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BCAS1 identifies active cortical remyelination in early and late stage multiple sclerosis
Author(s): ,
F. van der Meer
Affiliations:
Neuropathology, University Medical Center Göttingen, Göttingen
,
C. Sergiou
Affiliations:
Neuropathology, University Medical Center Göttingen, Göttingen
,
C. Wrzos
Affiliations:
Neuropathology, University Medical Center Göttingen, Göttingen
,
A. Winkler
Affiliations:
Neuropathology, University Medical Center Göttingen, Göttingen
,
S. Nessler
Affiliations:
Neuropathology, University Medical Center Göttingen, Göttingen
,
M. Simons
Affiliations:
Technical University of Munich, Munich, Germany
C. Stadelmann
Affiliations:
Neuropathology, University Medical Center Göttingen, Göttingen
ECTRIMS Online Library. van der Meer F. Oct 12, 2018; 228121; P1743
Franziska van der Meer
Franziska van der Meer
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Abstract: P1743

Type: Poster Sessions

Abstract Category: N/A

Background: In multiple sclerosis (MS), remyelination of cortical demyelinated lesions has been shown to be more efficient than remyelination of white matter plaques. However, remyelination in the cortex is difficult to detect immunohistochemically, and it is still not clear when cortical remyelination is most efficient.
Methods: In the present work we utilized a recently characterized protein, breast cancer-associated sequence 1 (BCAS1), that identifies actively myelinating oligodendrocytes during development and in disease. We specifically focused on cortical demyelination in early as well as late-stage MS and analyzed biopsy and autopsy tissue, respectively. We performed multi-fluorescent immunolabellings with antibodies against BCAS1 and myelin proteins. In addition, we assessed the time course of BCAS1-positive cell densities in a recently developed mouse model, where cytokine injection leads to robust focal cortical demyelination.
Results: We identified numerous BCAS1-positive oligodendrocytes in cortical demyelinating lesions of patients early in the disease course, and the density of BCAS1-positive cells in these patients exceeded that in late stage disease. Determining the fraction of BCAS1-positive cells with a myelinating morphology enabled a clear distinction of remyelination from incomplete cortical demyelination. In areas with cortical remyelination, BCAS1-positive myelinating cells in part expressed MAG, but not MBP or PLP. After experimental cortical demyelination, BCAS1-positive oligodendrocytes reached their highest values 5 days after injection and then decreased 10 and 20 days thereafter, reflecting the course of remyelination.
Conclusion: Our results highlight the cortex as a prime site of lesion formation and repair in MS and demonstrate BCAS1 as a highly useful cellular marker protein to identify active, ongoing cortical remyelination.
Disclosure:
Franziska van der Meer: nothing to disclose Christina Sergiou: nothing to disclose
Claudia Wrzos: nothing to disclose
Anne Winkler: nothing to disclose
Stefan Nessler: received research support from TEVA
Mikael Simons: nothing to disclose
Christine Stadelmann: She received honoraria for speaking and travel reimbursement from Novartis Pharma GmbH, Merck, Teva Pharmaceutical Industries Ltd., Biogen, and Bayer Health Care. She served on scientific advisory boards of Novartis, Merck, Roche, and Teva. She received research support from Teva. She is a member of the editoral board of Neurology: Neuroimmunology & Neuroinflammation.

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