Multiple Sclerosis MS models
Multiple sclerosis (MS) is a demyelinating disorder leading to physical and cognitive disability.
Cuprizone model (de- and remyelination)
The core neuropathology of multiple sclerosis is loss of oligodendrocytes and myelin sheats, leading to axonal damage and neuroinflammation. Cuprizone is a copper-chelator that induces death of oligodendrocytes and reversible demyelination in mice. Using PhenoTyper home-cages, behavioral changes were detected in this model in spontaneous behavior as well as in the CognitionWall test. For more information please contact us.
Cuprizone + rapamycin model (demyelination)
Cuprizone is a copper-chelator that induces death of oligodendrocytes and reversible demyelination in mice, thereby closely recapitulating multiple sclerosis (MS) disease mechanisms. Addition of mTor inhibitor rapamycin prevents spontaneous re-myelination by newly differentiated oligodendrocytes, thereby creating a more severe demyelinating phenotype. Sylics has detected profound changes in spontaneous behaviors in this model using PhenoTyper home-cages. For more information please contact us.
Experimental autoimmune encephalomyelitis (EAE) model
Multiple sclerosis is thought to be an immune-mediated inflammatory disorder. Immunization with myelin-based self-antigens (e.g. MBP, PLP, MOG) leads to an immune-mediated demyelination phenotype that mimics the core phenotypes of MS. The use of different adjuvants or targets allows induction of either relapsing remitting or progressive disease. EAE is therefore a versatile and disease-relevant MS mouse model. Sylics has extensive experience with induced mouse models. For more information please contact us.
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