The Experimental autoimmune encephalomyelitis (EAE) Mouse Model
Investigate neuroinflammation and CNS autoimmunity with translational relevance to multiple sclerosis.
Our EAE models are well-established platforms for investigating immune-mediated damage in the central nervous system (CNS). These models simulate multiple sclerosis (MS) using two distinct induction methods: proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG). Both variants reproduce key pathological features of MS, including demyelination, paralysis, and neuroinflammation.
A Model That Mirrors Human Autoimmune Demyelination
EAE models (both PLP- and MOG-induced) are the gold standard for mechanistically understanding autoimmune-generated CNS damage and testing new potential multiple sclerosis (MS) treatments in an animal model. Our EAE mouse model platform allows researchers to assess distinct disease mechanisms, including T-cell– and B-cell–driven pathology, across well-defined timelines and reproducible disease courses.
Both EAE models follow a standard 3-week study duration, providing efficient timelines for screening or in-depth mechanistic studies. While the platform is ideal for assessing immune-mediated pathways and therapeutic response, Melior also offers a cuprizone model of MS for studies specifically focused on demyelination and remyelination.
With extensive expertise in neuroinflammation and in vivo immunology, Melior helps you generate the translational data needed to move confidently toward clinical development.
Advantages of the PLP and MOG-induced EAE Models
The PLP model is best suited for evaluating test compounds in a remitting or fluctuating form of multiple sclerosis, while the MOG model is ideal for studying chronic inflammation or testing therapies targeting adaptive immune mechanisms.
PLP-Induced EAE Model | MOG-Induced EAE Model |
---|---|
Model relapsing-remitting disease using a clinically mild profile that includes clear relapse and remission phases. | Customize immune targeting by selecting MOG35–55 for T-cell–driven inflammation or MOG1–125 for B-cell–mediated disease. |
Replicate immune fluctuations with PLP139–151 induction in SJL mice, a well-established system for relapsing MS. | Simulate progressive MS with a chronic disease course suited for both preventative and therapeutic interventions. |
Evaluate remitting-stage treatments in a platform tailored to therapies that target immune modulation during disease variability. | Quantify motor deficits through Open Field testing to assess EAE-induced fatigue as a functional endpoint. |
Ready to get started or looking for a custom model?
We offer customizable EAE mouse model studies, with flexible protocols, endpoints, and treatment regimens tailored to your research goals.
MOG35-55-Induced EAE Model
Body weights. Body weights were taken daily beginning on Day 7 of the study. Beginning on Day 14, MOG35-55- treated mice were administered vehicle or 0.1 mg/kg FTY-720 once per day via PO route. Untreated mice showed a slight increase in body weight throughout the study. The FTY-720 and vehicle-treated mice showed body weight loss following the injection of MOG35-55/CFA. FTY-720-treated animals had a significant increase in body weight compared to vehicle-treated animals on Days 17-21 (p<0.05).
Average clinical scores over time. EAE mice were randomized into treatment groups (vehicle or 0.1 mg/kg FTY-720) according to clinical score on Day 7 of the study. Clinical scores were assessed daily beginning on Day 7 and ending on Day 21 using the following scale:
0- No clinical signs; normal
1- Limp tail or hind limb weakness, but not both
2- Limp tail AND hind limb weakness
3- Partial hind limb paralysis, affecting one limb
4- Complete hind limb paralysis, affecting both limbs
5- Moribund
Beginning on Day 14, MOG35-55- treated mice were administered vehicle or 0.1 mg/kg FTY-720 once per day via PO route. The FTY-720-treated mice showed a decrease in impairment following drug administration compared to the vehicle-treated mice, which became statistically significant on Day 21 (*p<0.05).
PLP139-151-Induced EAE Model
Body weights.The untreated mice showed an increase in body weight throughout the study. The FTY-720 and vehicle treated mice displayed a decrease in body weights following injection of PLP139-151/CFA, which was maintained throughout the study.
Average clinical scores over time. Clinical scores were assessed daily beginning on Day 7 and ending on Day 21. Based on the clinical score system, vehicle-treated mice showed a progressive increase in impairment severity throughout the study. Mice treated with 0.1 mg/kg FTY-720 displayed a reduction in clinical score following drug administration that became statistically significant compared to vehicle on Days 17–21. Data are mean ± SEM; *p < 0.05, **p < 0.01 compared to vehicle.
Clinical scoring was performed using the following scale:
0 – No clinical signs; normal activity
1 – Limp tail or hind limb weakness, but not both
2 – Limp tail and hind limb weakness
3 – Partial hind limb paralysis
4 – Complete hind limb paralysis
5 – Moribund or death due to EAE
Did you know fatigue can be functionally measured in EAE mice?
One of the most common symptoms of MS, fatigue, can be assessed in vivo using Open Field testing within Melior’s MOG-induced EAE model.
Related Services and Solutions
Target Demyelination with the Cuprizone Model
Our cuprizone model is ideal for investigating demyelination and remyelination in MS and for complimenting EAE mouse model studies focused on immune mechanisms.
Study Chronic Disease Progression with Aging Models
Melior’s aging mouse models support research into inflammation, neurodegeneration, metabolism, and other age-associated conditions using naturally aged animals.
Uncover New Indications with theraTRACE®
Melior’s theraTRACE® platform screens compounds across 40+ models, helping identify unexpected efficacy signals and multi-indication potential.
Publications
Nuesslein-Hildesheim B, Ferrero E, Schmid C, Huck C, Smith P, Tisserand S, Rubert J, Bornancin F, Eichlisberger D, Cenni B. Remibrutinib (LOU064) inhibits neuroinflammation driven by B cells and myeloid cells in preclinical models of multiple sclerosis. J Neuroinflammation. 2023 Aug 26;20(1):194. doi: 10.1186/s12974-023-02877-9.
Schrader TO, Xiong Y, Lorenzana AO, Broadhead A, Stebbins KJ, Poon MM, Baccei C, Lorrain DS. Discovery of PIPE-359, a Brain-Penetrant, Selective M1 Receptor Antagonist with Robust Efficacy in Murine MOG-EAE. ACS Med Chem Lett. 2020 Dec 24;12(1):155-161. doi: 10.1021/acsmedchemlett.0c00626.
Weiss L, Or R, Jones RC, Amunugama R, JeBailey L, Ramu S, Bernstein SA, Yekhtin Z, Almogi-Hazan O, Shainer R, Reibstein I, Vortmeyer AO, Paidas MJ, Zeira M, Slavin S, Barnea ER. Preimplantation factor (PIF*) reverses neuroinflammation while promoting neural repair in EAE model. J Neurol Sci. 2012 Jan 15;312(1-2):146-57. doi: 10.1016/j.jns.2011.07.050.
Frequently Asked Questions
Yes. The MOG-induced EAE model is especially well-suited for both preventative and therapeutic treatment regimens. Our study designs can be customized to match your dosing strategy and disease stage of interest.
Standard readouts include clinical scoring and histological analysis. Melior also offers functional assessments such as locomotor activity (e.g., Open Field testing) to quantify fatigue and motor deficits.
The PLP model is better suited for studying relapsing-remitting MS with a milder clinical course, while the MOG model is ideal for chronic or progressive disease and offers greater flexibility for targeting T-cell or B-cell mechanisms.