Remyelination by surviving oligodendrocytes is inefficient in the inflamed mammalian cortex.

Autor:	Mezydlo A; Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany., Treiber N; Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany., Ullrich Gavilanes EM; Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany., Eichenseer K; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; Hertie Institute for Clinical Brain Research, Tübingen, Germany., Ancău M; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany., Wens A; Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany., Ares Carral C; Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany., Schifferer M; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany., Snaidero N; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; Hertie Institute for Clinical Brain Research, Tübingen, Germany., Misgeld T; Institute of Neuronal Cell Biology, Technical University of Munich, Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Electronic address: thomas.misgeld@tum.de., Kerschensteiner M; Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians Universität München, Munich, Germany; Biomedical Center (BMC), Faculty of Medicine, Ludwig-Maximilians Universität München, Martinsried, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Electronic address: martin.kerschensteiner@med.uni-muenchen.de.
Jazyk:	angličtina
Zdroj:	Neuron [Neuron] 2023 Jun 07; Vol. 111 (11), pp. 1748-1759.e8. Date of Electronic Publication: 2023 Apr 17.
DOI:	10.1016/j.neuron.2023.03.031
Abstrakt:	In multiple sclerosis, an inflammatory attack results in myelin loss, which can be partially reversed by remyelination. Recent studies suggest that mature oligodendrocytes could contribute to remyelination by generating new myelin. Here, we show that in a mouse model of cortical multiple sclerosis pathology, surviving oligodendrocytes can indeed extend new proximal processes but rarely generate new myelin internodes. Furthermore, drugs that boost myelin recovery by targeting oligodendrocyte precursor cells did not enhance this alternate mode of myelin regeneration. These data indicate that the contribution of surviving oligodendrocytes to myelin recovery in the inflamed mammalian CNS is minor and inhibited by distinct remyelination brakes. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2023 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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