Cellular and molecular neuropathology of the cuprizone mouse model: Clinical relevance for multiple sclerosis

Praet, Jelle; Guglielmetti, Caroline; Berneman, Zwi; Van der Linden, Annemie; Ponsaerts, Peter

doi:10.1016/j.neubiorev.2014.10.004

Cited by 435Multiple Sclerosis Research StudiesNeurogenesis and neuroplasticity mechanismsNeurological Disease Mechanisms and Treatments

Cellular and molecular neuropathology of the cuprizone mouse model: Clinical relevance for multiple sclerosis

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Praet, Jelle, Guglielmetti, Caroline, Berneman, Zwi, Van der Linden, Annemie, Ponsaerts, Peter·2014·Neuroscience & Biobehavioral Reviews

DOI 10.1016/j.neubiorev.2014.10.004

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Abstract

The cuprizone mouse model allows the investigation of the complex molecular mechanisms behind nonautoimmune-mediated demyelination and spontaneous remyelination. While it is generally accepted that oligodendrocytes are specifically vulnerable to cuprizone intoxication due to their high metabolic demands, a comprehensive overview of the etiology of cuprizone-induced pathology is still missing to date. In this review we extensively describe the physico-chemical mode of action of cuprizone and discuss the molecular and enzymatic mechanisms by which cuprizone induces metabolic stress, oligodendrocyte apoptosis, myelin degeneration and eventually axonal and neuronal pathology. In addition, we describe the dual effector function of the immune system which tightly controls demyelination by effective induction of oligodendrocyte apoptosis, but in contrast also paves the way for fast and efficient remyelination by the secretion of neurotrophic factors and the clearance of cellular and myelinic debris. Finally, we discuss the many clinical symptoms that can be observed following cuprizone treatment, and how these strengthened the cuprizone model as a useful tool to study human multiple sclerosis, schizophrenia and epilepsy.

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Cuprizone-induced apoptosis precedes massive demyelination, indicating that oligodendrocyte degeneration is the main cause, as opposed to a secondary immune response.
“Importantly this apoptosis precedes the massive demyelination caused by cuprizone administration [18], indicating that oligodendrocyte degeneration is the main cause, as opposed to a secondary immune response.”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [18]
The involvement of brain resident neuroinflammatory cells such as microglia and astrocytes is believed to be responsible for the massive demyelination occurring at 4 weeks of cuprizone exposure.
“In addition to the direct effect of cuprizone on oligodendrocytes, the involvement of the brain’s resident neuroinflammatory cells such as microglia and astrocyes is also believed to be responsible for the massive demyelination occurring at 4 weeks time point of cuprizone exposure [18].”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [18]
Cuprizone selectively affects oligodendrocytes.
“Nevertheless, a consensus seems to be that cuprizone selectively affects oligodendrocytes.”
From Strain differences in cuprizone induced demyelination (2017) · cites this paper as [18]
Astrocytes and microglia collaborate through the release of cytokines, chemokines, and other factors to drive demyelination; preventing the release of specific cytokines or chemokines, restricting astrocyte reactivity, or ablating microglia all reduce cuprizone-induced demyelination.
“Astrocytes and microglia collaborate through the release of cytokines, chemokines, and other, yet to be identified factors, to drive demyelination [79, 107], preventing the release of specific cytokines or chemokines, restricting astrocyte reactivity, or ablating microglia all reduce cuprizone-induced demyelination [107, 181, 189, 243].”
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 [107]
The cuprizone model is based on oral ingestion of the copper chelator cuprizone, causing metabolic oligodendrocyte injury.
“The cuprizone model is based on oral ingestion of the copper chelator cuprizone, causing metabolic oligodendrocyte injury.”
From Insights and challenges on animal models for progressive multiple sclerosis (2026) · cites this paper as [183]

