Multiple sclerosis: The resolving lesion revealed

Cedric S Raine1

  • 1Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, New York City, NY, USA; Department of Neurology, Albert Einstein College of Medicine, Bronx, New York City, NY, USA; Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York City, NY, USA.

Insights

This study describes resolving lesions in multiple sclerosis (MS), revealing foamy microglia/macrophages and later stages with remyelination. These findings suggest a role for anti-inflammatory M2 cells in MS repair.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system.
  • The pathology of resolving lesions in MS remains poorly understood.
  • Identifying reparative mechanisms in MS is crucial for developing effective therapies.

Purpose of the Study:

  • To characterize the cellular and histological features of resolving lesions in multiple sclerosis.
  • To investigate the potential role of microglia/macrophages in lesion resolution and repair.
  • To explore the presence and significance of alternatively-activated (M2) microglia/macrophages in MS lesions.

Main Methods:

  • Histological examination of brain tissue from MS patients.
  • Immunohistochemistry to identify cell types, including microglia/macrophages.
  • Assessment of myelin integrity and astrogliosis.

Main Results:

  • Early resolving lesions showed fibrous astrogliosis and abundant lipid-laden microglia/macrophages at plaque edges.
  • No ongoing myelin breakdown or remyelination was observed in early lesions.
  • Later resolving lesions exhibited macrophages alongside evidence of remyelination within the gliotic parenchyma.

Conclusions:

  • Resolving lesions in MS possess distinct histological characteristics.
  • The presence of M2 microglia/macrophages suggests a potential role in modulating inflammation and promoting repair.
  • These findings offer novel insights into endogenous repair mechanisms in multiple sclerosis.