Search the webpage

Category: Inflammation
Animals used for research:  Mouse 

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 demyeination of the optic nerve.


Animal species

Mouse (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)

  • Standard readouts: 
    • Behavioral analysis and scoring
    • Infiltration of cervical spinal cord
    • Assessment of demyelination
  • Optional: 
    • 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)
Please contact us, if you would like to receive more information:


Phenotypic progression of EAE is monitored daily

Systemic scoring of the behavioural phenotype of mice that received either 50 ng dose of PTX or 60 ng dose of PTX. Data are expressed as mean.


  • Gran,B., Zhang, G.-X., Yu, S., Li, J., Chen, X.H., Ventura, E.S., Kamoun, M., and Rostami, A. (2002). IL-12p35-deficient mice are susceptible to experimental autoimmune encephalomyelitis: evidence for redundancy in the IL-12 system in the induction of central nervous system autoimmune demyelination. J. Immunol. 169, 7104–7110.


  • Lo, A.C., Saab C.Y., Black J.A., Waxman S.G. (2003). Phenytoin protects spinal cord axons and preserves axonal conduction and neurological function in a model of neuroinflammation in vivo. J Neurophysiol. 90(5):3566-71.