Abstract
EAE in rodents has been the most widely-studied research analog of human demyelinating disease, especially multiple sclerosis. However, accumulating evidence indicates that classical, axon-sparing demyelination cannot be solely responsible for typical behavioral deficits during EAE. The puzzle of clinical pathologic correlation during EAE in rodents is reviewed, emphasizing the discrepancy between the consistent occurrence of “ascending” hind paralysis and the variability of histopathologic changes in the central nervous system (CNS). Several alternative hypotheses of the cause of paralysis during EAE are briefly discussed, including a recently-developed theory based on functional disturbance of peripheral nodes of Ranvier in nerve root myelinated fibers. It is argued that such a theory has definite advantages in explaining typical clinical signs of EAE in rodents.
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Simmons, R.D., Bernard, C.C.A., Carnegie, P.R. (1983). Factors Underlying Ascending Paralysis in Rodents During Experimental Autoimmune Encephalomyelitis (EAE). In: Kidman, A.D., Tomkins, J.K., Morris, C.A., Cooper, N.A. (eds) Molecular Pathology of Nerve and Muscle. Experimental and Clinical Neuroscience. Humana Press. https://doi.org/10.1007/978-1-4612-5308-2_7
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DOI: https://doi.org/10.1007/978-1-4612-5308-2_7
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