Cuprizone (Standard)

[1]. Vega-Riquer JM, et al. Five Decades of Cuprizone, an Updated Model to Replicate Demyelinating Diseases. Curr Neuropharmacol. 2019;17(2):129-141. [Content Brief]

[2]. Zirngibl M, et al. Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination. Mol Neurodegener. 2022 May 7;17(1):34. [Content Brief]

[3]. Kipp M, et al. The cuprizone animal model: new insights into an old story. Acta Neuropathol. 2009 Dec;118(6):723-36. [Content Brief]

[4]. Torkildsen Ø, et al. The cuprizone model for demyelination[J]. Acta neurologica scandinavica, 2008, 117: 72-76.

[5]. Goldberg J, et al. Anatomical Distribution of Cuprizone-Induced Lesions in C57BL6 Mice. J Mol Neurosci. 2015 Oct;57(2):166-75. [Content Brief]

[6]. Benetti F, et al. Cuprizone neurotoxicity, copper deficiency and neurodegeneration. Neurotoxicology. 2010 Sep;31(5):509-17. [Content Brief]

[7]. Zatta P, et al. Copper and zinc dismetabolism in the mouse brain upon chronic cuprizone treatment. Cell Mol Life Sci. 2005 Jul;62(13):1502-13. [Content Brief]

[8]. Gudi V, et al. (2014) Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned. Front. Cell. Neurosci. 8:73.

[9]. Matsushima GK, et al. The neurotoxicant, cuprizone, as a model to study demyelination and remyelination in the central nervous system. Brain Pathol. 2001 Jan;11(1):107-16. [Content Brief]

[10]. Zhan J, et al. The Cuprizone Model: Dos and Do Nots. Cells. 2020 Mar 31;9(4):843. [Content Brief]

[11]. Praet J, et al. Cellular and molecular neuropathology of the cuprizone mouse model: clinical relevance for multiple sclerosis. Neurosci Biobehav Rev. 2014 Nov;47:485-505. [Content Brief]