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

H. Michael Tucker, James Simpson, Muthoni Kihiko-Ehmann, Linda H. Younkin, Joseph P. McGillis, Steven G. Younkin, Jay L. Degen, Steven Estus

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Deposition of amyloid beta (Aβ) 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 Aβ degradation; data supporting the role of the latter three enzymes have included increased levels of endogenous murine Aβ in mice genetically deficient for the respective enzyme. In this study, we sought to determine if plasminogen deficiency increases endogenous Aβ. We report that plasminogen deficiency did not result in an Aβ increase in the brain or in the plasma of adult mice. Hence, although plasmin is potentially important in the degradation of Aβ aggregates, we interpret these data as suggesting that plasmin does not regulate steady-state Aβ levels in non-pathologic conditions.

Original languageEnglish
Pages (from-to)285-289
Number of pages5
JournalNeuroscience Letters
Issue number3
StatePublished - Sep 30 2004

Bibliographical note

Funding Information:
This study was supported by grant numbers NIH R01 AG021362-01 and AG21545-02.


  • Alzheimers disease
  • Amyloid
  • Plasmin
  • Proteolysis

ASJC Scopus subject areas

  • General Neuroscience


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