| Quantity: | |
|---|---|
Clinical Relevance - Summarizes the main features of MS pathology: oligodendrocyte loss, demyelination, gliosis, and motor dysfunction.
Quantifiable endpoints - body weight, Rotarod test (motor coordination), myelin area measurement (histology), Luxol fast blue staining and scoring.
Mechanism driven - Cuprizone induces oligodendrocyte stress via copper chelation, leading to mitochondrial dysfunction and apoptosis, with subsequent activation of glial cells.
Translational value – ideal for testing remyelinating therapies, neuroprotective agents and anti-inflammatory drugs for multiple sclerosis and other demyelinating diseases.
IND Ready Packet – Research can be conducted in accordance with GLP principles.
Cuprizone-induced demyelination model
• Efficacy testing of remyelination therapies (anti-LINGO-1, muscarinic receptor antagonists, thyroid hormone agonists)
• Evaluating neuroprotective and anti-inflammatory drugs in multiple sclerosis
• Target validation of oligodendrocyte survival and differentiation pathways
• Biomarker discovery (myelin proteins, glial markers)
• Pharmacology and toxicology studies to support IND
scope | Specification |
Species/Strain | C57BL/6 mouse |
induction method | Mix 0.2–0.5% cuprizone in standard rodent feed for 3–6 weeks |
study time | 3–8 weeks (demyelination phase) + optional 2–6 weeks (remyelination phase after cuprizone discontinuation) |
critical endpoint | Body weight, Rotarod test (motor coordination), myelin area measurement (histology, corpus callosum), Luxol Fast Blue staining and scoring, immunohistochemistry for oligodendrocytes (CC1, Olig2), astrocytes (GFAP), microglia (Iba1), optional: electron microscopy for myelin thickness, qPCR for determination of myelin genes (MBP, PLP, MAG) |
packet | Raw data, analysis reports, behavioral data, histological sections (LFB, IHC), image analysis files, bioinformatics (optional) |
Q: How does cuprizone induce demyelination?
A: Cuprizone is a copper chelator that disrupts mitochondrial function in oligodendrocytes, leading to metabolic stress, oxidative damage, and apoptosis. This triggers microglial activation and phagocytosis of myelin fragments, leading to demyelination, particularly in the corpus callosum.
Q: What are the key similarities to multiple sclerosis in humans?
A: This model exhibits oligodendrocyte loss, primary demyelination, astrogliosis, microglial activation, and motor function deficits. Unlike EAE, it lacks a significant peripheral immune component, making it ideal for studying central demyelination and remyelination processes.
Q: Can this model be used for IND support studies?
Answer: Yes. Studies can be conducted according to GLP principles for regulatory submissions (FDA, EMA).
Q: Do you offer customized study protocols (e.g., different cuprizone concentrations, durations, remyelination studies)?
Answer: Of course. Our scientific team tailors cuprizone dosing regimens, study timelines (acute vs. chronic demyelination, remyelination phases) and endpoint analyzes for your specific drug candidate.
