Characterization of Rab32 and HMGB1 involved in the disease course of Experimental Autoimmune Encephalomyelitis, An animal model of Multiple Sclerosis.

Abstract

Multiple Sclerosis (MS) is the most common chronic inflammatory, neurodegenerative and demyelinating disease of the central nervous system among young adults which leads to permanent neurological damage. Despite the rapid advancement of experimental and clinical research into MS, the exact molecular mechanism behind the disease progression remains elusive. Currently, available MS medications will only slow down the disease's progression and do not function for all patients therefore, more successful therapies are needed. One of the most well-studied and well-established models to investigate neuroinflammatory pathways involved in MS is Experimental Autoimmune Encephalomyelitis (EAE). EAE can be induced in different animal models but mice are the most widely used species for this model. High Mobility box 1 group (HMGB1) has emerged as a possible candidate because of its role in EAE/MS pathogenesis. The objective of this study was to determine whether HMGB1 can be a therapeutic target for EAE. To achieve this objective, we created an Animal model of MS by administrating the MOG35-55 peptide. This study will allow a wide range of possible therapeutic interventions to be developed and preclinically tested.