Summary: EAE models aspects of autoimmunity, inflammation, demyelination, cell trafficking and tolerance induction seen in Multiple Sclerosis.
Experimental autoimmune encephalomyelitis (EAE) is the most commonly used model for the preclinical development of drug candidates for treatment of multiple sclerosis (MS).
As the EAE model models aspects of autoimmunity, inflammation, demyelination, cell trafficking and tolerance induction seen in MS, it provides a versatile tool for a broad array of drug candidates.
The model is characterized by paralysis, CNS inflammation and demyelination. We are using MOG35-55 antigen to induce a phenotype reminiscent of MS with a well-defined onset of development of EAE and EAE severity. In addition, the EAE model mimics aspects of optic neuritis and demyelination of the optic nerve.
|Animal species||Mice (C57BL/6)|
|Method of induction||– MOG35-55/mL emulsion|
– Killed mycobacterium tuberculosis H37Ra/mL emulsion
– Pertussis toxin (PTX)
|Follow-up period||Up to 28 days|
|Route of compound administration||Topical, systemic, intravitreal, intravenous (infusion)|
– Behavioral analysis and scoring
– Infiltration of cervical spinal cord
– Assessment of demyelination
– Assessment of functional vision by electroretinogram and visually-evoked potentials
– Infiltration of optic nerve and assessment of demyelination
– Unbiased estimation of the total number of retinal ganglion cells (stereology)
Outcomes and Read-Outs
Scoring of behavioral phenotype
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