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Literature DB >> 21366663

Lack of cuprizone-induced demyelination in the murine spinal cord despite oligodendroglial alterations substantiates the concept of site-specific susceptibilities of the central nervous system.

V Herder, F Hansmann, M Stangel, T Skripuletz, W Baumgärtner, A Beineke.

Abstract

Entities: Chemical Disease Species

Mesh：

Substances：
Cuprizone

Year: 2011 PMID： 21366663 DOI： 10.1111/j.1365-2990.2011.01168.x

Source DB: PubMed Journal: Neuropathol Appl Neurobiol ISSN： 0305-1846 Impact factor: 8.090

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Cited

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12 in total

1. Anatomical Distribution of Cuprizone-Induced Lesions in C57BL6 Mice.

Authors: Johannes Goldberg; Tim Clarner; Cordian Beyer; Markus Kipp
Journal: J Mol Neurosci Date: 2015-06-12 Impact factor: 3.444

2. Cuprizone Intoxication Induces Cell Intrinsic Alterations in Oligodendrocyte Metabolism Independent of Copper Chelation.

Authors: Alexandra Taraboletti; Tia Walker; Robin Avila; He Huang; Joel Caporoso; Erendra Manandhar; Thomas C Leeper; David A Modarelli; Satish Medicetty; Leah P Shriver
Journal: Biochemistry Date: 2017-02-28 Impact factor: 3.162

3. Regional heterogeneity of cuprizone-induced demyelination: topographical aspects of the midline of the corpus callosum.

Authors: T Schmidt; H Awad; A Slowik; C Beyer; M Kipp; T Clarner
Journal: J Mol Neurosci Date: 2012-10-05 Impact factor: 3.444

Review 4. Heterogeneity in oligodendroglia: Is it relevant to mouse models and human disease?

Authors: Isis M Ornelas; Lauren E McLane; Aminat Saliu; Angelina V Evangelou; Luipa Khandker; Teresa L Wood
Journal: J Neurosci Res Date: 2016-08-25 Impact factor: 4.164

Review 5. The mechanistic target of rapamycin as a regulator of metabolic function in oligodendroglia during remyelination.

Authors: Marie L Mather; Marisa A Jeffries; Teresa L Wood
Journal: Curr Opin Pharmacol Date: 2022-03-01 Impact factor: 5.547

6. mTOR Signaling Regulates Metabolic Function in Oligodendrocyte Precursor Cells and Promotes Efficient Brain Remyelination in the Cuprizone Model.

Authors: Marisa A Jeffries; Lauren E McLane; Luipa Khandker; Marie L Mather; Angelina V Evangelou; Divyangi Kantak; Jennifer N Bourne; Wendy B Macklin; Teresa L Wood
Journal: J Neurosci Date: 2021-08-20 Impact factor: 6.709

Lack of cuprizone-induced demyelination in the murine spinal cord despite oligodendroglial alterations substantiates the concept of site-specific susceptibilities of the central nervous system.

1. Anatomical Distribution of Cuprizone-Induced Lesions in C57BL6 Mice.

2. Cuprizone Intoxication Induces Cell Intrinsic Alterations in Oligodendrocyte Metabolism Independent of Copper Chelation.

3. Regional heterogeneity of cuprizone-induced demyelination: topographical aspects of the midline of the corpus callosum.

Review 4. Heterogeneity in oligodendroglia: Is it relevant to mouse models and human disease?

Review 5. The mechanistic target of rapamycin as a regulator of metabolic function in oligodendroglia during remyelination.

6. mTOR Signaling Regulates Metabolic Function in Oligodendrocyte Precursor Cells and Promotes Efficient Brain Remyelination in the Cuprizone Model.

Review 7. PART 2: Mouse models for multiple sclerosis research.

8. Transcriptomic meta-analysis of multiple sclerosis and its experimental models.

Review 9. The Cuprizone Model: Dos and Do Nots.

10. Revisiting the Pathoetiology of Multiple Sclerosis: Has the Tail Been Wagging the Mouse?