Mouse Experimental Demyelination (Cuprizone Model)

Demyelination is a pathological process characterized by the loss of myelin sheaths around axons, leading to neurological dysfunction in diseases such as multiple sclerosis (MS). The cuprizone model is a widely used and well-characterized experimental model of demyelination and remyelination. Cuprizone (bis-cyclohexanone oxaldihydrazone), a copper chelator, is administered in the diet to young adult mice, inducing oligodendrocyte stress and apoptosis, followed by astrocyte and microglial activation, and subsequent demyelination of distinct brain regions (particularly the corpus callosum). HKeyBio offers a validated cuprizone induced demyelination model in C57BL/6 mice, which recapitulates key features of human demyelinating diseases including oligodendrocyte loss, microgliosis, astrogliosis, and motor function deficits. This model provides a robust platform for preclinical efficacy testing of novel remyelinating and neuroprotective therapeutics for multiple sclerosis and other demyelinating disorders.

Quantity:
Availability:





Inquire Add to Basket

Product Description

Key Features & Benefits

Clinically relevant – Recapitulates key features of multiple sclerosis 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 through copper chelation, leading to mitochondrial dysfunction and apoptosis, with subsequent glial activation.

Translational value – Ideal for testing remyelinating therapies, neuroprotective agents, and anti-inflammatory drugs for multiple sclerosis and other demyelinating diseases.

IND-ready data packages – Studies can be conducted in accordance with GLP principles.

Technical Data & Validation

Cuprizone Induced Demyelination Model

3fb93a8040c095473c820d017582a333

Applications

• Efficacy testing of remyelinating therapies (anti-LINGO-1, muscarinic receptor antagonists, thyroid hormone agonists)

• Evaluation of neuroprotective agents and anti-inflammatory drugs for multiple sclerosis

• Target validation for oligodendrocyte survival and differentiation pathways

• Biomarker discovery (myelin proteins, glial markers)

• IND-enabling pharmacology and toxicology studies

Model Specifications

Parameter	Specification
Species/Strain	C57BL/6 mouse
Induction method	Dietary administration of 0.2–0.5% cuprizone mixed in standard rodent chow for 3–6 weeks
Study duration	3–8 weeks (demyelination phase) + optional 2–6 weeks (remyelination phase after cuprizone withdrawal)
Key endpoints	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 myelin genes (MBP, PLP, MAG)
Data package	Raw data, analysis reports, behavioral data, histology slides (LFB, IHC), image analysis files, bioinformatics (optional)

❓ Frequently Asked Questions

Q1: What demyelination preclinical model do you provide?

A1: We offer a cuprizone-induced demyelination model using C57BL/6 mice for central nervous system demyelination disease research.

Q 2: What is the modeling mechanism?

A2: Cuprizone disrupts copper balance and causes mitochondrial dysfunction. It triggers oligodendrocyte injury, glial cell activation and myelin sheath loss, simulating pathological changes of human demyelinating disorders.

Q3: What evaluation indicators are adopted?

A3: We monitor body weight and conduct Rotarod tests for motor function assessment. We detect IL-17 and Th1 cells, and perform Luxol fast blue staining to evaluate brain demyelination.

Q4: What is the experimental schedule?

A4: Cuprizone is administered three times per day starting from Day 0. The whole experiment lasts 35 days until all tests are completed.

Q5: What are the advantages and applications?

A5: This model features stable demyelinating lesions and easy operation. It is widely used for efficacy screening and mechanism study of drugs targeting demyelinating diseases.