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Delayed Demyelination and Impaired Remyelination in Aged Mice in the Cuprizone Model.

GND
1033699489
ORCID
0000-0002-6055-5695
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Gingele, Stefan;
ORCID
0000-0003-1465-8172
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Henkel, Florian;
GND
1057884502
ORCID
0000-0001-8833-1709
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Heckers, Sandra;
ORCID
0000-0003-4607-3515
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Moellenkamp, Thiemo M;
GND
1217289003
ORCID
0000-0002-5928-2343
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Hümmert, Martin W;
GND
132929899
ORCID
0000-0001-8550-335X
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Skripuletz, Thomas;
GND
133799158
ORCID
0000-0003-2504-5398
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Stangel, Martin;
GND
143278363
ORCID
0000-0002-0438-2339
Affiliation
Department of Neurology, Hannover Medical School, D-30625 Hannover, Germany.
Gudi, Viktoria

To unravel the failure of remyelination in multiple sclerosis (MS) and to test promising remyelinating treatments, suitable animal models like the well-established cuprizone model are required. However, this model is only standardized in young mice. This does not represent the typical age of MS patients. Furthermore, remyelination is very fast in young mice, hindering the examination of effects of remyelination-promoting agents. Thus, there is the need for a better animal model to study remyelination. We therefore aimed to establish the cuprizone model in aged mice. 6-month-old C57BL6 mice were fed with different concentrations of cuprizone (0.2-0.6%) for 5-6.5 weeks. De- and remyelination in the medial and lateral parts of the corpus callosum were analyzed by immunohistochemistry. Feeding aged mice 0.4% cuprizone for 6.5 weeks resulted in the best and most reliable administration scheme with virtually complete demyelination of the corpus callosum. This was accompanied by a strong accumulation of microglia and near absolute loss of mature oligodendrocytes. Subsequent remyelination was initially robust but remained incomplete. The remyelination process in mature adult mice better represents the age of MS patients and offers a better model for the examination of regenerative therapies.

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