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Disruption of Myelin Leads to Ectopic Expression of KV1.1 Channels with Abnormal Conductivity of Optic Nerve Axons in a Cuprizone-Induced Model of Demyelination
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PERK Activation Preserves the Viability and Function of Remyelinating Oligodendrocytes in Immune-Mediated Demyelinating Diseases
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Evaluation of [123I]-CLINDE as a potent SPECT radiotracer to assess the degree of astroglia activation in cuprizone-induced neuroinflammation
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The cyclooxygenase‐2 pathway via the PGE2 EP2 receptor contributes to oligodendrocytes apoptosis in cuprizone‐induced demyelination
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Demyelination caused by the copper chelator cuprizone halts T cell mediated autoimmune neuroinflammation
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Local Overexpression of Interleukin-11 in the Central Nervous System Limits Demyelination and Enhances Remyelination
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Multimodal imaging of subventricular zone neural stem/progenitor cells in the cuprizone mouse model reveals increased neurogenic potential for the olfactory bulb pathway, but no contribution to remyelination of the corpus callosum
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G protein‐coupled receptor 30 contributes to improved remyelination after cuprizone‐induced demyelination
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TREM2 regulates microglial cholesterol metabolism upon chronic phagocytic challenge
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Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases
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Animal models of multiple sclerosis: Focus on experimental autoimmune encephalomyelitis
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Neuroprotective Potential of Ellagic Acid: A Critical Review
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Diffusion kurtosis imaging probes cortical alterations and white matter pathology following cuprizone induced demyelination and spontaneous remyelination
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Microglial Phenotypes and Functions in Multiple SclerosisPreprint
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Infection as an Environmental Trigger of Multiple Sclerosis Disease Exacerbation
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Zhang, Y., Li, X., Ćirić, B., Curtis, M. T., Chen, W., Rostami, A. M., & Zhang, G. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2000208117 · Cited by 103 · see citing works
Blood-brain barrier hyperpermeability precedes demyelination in the cuprizone model
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Behavioural phenotypes in the cuprizone model of central nervous system demyelination.
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NLR-Dependent Regulation of Inflammation in Multiple Sclerosis
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Diversity of Reactive Astrogliosis in CNS Pathology: Heterogeneity or Plasticity?
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Physical Exercise Improves Cognitive Function Together with Microglia Phenotype Modulation and Remyelination in Chronic Cerebral Hypoperfusion
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Nanocatalytic activity of clean-surfaced, faceted nanocrystalline gold enhances remyelination in animal models of multiple sclerosis
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Cytokine Signaling in Multiple Sclerosis and Its Therapeutic Applications
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Fundamentally different roles of neuronal TNF receptors in CNS pathology: TNFR1 and IKKβ promote microglial responses and tissue injury in demyelination while TNFR2 protects against excitotoxicity in mice
Papazian, I., Tsoukala, E., Boutou, A., Καραμίτα, Μ., Kambas, K., Iliopoulou, L., Fischer, R., Kontermann, R. E., Denis, M. C., Kollias, G. A., et al. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02200-4 · Cited by 86 · see citing works
Hyperpolarized 13 C MR metabolic imaging can detect neuroinflammation in vivo in a multiple sclerosis murine model
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Microglial NLRP3 inflammasome activation in multiple sclerosis
(2020) · Advances in Protein Chemistry and Structural Biology · doi:10.1016/bs.apcsb.2019.08.007 · Cited by 83 · see citing works
Opposing effects of apoE2 and apoE4 on microglial activation and lipid metabolism in response to demyelination
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Fluorescent flavonoids for endoplasmic reticulum cell imaging
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Ketogenic diet ameliorates axonal defects and promotes myelination in Pelizaeus–Merzbacher disease
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An overall view of the most common experimental models for multiple sclerosis
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Antipsychotic drugs counteract autophagy and mitophagy in multiple sclerosis
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Interleukin-13 immune gene therapy prevents CNS inflammation and demyelination via alternative activation of microglia and macrophages: Modulation of CNS Inflammation by Interkeukin-13
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Evaluation of the cuprizone model
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Authors: Praet, J., Guglielmetti, C., Berneman, Z., Van der Linden, A., & Ponsaerts, P.
Affiliations: University of Antwerp (BE)
Corresponding author: Praet, Jelle
ORCID: Praet, Jelle
Guglielmetti, Caroline
Berneman, Zwi
Ponsaerts, Peter
Venue: Neuroscience & Biobehavioral Reviews
Publisher: Elsevier BV
Published: 2014-11
Volume: 47
Pages: 485-505
ISSN: 0149-7634 (ISSN-L)
DOI: 10.1016/j.neubiorev.2014.10.004
OpenAlex: W1991883207
Cited by: 435
References: 268
Citations by year: 2026: 29 · 2025: 36 · 2024: 29 · 2023: 37 · 2022: 51 · 2021: 49 · 2020: 48 · 2019: 49 · 2018: 41 · 2017: 35 · 2016: 19 · 2015: 12
FWCI: 3.11
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by-nc-nd/3.0/ (vor)
Locations: Neuroscience & Biobehavioral Reviews (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Funders: Fund for Scientific Research-Flanders
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 › Neurological Disease Mechanisms and Treatments
Keywords: cuprizone, multiple sclerosis, demyelination, remyelination, oligodendrocyte apoptosis, myelin degeneration, metabolic stress, neuroinflammation, neurotrophic factors, myelin debris clearance, axonal pathology, neuronal pathology, schizophrenia, epilepsy, mouse model
MeSH terms: Animals, Brain, Cuprizone, Disease Models, Animal, Multiple Sclerosis, Myelin Sheath, Neuroglia, Neurons, Oxidative Stress, Mice

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Cellular and molecular neuropathology of the cuprizone mouse model: Clinical relevance for multiple sclerosis

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