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Oligodendrocyte and Myelin Pathophysiology in Multiple Sclerosis

Eneritz López-Muguruza1,2, Carla Peiró-Moreno1,2, Asier Ruiz3

  • 1Department of Neurosciences, University of the Basque Country UPV/EHU, IIS-BioBizkaia and CIBERNED, Leioa, Spain.

Advances in Neurobiology
|June 11, 2025
PubMed

Insights

Multiple sclerosis (MS) is a progressive neurodegenerative disease targeting the central nervous system (CNS). Understanding oligodendrocyte and myelin damage is key to developing therapies for tissue repair and halting MS progression.

Area of Science:

  • Neuroimmunology
  • Neurodegeneration
  • Central Nervous System Pathology

Background:

  • Multiple sclerosis (MS) is a chronic, autoimmune, and progressive neurodegenerative disease affecting the central nervous system (CNS).
  • MS pathology primarily targets myelin and oligodendrocytes, but also involves other glial cells and neurons.
  • Inflammation, initiated peripherally, spreads throughout the CNS, activating astrocytes and microglia.

Purpose of the Study:

  • To emphasize pathophysiological changes in oligodendrocytes and myelin due to the inflammatory cascade in MS.
  • To explore mechanisms of oligodendrocyte and myelin damage beyond immune attack for CNS protection.
  • To summarize experimental developments, clinical therapies, and trials for MS tissue repair and halting disease progression.

Main Methods:

  • Review of current literature on MS pathophysiology.
  • Analysis of inflammatory cascade mechanisms impacting CNS.
  • Examination of oligodendrocyte repopulation and remyelination strategies.

Main Results:

  • Inflammation drives oligodendrocyte and myelin damage in MS.
  • Understanding the axon-myelin unit is crucial for preventing axonal degeneration.
  • Oligodendrocyte repopulation and remyelination offer therapeutic potential.

Conclusions:

  • Targeting oligodendrocyte and myelin pathology is essential for MS treatment.
  • Preventing axonal degeneration is critical for managing MS symptoms and CNS atrophy.
  • Further research into remyelination strategies holds promise for halting MS progression.
Keywords:
Autoimmune diseaseMultiple sclerosisNeurodegenerationOligodendroglia

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