Chronic remitting experimental allergic encephalomyelitis in lewis rats as a model of multiple sclerosis

Abstract

Experimental allergic encephalomyelitis (EAE)is an autoimmune demyelinating disorder of the central nervous system (CNS), which can be elicited in genetically sensitive animals by immunization with nerve tissue homogenate or encephalitogenic components combined with a powerful adjuvant. The clinical and pathological changes of EAE are reminiscent of the changes which are seen in humans with the demyelinatiug disease multiple sclerosis (MS), and EAE can thus serve as a model of this disease [1,8,11,12]. The clinical form and extent of demyelination differ in different animal species and depend on the antigen used. In particular, chronic remitting EAE (crEAE) is characterized clinically by periods of exacerbation and remission, similar to analogous periods occurring in MS. The major pathological features of EAE are the inflammatory process and demyelination. In principle, the CNS of animals with acute EAE shows only small losses of myelin coatings, while in crEAE, demyelination is very well pronounced. The absence of conductivity in the CNS in crEAE has been shown to be associated with blockade due to demyelination [15]. Since the extent of demyelination varies in different models of crEAE, it is very important to assess the destruction of myelin coatings in each model.