Experimental Autoimmune Encephalomyelitis (EAE)

Summary: EAE models aspects of autoimmunity, inflammation, demyelination, cell trafficking and tolerance induction seen in Multiple Sclerosis.

Model Description

Experimental autoimmune encephalomyelitis (EAE) is the most commonly used model for the preclinical development of drug candidates for treatment of optic neuritis and 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 speciesMice (C57BL/6)
Method of induction– MOG35-55/mL emulsion
– Killed mycobacterium tuberculosis H37Ra/mL emulsion
– Pertussis toxin (PTX)
Follow-up periodUp to 28 days
Route of compound administrationTopical, systemic, intravitreal, intravenous (infusion)
Read-outsStandard 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)

Outcomes and Read-Outs 

Scoring of behavioral phenotype

Fig. 1. Systemic scoring of the behavioral phenotype of mice that received either 50 ng dose of PTX or 60 ng dose of PTX.
Figure 1. Systemic scoring of the behavioral phenotype of mice that received either 50 ng dose of PTX or 60 ng dose of PTX. Data are expressed as mean. Phenotypic progression of EAE is monitored daily.

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