Some key differences between EAE in mice, and MS in humans include:

B-cells: Some research points to anti-CD20 B-cells being the basis of the autoimmune attacks. This has been shown to be completely different in EAE and MS.
oxidative injury: Mitochondrial injury is seen in EAE and MS, but mitochondrial gene deletions have so far only been detected in MS lesions. microglia behaviour: In contrast to experimental models of inflammatory demyelination, lesion formation in multiple sclerosis occurs on a background of pro-inflammatory microglia activation, which is seen already in the normal white matter of age-matched controls, and this may contribute to neurodegeneration in the disease. pathological patterns: EAE is unable to reproduce MS pathological patterns III and IV. Secondary damage
Given that some conditions as MS show cortical damage together with the WM damage, there has been interest if this can appear as a secondary damage of the WM. Human Anti-MOG in mice
Anti-MOG associated encephalomyelitis can be passed from humans to mice, inducing MS type II demyelination (pattern II)

Immunogenetic interactions
Deficiency of TBX21 or STAT4 provides resistance against EAE, while interferon-γ-, interferon-γ-receptor-, interleukin-12 subunit α-, interleukin 12 receptor, β 2 subunit-, and interleukin 18-deficiency exacerbated disease. In humans
Sometimes the human equivalent to EAE has been triggered in humans by accident or medical mistake. The reactions have been diverse according to the sources of the disease The researchers in the last report have termed the condition "human autoimmune encephalitis" (HAE).
Thanks to these pattern III models some specific experimental treatments have appearedThe model for primary progressive MS is the Theilers virus model. This model presents features not available in others, like microglial activation. Alternatives
Recently it has been found that CSF from MS patients can carry the disease to rodents, opening the door to an alternative model. References
External links

Mult-sclerosis.org: information on EAE