Experimental Allergic Encephalomyelitis
From The MS Information Sourcebook, produced by the National MS Society.
Experimental allergic encephalomyelitis (EAE), and the related experimental autoimmune encephalomyelitis, are diseases of the brain and spinal cord, similar in many respects to MS, which are induced in laboratory animals. Animals with EAE serve as animal models for MS, allowing experimentation that would be impossible and unethical in humans who have the disease. Like MS, EAE is a demyelinating disease-it destroys the myelin, the fatty sheath that protects and surrounds nerve fibers. EAE can be induced in rats, mice, guinea pigs, rabbits, and monkeys. Like MS, it takes several clinical forms, including relapsing-remitting and progressive-relapsing.
EAE is induced in strains of lab animals that are susceptible to the disease by injecting myelin or specific myelin proteins in combination with an immune-exciting agent, called an adjuvent.
Animal Studies Yield Important Information About MS
Much of our current knowledge about the disease damage (pathology) and immune responses underlying MS has been gained from studies of animals with EAE. Information derived from microscopic and biochemical examination of the brain, blood, and spinal cord of animals with EAE includes:
- Identifying sites in the central nervous system that are more likely to develop MS lesions-damaged areas-also known as plaques;
- Finding out which immune cells are involved in the formation of plaques and how they interact; and
- Developing experimental treatments or manipulations that can stop or reverse the demyelinating process.
At least two of the currently available MS therapies—mitoxantrone (Novantrone) and glatiramer acetate (Copaxone) were developed because of promising findings in mice with EAE. Ongoing studies of EAE in the laboratory will continue to be an important early step in the development of new therapies for MS.
Kalb R. (ed.) Multiple Sclerosis: The Questions You Have; The Answers You Need (3rd ed.). New York: Demos Medical Publishing, 2004.
—Ch. 3 Treatments