Demyelination experimental models

Bieber, A. J. and Rodriguez, M. Experimental models of virus-induced demyelination. In R. A. Lazzarini (ed.), Myelin Biology and Disorders. San Diego, CA Elsevier Academic Press, 2004, pp. 1073-1100. 

To understand the role of the different constituents of oligodendrocytes, Schwann cells, and myelin, and the cellular interactions, it is necessary to consider each constituent and the abnormalities that occur in experimental models and in human pathology. Each specific compound of myelin, and many factors involved in myeli-nation, can give rise to genetic diseases or autoimmune diseases. There are many animal models and human diseases that help in understanding the demyelination process. 

Multiple sclerosis (MS) has traditionally been viewed as a disorder in which myelin is the primary target. However, there is recent evidence for abnormal SNS expression in experimental models of demyelination and in MS. Black et al (1999b) studied Na channel expression in the taiep rat, a mutant model in which myelin is initially formed normally, but then lost as a result of an oligodendrocyte abnormality. They observed the abnormal expression of SNS Na channel mRNA and protein in Purkinje cells following loss of myelin. More recently. Black et al (2000) demonstrated that SNS mRNA and protein, which are not detectable in normal Purkinje cells, are expressed within Purkinje cells in a mouse model of MS, chronic relapsing experimental allergic encephalomyelitis. Black et al (2000) have also demonstrated the expression of SNS mRNA (Fig. 7a, b) and protein (Fig. 7e, f) within cerebellar Purkinje cells from tissue obtained post-mortem from MS patients, but not in controls with no neurological disease (Fig. 7c, g). 

Brain oedema in humans may be a sequelae to a variety of conditions such as tumour, injuries, hypertension, infarct or hypercapnic hypoxia. In some instances there is overlapping of mechanisms, such as tumour causing increased intracranial pressure followed by haemorrhage. Brain oedema may be focal or diffuse, frequently occurring with exclusion of the arcuate fibres. It is now recognized by most authors that two types of brain oedema can be differentiated vasogenic and cytoxic [1]. Their chemical parameters can be elucidated better in experimental models and tend to differ with the type of the oedema. The term demyelination in this condition refers to the pallor of white matter seen in sections stedned for demonstration of myelin. 

Experimental allergic encephalomyelitis is an animal model of autoimmune demyelination 640... 

EAE experimental allergic/autoimmune encephalitis is an animal model for demyelinating diseases, such as multiple sclerosis. It is induced by injection of myelin basic protein or whole CNS tissue together with adjuvants. 

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