Comparative evaluation of EAE variants

Given the complexity of MS and its unclear aetiology, unsurprisingly, no animal model recapitulating the clinical features together with the pathophysiology of MS has been successfully developed to date. Currently, EAE generated by autoimmune-mediated demyelination, is the most widely accepted model. However, EAE itself is a complex disease which is not completely understood. Similarly to MS, it can follow multiple clinical courses and in a number of these variants, clinical profiles apparently mimicking those of MS subtypes, are actually associated with major deviations from MS in terms of hallmarks of pathology. Therefore each variant only reflects certain specific facets of MS.

In view of current developments in large-scale gene expression and protein profiling technology, as well as in drug design, it is important to continue to identify areas of coincidence in disease mechanisms between EAE variants and MS, so that the full capabilities provided by these technologies can be exploited with the aims of further elucidating molecular pathways underlying MS and generating more refined drugs.

Our lab has mapped the spatio-temporal evolution of disease, clinically and pathologically in 4 EAE variants, namely: (a) the NOD/Lt mouse strain induced with peptide 35-55 of myelin oligodendrocyte glycoprotein (MOG35-55), (b) the C57Bl/6 mouse strain induced with MOG35-55, (c) the BALB/c mouse strain induced with peptide 180-199 of proteolipid protein (PLP180-199) and (d) SJL/J mouse strain induced with peptide 139-151 of proteolipid protein (PLP139-151).