Lara-Maria Preuth - Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany
Susann Eichler - Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany
Niklas Huntemann - Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany
Anna Vogelsang - Department of Neurology with Institute of Translational Neurology, University of Muenster, Muenster, Germany

Patients suffering from multiple sclerosis (MS) have an augmented risk for cardiovascular diseases associated with abnormal platelet functions. However, platelet-mediated contributions to inflammatory disorders of the central nervous system (CNS), such asexperimental autoimmune encephalomyelitis (EAE), a model to study MS, remain poorly understood.In EAE, platelets were found accumulating in the CNS parenchyma, thereby amplifying the (neuro) inflammatory response. Materials and Methods: Here, we show that pharmacologic blockade of platelet-receptor P2Y12 with elinogrel renders mice less susceptible to EAE. Results: While disease onset was unaltered, elinogrel treatment was associated with a reduced (p<0.03) disease maximum and also with reduced prevalence of inflammatory infiltrates compared to the control group (5,1 ± 1,4% versus 9,6 ± 1,2%, n=6, p<0.05). Amelioration was ccompanied by reduced numbers of interleukin-17A-producing T-helper cells as determined via intracellular cytokine staining atthe disease peak (day 15). Further, an increase in CD8+ and CD8+CD11c+ cells, but no significant difference in macrophages, microglia, B-cells and plasmatic dendritic cells of elinogrel-treated mice was found. Conclusion: Overall, our findings show that inhibition of platelet activation is beneficial in an animal model of MS and thus indicate in addition to the classical immunological-orien ted pathophysiological concepts analternative strategy for the treatment of MS.