Plasmin deficiency does not alter endogenous murine amyloid beta levels in mice

Deposition of amyloid beta (Abeta) into extracellular plaques is a pathologic characteristic of Alzheimer's disease. Plasmin, neprilysin, endothelin-converting enzyme and insulin-degrading enzyme (IDE) have each been implicated in Abeta degradation; data supporting the role of the latter three enzymes have included increased levels of endogenous murine Abeta in mice genetically deficient for,the respective enzyme. In this study, we sought to determine if plasminogen deficiency increases endogenous Abeta. We report that plasminogen deficiency did not result in an Abeta increase in the brain or in the plasma of adult mice. Hence, although plasmin is potentially important in the degradation of Abeta aggregates, we interpret these data as suggesting that plasmin does not regulate steady-state Abeta levels in non-pathologic conditions. (C) 2004 Elsevier Ireland Ltd. All rights reserved.