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

Neurosci Lett. 2004 Sep 30;368(3):285-9. doi: 10.1016/j.neulet.2004.07.011.

Abstract

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

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Amyloid beta-Peptides / biosynthesis
  • Amyloid beta-Peptides / blood
  • Amyloid beta-Peptides / metabolism*
  • Animals
  • Female
  • Fibrinolysin / deficiency*
  • Fibrinolysin / genetics*
  • Fibrinolysin / physiology
  • Genetic Carrier Screening
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Peptide Fragments / biosynthesis
  • Peptide Fragments / blood
  • Peptide Fragments / metabolism*
  • Plasminogen / deficiency
  • Plasminogen / genetics

Substances

  • Amyloid beta-Peptides
  • Peptide Fragments
  • amyloid beta-protein (1-40)
  • amyloid beta-protein (1-42)
  • Plasminogen
  • Fibrinolysin