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The modification of experimental allergic encephalomyelitis with epsilon aminocaproic acid

Department of Neurology, University of Arizona College of Medicine and University Hospital, Tucson, AZ.

Epsilon aminocaproic acid, an inhibitor of plasminogen and trypsinogen activators, can decrease the severity of experimental allergic encephalomyelitis (EAE) in rats. The drug was tried because of a number of observations suggesting that neutral proteases, such as plasmin, might be chemical mediators of demyelination. The highest concentrations of plasminogen activator are found in the walls of veins and venules, around which demyelination is common in many demyelinating diseases, including MS. Indeed, the earliest lesion in MS is often demyelination with little cellular infiltration. In vitro studies have shown that neutral proteases secreted by activated macrophages selectively lyse myelin basic protein.

Dr. Sibley's address is Department of Neurology, University of Arizona Health Sciences Center, Tucson, AZ 87524.

Supported in part by a grant from the National Multiple Sclerosls Society (RG-1048-A-11) and by the William Brewster McKenna Fund for Multiple Sclerosis Research.

Accepted for publication May 8. 1978.