“…These problems are, in part, due to the lack of diversity in EAE models using inbred strains of mice, various misconceptions about our understanding of the pathophysiology of EAE from knockout mice, the relatively small numbers of animals used in EAE test systems, and the short time interval for testing even 'chronic' therapies in EAE, in which experiments might need to run for years, not weeks or months, to model chronic human therapy. Despite its pitfalls, EAE has been a useful model for predicting success with clinical trials in multiple sclerosis (MS).Currently, there are several approved therapies for MS, including glatiramer acetate [1-8], mitoxantrone [9-11], various b interferons (IFNs) [12,13] and natalizumab [14][15][16][17], which has been withdrawn currently from the market by its manufacturers. Glatiramer acetate is one of the hallmarks of current therapy and was developed based on its ability to modulate EAE [1][2][3][4][5][6][7][8].…”