Other EAE models include proteolipid protein inoculation in mice, which similarly induces a relapsing-remitting disease course. Infection of susceptible mouse strains with Theiler’s murine encephalomyelitis virus represents a well-established infectious animal model of MS. Inoculation of susceptible mice with low virulent strains of TMEV is Sipeimine followed by a characteristic biphasic disease course with an initial transitory polioencephalitis with predominant manifestation within the first week post infection, followed by a chronic progressive demyelinating leukomyelitis. Depending on the experimental setup and used assay, demyelination starts between two and six weeks after the infection, and reaches a plateau approximately three to five months after the infection. In addition, certain genetic modifications have shown to be associated with central nervous system demyelination and are used as another model system. As such, tumor necrosis factor -overexpressing mice develop a chronic progressive inflammatory demyelinating disease with Chlorhexidine hydrochloride oligodendrocyte apoptosis and microglial activation in the early stages, followed by demyelination and secondary axonal damage in late stages. Furthermore, a diversity of toxic models such as local ethidium bromide injection or systemic cuprizone feeding have been used to study demyelination and remyelination. The aims of the present study were 1.) to re-analyze publically available microarray data sets of MS and its animal models employing a consistent methodology, 2.) to compare the results across species, experimental models and platforms in order to detect highly conserved pathways that offer the broadest therapeutic potential, and 3.) to explore, if the transcriptional changes in the different animal models reflect the anticipated difference in the pathomechanisms. This study provides data of chronic-active MS plaques, chronic MS plaques, and control tissues of healthy individuals. Chronic active plaques were defined as chronic demyelinated lesions with sharply defined margins and recent areas of inflammatory demyelination at the edges. In contrast, chronic plaques showed demyelination with well demarcated borders and abundant astrogliosis, but lacked inflammatory cell infiltration. As only this single MS study matched the inclusion criteria, we lowered the criteria for MS in order to broaden the data base. Therefore, we re-screened the literature for MS microarray studies that fulfill the aforementioned inclusion criteria 1�C3, and at least provide a complete list of all differentially expressed genes with fold changes and pvalues. Two additional studies of MS matched these lowered criteria. Both studies provide complete lists of DEGs from patients diagnosed with secondary progressive MS in comparison to healthy controls. Here, one study investigated both active and chronic active lesions, while the other study focused on active MS lesions. In both studies, active lesions were defined as lesions with active demyelination as well as inflammatory infiltrates. Regarding the animal models, the original inclusion criteria were fulfilled by a study investigating three phases in MOG-induced EAE in Dark Agouti rats. In this study, female Dark Agouti rats were immunized with recombinant MOG, emulsified in complete Freund’s adjuvant. The acute phase of EAE was defined as the first EAE attack with clinical signs such as hind limb paralysis, whereas the recovery phase was defined as the first day at which the rats began to gain weight again. The relapsing phase presented as a second worsening of the clinical signs.