TY - JOUR
T1 - Plasmin deficiency does not alter endogenous murine amyloid beta levels in mice
AU - Tucker, H. Michael
AU - Simpson, James
AU - Kihiko-Ehmann, Muthoni
AU - Younkin, Linda H.
AU - McGillis, Joseph P.
AU - Younkin, Steven G.
AU - Degen, Jay L.
AU - Estus, Steven
N1 - Funding Information:
This study was supported by grant numbers NIH R01 AG021362-01 and AG21545-02.
PY - 2004/9/30
Y1 - 2004/9/30
N2 - 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.
AB - 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.
KW - Alzheimers disease
KW - Amyloid
KW - Plasmin
KW - Proteolysis
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U2 - 10.1016/j.neulet.2004.07.011
DO - 10.1016/j.neulet.2004.07.011
M3 - Article
C2 - 15364412
AN - SCOPUS:4544260590
SN - 0304-3940
VL - 368
SP - 285
EP - 289
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -