Multiple Sclerosis MS models

Mouse models for Parkinson’s disease (PD) mimic different aspects of the disease, such as substantia nigra degeneration, alpha-synuclein pathology, and dysfunction of intracellular pathways.

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.

Spontaneous behaviour of mice in the automated home-cage (PhenoTypers) is tracked at high resolution and analysed by AHCODA. Highly discriminative parameters are produced, detecting changes in domains of motor function, circadian rhythm and others.
Effect size plot showing the specific decrease in activity during the dark phase in Cuprizone treated mice in comparison with naturally ageing B6 mice and neurodegeneration models.

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.

Multiple sclerosis (MS): microglia cells damage the myelin sheath of neuron axons.

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