What is experimental autoimmune encephalomyelitis?

Experimental autoimmune encephalomyelitis (EAE) is a T-helper (Th) cell-mediated autoimmune disease characterized by T-cell and monocyte infiltration in the central nervous system (CNS) associated with local inflammation.

How do you induce experimental autoimmune encephalomyelitis?

In the treatment model, EAE disease is induced by myelin antigen immunization or by adoptive transfer of myelin antigen-specific CD4+ T cells before introducing hormonal and nutritional manipulations and assessing their impact.

What is experimental autoimmune encephalomyelitis and multiple sclerosis?

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.

Is EAE a good model for MS?

From the pathogenesis point of view, therefore, EAE is a good model for studying MS mechanisms, even more so than for testing or developing drugs (Farooqi et al., 2010).

How experimental autoimmune encephalomyelitis is mediated in mice?

In mice. Demyelination is produced by injection of brain extracts, CNS proteins (such as myelin basic protein), or peptides from such protein emulsified in an adjuvant such as complete Freund’s adjuvant. The presence of the adjuvant allows the generation of inflammatory responses to the protein/peptides.

What is Cuprizone used for?

Cuprizone is used to produce toxic demyelination that resembles the demyelination that occurs in MS (Torkildsen et al., 2008).

How does Cuprizone cause demyelination?

Oral intoxication with the copper-chelator cuprizone induces oligodendrocyte apoptosis within a few days, which is closely followed by the activation of the innate immune cells in the brain, i.e., astrocytes and microglia, finally leading to demyelination of distinct white and grey matter brain areas.

What is Cuprizone model?

The cuprizone model is a model for toxic demyelination. In this model, young mice are fed with the copper chelator cuprizone, leading to oligodendrocyte death and a subsequent reversible demyelination. Spontaneous remyelination can be seen as early as 4 days after withdrawal of cuprizone.

Experimental autoimmune encephalomyelitis (EAE) is the most commonly used experimental model for the human inflammatory demyelinating disease, multiple sclerosis (MS).

How does venlafaxine treat murine experimental autoimmune encephalomyelitis?

The antidepressant venlafaxine ameliorates murine experimental autoimmune encephalomyelitis by suppression of pro-inflammatory cytokines. Int J Neuropsychopharmacol. 2009;12:525–536.

What is the role of monoclonal antibodies in the treatment of encephalomyelitis?

[PubMed] [Google Scholar] Kent SJ, Karlik SJ, Cannon C, Hines DK, Yednock TA, Fritz LC, et al. A monoclonal antibody to alpha 4 integrin suppresses and reverses active experimental allergic encephalomyelitis.

What is the role of mesenchymal stem cells in autoimmune encephalomyelitis?

Human mesenchymal stem cells infiltrate the spinal cord, reduce demyelination, and localize to white matter lesions in experimental autoimmune encephalomyelitis. J Neuropathol Exp Neurol. 2010;69:1087–1095.