Fibrinolytic activity of plaques and white matter in multiple sclerosis

Insights

Multiple sclerosis (MS) plaques show increased fibrinolysis around blood vessels. This fibrinolytic activity, linked to vascular endothelium, may contribute to MS plaque development, not macrophages.

Area of Science:

  • Neuroimmunology
  • Vascular Biology
  • Demyelinating Diseases

Background:

  • Plasminogen activator from macrophages is a suspected mediator of demyelination in experimental allergic encephalomyelitis and multiple sclerosis (MS).
  • Investigating fibrinolysis in MS is crucial for understanding disease pathogenesis.

Purpose of the Study:

  • To investigate the fibrinolytic activity in white matter and MS plaques.
  • To determine the cellular and tissue localization of fibrinolysis in MS lesions.
  • To explore the potential role of fibrinolytic enzymes in the genesis of MS plaques.

Main Methods:

  • Histochemical techniques were used to assess fibrin clot breakdown capacity.
  • Fibrinolytic activity was localized in white matter and plaques from MS patients and controls.
  • Correlation with disease activity, plaque age, lymphocytic infiltrates, gliosis, and macrophages was examined.

Main Results:

  • Fibrinolytic activity was localized exclusively around blood vessels and capillaries in both MS patients and controls.
  • MS plaques exhibited more numerous and intense foci of lysis compared to adjacent unaffected white matter.
  • No correlation was found between fibrinolysis and disease activity, plaque age, or the presence of inflammatory cells/macrophages.

Conclusions:

  • Fibrinolysis in MS lesions is primarily associated with blood vessels, suggesting a role for vascular endothelium rather than macrophages.
  • The increased fibrinolysis in MS plaques may contribute to their development, particularly in perivascular areas.
  • Further research is needed to fully elucidate the role of fibrinolytic enzymes in MS pathogenesis.

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