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   <subfield code="a">The hippocampal fimbria of cuprizone-treated animals as a structure for studying neuroprotection in multiple sclerosis</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[M. Kipp, A. Norkus, B. Krauspe, T. Clarner, K. Berger, P. van der Valk, S. Amor, C. Beyer]</subfield>
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   <subfield code="a">Objective and design: It has been demonstrated that changes in the normal-appearing white matter (NAWM) in multiple sclerosis precede the appearance of classical lesions. The understanding of NAWM biology in an established disease model might help to clarify why some of them progress to active demyelinating lesions. Material or subjects: C57BL6 male mice (19-21g) were used in this study. Treatment: Demyelination was induced by feeding mice a diet containing 0.2% cuprizone for up to 5weeks. Methods: Routine stainings (luxol fast blue, and hematoxylin and eosin) and immunohistochemistry were performed to assess myelin status and the inflammatory infiltrate. Results: We demonstrated that, in the toxic demyelination cuprizone model, the corpus callosum is severely demyelinated after a 5-week cuprizone challenge (acute demyelination) whereas the fimbria of the hippocampus appear normal in routine myelin stainings. Microgliosis but not astrogliosis is evident after acute demyelination in the fimbria. Interestingly, both regions, the fimbria and the corpus callosum, demonstrated early oligodendrocyte apoptosis as well as intense microglia accumulation and activation. However, only the corpus callosum progresses to actively demyelination lesions whereas the fimbria does not. Conclusions: The applied model appears suitable for elucidating pathways which promote progression of affected tissue to an active lesion.</subfield>
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   <subfield code="a">The Author(s), 2011</subfield>
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   <subfield code="D">M.</subfield>
   <subfield code="u">Institute of Neuroanatomy, Faculty of Medicine, RWTH Aachen University, Wendlingweg 2, 52074, Aachen, Germany</subfield>
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