas of mouse brain. Its references include Hiremath’s cuprizone study and a study of demyelination in the superior cerebellar peduncle. The available text does not identify the corpus callosum or hippocampus as affected regions, or say that Hiremath standardized the model, so those specifics are not supported by this source. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIn the cuprizone model, microglial activation and axonal loss positively correlate with demyelination, and lesion localization is reproducible primarily in the corpus callosum, cerebellar peduncle, hippocampus, and cortex.
“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]
The main text (page not provided) describes reproducible cuprizone-induced demyelination and microglial recruitment, while the references (page not provided) identify studies of demyelination in the superior cerebellar peduncle. Our copy does not establish axonal loss as positively correlated with demyelination or specifically locate lesions in the corpus callosum. The citing sentence assigns the hippocampus and cortex to other citations, not this source. (LLM, conf=0.83)
Experimental — accuracy not yet measuredRemyelination is very robust in the cuprizone model and starts directly after demyelination is complete, irrespective of whether cuprizone is further fed or not.
“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
The paper’s summary reports almost complete remyelination within weeks after cuprizone is stopped. It also reports progenitor-cell proliferation during continued exposure, but that is not evidence that remyelination starts immediately after demyelination is complete or proceeds irrespective of continued feeding. The retrieved passages have no section or page labels. (LLM, conf=0.85)
Experimental — accuracy not yet measuredDepletion of microglia prevented the loss of oligodendrocytes in the corpus callosum that normally results from CUP treatment.
“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 <scp>CSF1R</scp> signaling (2021) · cites this paper as Matsushima & Morell, 2001
The opening overview (section and page not provided) says cuprizone-treated mice experience mature oligodendrocyte apoptosis, followed by microglial recruitment. It does not report that depleting microglia prevents oligodendrocyte loss in the corpus callosum. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe cuprizone model involves administration of cuprizone to induce oligodendrocyte apoptosis.
“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]
The cuprizone model is a well-established toxin-induced model of demyelination in the CNS.
“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]
In the cuprizone model, these events lead to OPC recruitment, differentiation into mature oligodendrocytes, and then remyelination which is almost complete within a few weeks from toxin withdrawal.
“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]
NODDI could be a sensitive biomarker to probe different stages of white matter pathology between acute and chronic demyelination.
“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
The paper’s discussion of the cuprizone model describes the time course of demyelination and remyelination in mice, but does not assess an imaging biomarker. Searches for NODDI and for acute versus chronic demyelination found no passage supporting the attributed claim about NODDI’s sensitivity. (LLM, conf=0.76)
Experimental — accuracy not yet measuredHistorically, T-cells are not linked to demyelination following cuprizone treatment because loss of RAG-1 does not alter demyelination and T-cell accumulation in the corpus callosum.
“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]
The available text describes cuprizone-induced oligodendrocyte loss and subsequent microglial recruitment, but does not address whether T cells contribute to demyelination. Searches for RAG-1, T cells, and lymphocyte accumulation in the corpus callosum found no passage reporting the claimed knockout result. The available copy appears to contain an introductory summary and references rather than the decisive discussion. (LLM, conf=0.72)
Experimental — accuracy not yet measuredDemyelination peaks between 4.5 and 5 weeks of cuprizone exposure in the corpus callosum and between 5 and 6 weeks in the cortex and hippocampus.
“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
The available paper text describes cuprizone-induced demyelination in mouse brain but gives no peak times for the corpus callosum, cortex, or hippocampus. Searches for the named regions and the 4.5–6-week intervals found no passage addressing those specific timings; the returned passages have no section or page labels. (LLM, conf=0.72)
Experimental — accuracy not yet measuredStrong astrogliosis comprising hypertrophy and hyperplasia of astrocytes occurs as a response to cuprizone treatment in different white and gray matter structures including the corpus callosum, hippocampus, cerebellum, cortex, and basal ganglia.
“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
The available summary describes cuprizone-induced demyelination, microglial recruitment, and remyelination, but does not describe astrogliosis in the corpus callosum. Searches for astrocyte hypertrophy, hyperplasia, astrogliosis, and corpus callosum found no passage establishing the response attributed to Matsushima and Morell; the other named regions have separate citations in the citing sentence. (LLM, conf=0.70)
Experimental — accuracy not yet measuredAstrogliosis is an additional pathological hallmark of CUP treatment.
“Astrogliosis is an additional pathological hallmark of CUP treatment (Matsushima & Morell, 2001).”
From Activated microglia drive demyelination via <scp>CSF1R</scp> signaling (2021) · cites this paper as Matsushima & Morell, 2001
The available paper text describes cuprizone-induced demyelination and microglial recruitment, but does not describe astrogliosis as a consequence of treatment. Searches for “astrogliosis” and reactive astrocytes returned only related reference titles, not a passage establishing the claimed hallmark. (LLM, conf=0.70)
Experimental — accuracy not yet measured
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Statin Therapy Inhibits Remyelination in the Central Nervous System
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- 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 › Pathology and Forensic Medicine › 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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