Plasmin deficiency does not alter endogenous murine amyloid beta levels in mice.
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.
Tucker
H Michael
HM
Department of Physiology, Sanders-Brown Center on Aging, University of Kentucky, 800 S. Limestone St., Lexington, KY 40536-0230, USA.
Simpson
James
J
Kihiko-Ehmann
Muthoni
M
Younkin
Linda H
LH
McGillis
Joseph P
JP
Younkin
Steven G
SG
Degen
Jay L
JL
Estus
Steven
S
D016229:Amyloid beta-Peptides / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D000818:Animals; D005260:Female; D005341:Fibrinolysin / Q000172:deficiency* / Q000235:genetics* / Q000502:physiology; D006580:Genetic Carrier Screening; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D010446:Peptide Fragments / Q000096:biosynthesis / Q000097:blood / Q000378:metabolism*; D010958:Plasminogen / Q000172:deficiency / Q000235:genetics
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42); D010958:Plasminogen; D005341:Fibrinolysin