Journal
BRITISH JOURNAL OF PHARMACOLOGY
Volume 164, Issue 4, Pages 1079-1106Publisher
WILEY
DOI: 10.1111/j.1476-5381.2011.01302.x
Keywords
animal models; autoimmunity; demyelination; experimental autoimmune encephalomyelitis; immunomodulation; multiple sclerosis; neurodegeneration; neuroinflammation; neuroprotection; therapy
Categories
Funding
- Multiple Sclerosis Society of Great Britain and Northern Ireland
- University of Nottingham
- European Union
- pharmaceutical industry
- Bayer Schering
- Biogen Idec
- Centocor
- Cephalon
- GlaxoSmithKline
- GW Pharma
- Merck Serono
- Teva
- Novartis
- Roche
- UCB
- Almirall
Ask authors/readers for more resources
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. There is great heterogeneity in the susceptibility to the induction, the method of induction and the response to various immunological or neuropharmacological interventions, many of which are reviewed here. This makes EAE a very versatile system to use in translational neuro-and immunopharmacology, but the model needs to be tailored to the scientific question being asked. While creating difficulties and underscoring the inherent weaknesses of this model of MS in straightforward translation from EAE to the human disease, this variability also creates an opportunity to explore multiple facets of the immune and neural mechanisms of immune-mediated neuroinflammation and demyelination as well as intrinsic protective mechanisms. This allows the eventual development and preclinical testing of a wide range of potential therapeutic interventions.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available