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Open AccessArticle

Laquinimod Supports Remyelination in Non-Supportive Environments

Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany
Institute of Neuroanatomy and JARA-BRAIN, Faculty of Medicine, RWTH Aachen University, 52074 Aachen, Germany
Department of Anatomy II, Ludwig-Maximilians-University of Munich, 80336 Munich, Germany
AyalaPharma, VP Research & Nonclinical Development, Rehovot 7670104, Israel
Centre for Transdisciplinary Neurosciences, Rostock University Medical Center, 18057 Rostock, Germany
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Sassan Hafizi
Cells 2019, 8(11), 1363;
Received: 10 October 2019 / Revised: 21 October 2019 / Accepted: 22 October 2019 / Published: 31 October 2019
(This article belongs to the Special Issue Oligodendrocyte Physiology and Pathology Function)
Inflammatory demyelination, which is a characteristic of multiple sclerosis lesions, leads to acute functional deficits and, in the long term, to progressive axonal degeneration. While remyelination is believed to protect axons, the endogenous-regenerative processes are often incomplete or even completely fail in many multiple sclerosis patients. Although it is currently unknown why remyelination fails, recurrent demyelination of previously demyelinated white matter areas is one contributing factor. In this study, we investigated whether laquinimod, which has demonstrated protective effects in active multiple sclerosis patients, protects against recurrent demyelination. To address this, male mice were intoxicated with cuprizone for up to eight weeks and treated with either a vehicle solution or laquinimod at the beginning of week 5, where remyelination was ongoing. The brains were harvested and analyzed by immunohistochemistry. At the time-point of laquinimod treatment initiation, oligodendrocyte progenitor cells proliferated and maturated despite ongoing demyelination activity. In the following weeks, myelination recovered in the laquinimod- but not vehicle-treated mice, despite continued cuprizone intoxication. Myelin recovery was paralleled by less severe microgliosis and acute axonal injury. In this study, we were able to demonstrate that laquinimod, which has previously been shown to protect against cuprizone-induced oligodendrocyte degeneration, exerts protective effects during oligodendrocyte progenitor differentiation as well. By this mechanism, laquinimod allows remyelination in non-supportive environments. These results should encourage further clinical studies in progressive multiple sclerosis patients. View Full-Text
Keywords: multiple sclerosis; remyelination; cuprizone; neurodegeneration; laquinimod multiple sclerosis; remyelination; cuprizone; neurodegeneration; laquinimod
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Nyamoya, S.; Steinle, J.; Chrzanowski, U.; Kaye, J.; Schmitz, C.; Beyer, C.; Kipp, M. Laquinimod Supports Remyelination in Non-Supportive Environments. Cells 2019, 8, 1363.

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