Multiple Sclerosis Models
Experimental autoimmune encephalomyelitis (EAE) multiple sclerosis models are standard models for brain inflammation and demyelination studies. EAE MS models are induced via injection of myelin oligodendrocyte glycoprotein (MOG) or proteolipid protein (PLP). Validated for rats and mice, our EAE multiple sclerosis models allow you to effectively evaluate novel MS therapies that target the inflammatory response:
- MOG35-55 EAE in C57BL/6 mice
- Spinal cord homogenate (SCH) EAE in rats
- MOG1-125 EAE in Dark Agouti rats
We’ve validated our MS mouse models with positive control compounds and drugs, including dexamethasone, glatiramer acetate, and fingolimod. These EAE mouse models are used in concert with a collection of assays that allow you to both monitor disease progression and therapeutic response. The assays include:
- Spinal cord and brain pathology monitored via histological techniques and ELISA assays
- SPECT/CT monitoring of inflammation in the brain and spinal cord
- Flow cytometry-based immunophenotyping of peripheral and central nervous system tissues
- NanoString Autoimmunity Gene Expression Profiling Panel
Studies using large animal EAE models include MRI analysis and pathological assessment of lesions.
Demyelination Multiple Sclerosis Models
Our cuprizone- and lysolecithin-induced rodent models are well suited for the study of the independent mechanisms of demyelination. The cuprizone model uses a validated study design where demyelination is induced followed by a recovery period of remyelination. During the study, motor performance using rotarod tests or fine motor kinematic analysis, anxiety, and cognition are measured at specific intervals along with confirmation histology and IHC studies.
Frequently Asked Questions (FAQs) about Multiple Sclerosis Models
Is the EAE model the best model for multiple sclerosis studies?
Several MS models exist, but by far the best understood and most commonly used is the rodent model of EAE. EAE mouse models are more frequently used because of the inbred genotype of laboratory mice, their rapid breeding capacity, the ease of genetic manipulation and the accessibility of transgenic and knockout mice to facilitate mechanistic studies.
What are some of the parameters that change in the cuprizone Multiple Sclerosis model?
Along with cognitive disturbance, the following parameters have been observed in cuprizone-induced MS models:
- Increased neuroinflammation measured by SPECT imaging of TSPO, a translocated protein
- Decreased 18F-deoxyglucose consumption by PET imaging after longer exposures to cuprizone
- Decreased immunostaining of myelin basic protein (MBP) in the brain
- Mild neurological consequences, but alterations in the open field-testing results
- Changes in specific parameters of fine motor kinematic analysis suggesting gait changes
Do sensory deficits, such as visual impairment, contribute to reduced touchscreen performance versus a true cognitive deficit in cuprizone-induced mice?
Touchscreen testing does rely on visual abilities. However, most cuprizone-induced MS models showed very specific stimulus-oriented behavior and interacted with the stimulus by the end of the touchscreen testing training, excluding the possibility that the cognitive changes were not because the mice were blind. While we cannot exclude the possibility that the vision in cuprizone-induced mice was impaired, visual impairment alone does not sufficiently explain the findings.