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A Perspective of Coagulation Dysfunction in Multiple Sclerosis and in Experimental Allergic Encephalomyelitis
Domenico Plantone1, Matilde Inglese2, Marco Salvetti3,4
1S.O.C. Neurologia, Ospedale San Biagio, Domodossola, Italy.
Frontiers in Neurology
|January 30, 2019
Summary
The coagulation pathway, involving fibrinogen and thrombin, plays a significant role in multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE). Targeting coagulation factors may offer new therapeutic strategies for MS.
Area of Science:
- Neuroimmunology
- Hematology
Background:
- Coagulation and vascular thrombosis are implicated in multiple sclerosis (MS) pathophysiology.
- Fibrinogen deposition correlates with clinical signs in experimental allergic encephalomyelitis (EAE), an MS model.
Purpose of the Study:
- To investigate the role of coagulation factors, including thrombin and fibrinogen, in MS and EAE.
- To explore the impact of platelets and anticoagulant agents on EAE.
Main Methods:
- Review of studies on fibrinogen leakage, thrombin effects on glial cells, heparin's efficacy, platelet depletion, and anticoagulant treatments in EAE.
- Analysis of microglia activation, astrocyte reactivity, and inflammatory mediator production.
Main Results:
- Fibrinogen leakage triggers microglial activation in early EAE and MS lesions.
- Thrombin at high concentrations induces reactive astrocytes and pro-inflammatory microglia.
- Heparin suppresses EAE, platelet depletion ameliorates EAE, and anticoagulants improve EAE outcomes.
Conclusions:
- The coagulation pathway is integral to MS pathophysiology.
- Coagulation factors represent potential therapeutic targets for MS, complementing current treatments.
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