Hemostasis Components as Therapeutic Targets in Autoimmune Demyelination

Several studies in both multiple sclerosis (MS) and experimental autoimmune encephalitis (EAE) have shed light on the vascular mechanisms contributing to MS pathogenesis. The dysregulation of the hemostatic pathways revealed to play a pivotal role. Here, we review the numerous findings providing evidence on the involvement of hemostasis components in MS pathogenesis to highlight why they might be considered potential therapeutic targets in the disease. A literature search for articles from January 1950 to September 2021 was conducted in PubMed and Scopus. A consistent body of evidence supports the pro-inflammatory activity of activated platelets in MS pathogenesis and the beneficial effect of aspirin administration on the EAE clinical course. Further, neuropathological findings in subjects with MS and experimental studies in EAE have revealed dysregulation of coagulation/fibrinolysis system in autoimmune demyelination. Fibrin deposition in the central nervous system and its interaction with the CD11b receptor on microglia cells seems to drive neuroinflammation and autoimmune demyelination. However, at present, few and controversial clinical data are available on the implementation of drugs targeting fibrin deposition in MS therapy. In conclusion, targeting platelet activation and receptors for fibrin(ogen) deserve further research to hopefully purpose new drugs in the pharmacologic paraphernalia of MS neurologists.