Sep 5, 1989

Some pathophysiological aspects of experimental autoimmune encephalomyelitis

Schweizerische Rundschau für Medizin Praxis = Revue suisse de médecine Praxis
C G Honegger, H Langemann

Abstract

Three aspects of the pathophysiology of experimental autoimmune encephalomyelitis (EAE) are discussed: firstly, the possible electrophysiological effects in the CNS of myelin basic protein, which is released during demyelination; secondly, the partial degeneration of monoaminergic and glutamatergic neurons which occurs during an attack of EAE in addition to demyelination; thirdly, the importance of ischemic events, accompanied by free radical release, in EAE. Especially the third aspect could have therapeutic implications. Treatment with radical scavengers, N-methyl-D-aspartate receptor blockers, or calcium blockers (as suggested for ischemia) might prove effective for EAE. Our present aim is to investigate whether these results are also relevant for MS, for which EAE is an animal model.

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Mentioned in this Paper

Ischemia
Calcium [EPC]
Abnormal Degeneration
Calcium
Neurons
Brain
Free Radicals
Nerve Degeneration
Synaptic Transmission
Experimental Autoimmune Encephalomyelitis

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