Abstract
EXPERIMENTAL allergic encephalomyelitis (EAE) is an autoimmune, paralytic disease that can be induced in experimental animals by injection of whole tissue from the central nervous system (CNS), or the purified myelin basic protein (PBP) homogenised in Freund's adjuvant. In some respects, it resembles certain human demyelinating diseases1,2. Preferential changes occur in the metabolism of glycosphingolipids in the CNS3–6, some of which do not seem to be directly related to the presence of clinical symptoms4. In the guinea pig, changes in some of the myelin components seem to depend on the disease-inducing substance used. The cerebroside content of the CNS changes when this animal is sensitised with whole CNS, or with PBP and CNS lipids, but not when PBP alone is used as encephalitogen. The content of sulphatides changes the extent depending on the composition of the encephalitogenic preparation injected6. We report here that changes in the level of glycosphingolipids may arise in response to components other than the myelin basic protein and without the simultaneous occurrence of paralytic symptoms.
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MAGGIO, B., CUMAR, F. Experimental allergic encephalomyelitis: dissociation of neurological symptoms from lipid alterations in brain. Nature 253, 364–365 (1975). https://doi.org/10.1038/253364a0
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DOI: https://doi.org/10.1038/253364a0
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