Remyelination by surviving oligodendrocytes is inefficient in the inflamed mammalian cortex

Aleksandra Mezydlo, Nils Treiber, Emily Melisa Ullrich Gavilanes, Katharina Eichenseer, Mihai Ancău, Adinda Wens, Carla Ares Carral, Martina Schifferer, Nicolas Snaidero, Thomas Misgeld, Martin Kerschensteiner

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)1748-1759.e8
JournalNeuron
Volume111
Issue number11
DOIs
StatePublished - 7 Jun 2023
Externally publishedYes

Keywords

  • CLEM
  • demyelination
  • in vivo microscopy
  • multiple sclerosis
  • myelin
  • oligodendrocyte precursor cell
  • oligodendrocytes
  • remyelination

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