experimental autoimmune encephalomyeltis (EAE)

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MOG-induced EAE preclinical disease model

Using the MOG (myelin oligodendrocyte glycoprotein) to induce disaese results in an encephalitogenic T-cell response and a demyelinating auto-antibody response. MOG 35-55 peptide together with pertussis toxin (PT) will result in a chronic-progressive form of EAE in the C57BL/6. In addition to paralysis, this model is characterized with deyelination both of the spinal cord and the brain.

MOG-induced EAE preclinical contract research model*
Length 35 days
Induction MOG 35-55 peptide plus PT. Onset of disease occurs between days 10-12
Positive Control Dexamethasone
Assessments clinical sign/score, body weight,
Additional Options Rotarod, histopathology, demyelination analysis, Immunohistochemistry, cytokine analysis, gene expression

*Models can be customized to sponsors criteria. Contact a scientist.

Figures: Correlation between rotarod (used to evaluate cognitive function) and clinical scores in MOG-induced EAE. RPM = rotations/minute.

Rotarod for evaluating cognitive functionMOG-EAE clinical score