Multiple Sclerosis (MS) Models

Multiple Sclerosis (MS) is a chronic autoimmune disorder characterized by the immune system attacking the central nervous system, leading to inflammation, demyelination, and neurodegeneration. This progressive disease affects millions worldwide and results in symptoms such as muscle weakness, fatigue, cognitive impairment, and coordination difficulties, which worsen over time.

At Naason Science, our Preclinical Research Models are vital for advancing MS research, offering insights into immune response mechanisms, myelin damage, and neuronal loss. Our models replicate core aspects of MS pathology, such as inflammation and demyelination, enabling the evaluation of new therapies aimed at slowing disease progression, reducing symptoms, and improving patient quality of life. These preclinical models provide a foundation for translating discoveries from the lab to clinical applications in MS treatment.

Updated Cuprizone-Induced Demyelination Model for MS

At Naason Science, we have refined our cuprizone model to improve reproducibility and provide more detailed insights into demyelination and remyelination dynamics. This updated version offers researchers a powerful platform to investigate neuroinflammation, glial responses, and therapeutic strategies aimed at protecting or restoring myelin. By enhancing the precision and reliability of the model, we enable scientists to move closer to effective solutions for MS and other demyelinating disorders.

Model description:
The cuprizone mouse model is a non-autoimmune experimental model widely used to study demyelination and remyelination in the central nervous system (CNS), particularly relevant to multiple sclerosis (MS). The model is induced by feeding mice a diet containing cuprizone, a copper-chelating agent that selectively causes oligodendrocyte death and subsequent myelin loss, especially in the corpus callosum.

Applications:

Studying the mechanisms of demyelination and remyelination
Investigating neuroinflammatory processes
Evaluating potential therapeutic interventions for MS and other demyelinating diseases

Histology markers:

GFAP – astrocyte marker
Iba1 – microglia marker
Olig2 – oligodendrocyte marker
MBP (Myelin Basic Protein) – myelin protein marker
Luxol Fast Blue (LFB) – myelin staining

Representative readouts:

Immunohistochemistry showing changes in astrocytes, microglia, and oligodendrocytes
Myelin staining (MBP, LFB) to visualize demyelination in the striatum and corpus callosum

EAE-MOG induced Multiple Sclerosis Model

Experimental autoimmune encephalomyelitis (EAE) is the most commonly used experimental model for the human inflammatory demyelinating disease, multiple sclerosis (MS). EAE is a complex condition in which the interaction between a variety of immunopathological and neuropathological mechanisms leads to an approximation of the key pathological features of MS: inflammation, demyelination, axonal loss and gliosis. The counter-regulatory mechanisms of resolution of inflammation and remyelination also occur in EAE, which, therefore can also serve as a model for these processes. Moreover, EAE is often used as a model of cell-mediated organ-specific autoimmune conditions in general. EAE has a complex neuropharmacology, and many of the drugs that are in current or imminent use in MS have been developed, tested or validated on the basis of EAE studies.

Multiple Sclerosis (MS) Models

Updated Cuprizone-Induced Demyelination Model for MS

EAE-MOG induced Multiple Sclerosis Model

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