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Inflammatory microglia correlate with impaired oligodendrocyte maturation in multiple sclerosis
J Q Alida Chen1, Dennis D Wever1, Niamh B McNamara1
1Neuroimmunology Research Group, Netherlands Institute for Neuroscience, Amsterdam, Netherlands.
Frontiers in Immunology
|January 29, 2025
Summary
Inflammatory microglia (iNOS+) correlate with early-stage oligodendrocyte deficits, hindering myelin repair in multiple sclerosis (MS). This suggests inflammatory responses impair remyelination in MS patients.
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Remyelination is a natural repair process in multiple sclerosis (MS) but is often inefficient.
- The mechanisms driving variable remyelination efficacy in MS are poorly understood.
- Microglia activation is implicated in MS pathology and repair processes.
Purpose of the Study:
- To investigate the relationship between microglia activation states and remyelination activity in MS lesions.
- To compare cellular and molecular markers of remyelination in efficiently remyelinating donors (ERDs) versus poorly remyelinating donors (PRDs).
Main Methods:
- Correlated CD163+ (regenerative) and iNOS+ (inflammatory) microglia with BCAS1+ oligodendrocytes in MS brain donors.
- Subdivided oligodendrocytes into early-stage (<3 processes) and late-stage (≥3 processes).
- Analyzed lesions from ERDs (n=25) and PRDs (n=17) based on remyelinated lesion proportions.
Main Results:
- No differences in CD163+ microglia between MS lesions or donor groups.
- Increased iNOS+ microglia in remyelinated lesions of PRDs compared to ERDs.
- More early-stage BCAS1+ oligodendrocytes found in PRDs, correlating positively with iNOS+ microglia.
Conclusions:
- Impaired maturation of early-stage BCAS1+ oligodendrocytes in the presence of inflammatory microglia may contribute to remyelination deficits in MS.
- Inflammatory microglia may hinder successful lesion repair and endogenous myelin regeneration in MS.
- Understanding these interactions is crucial for developing strategies to enhance remyelination in MS.
