Skip to content
RDL
Network
Ekosistem
Uygulama değiştir
EN
Hakkımızda
SSS
Giriş yap
Başla
Ageing and amyloid-beta peptide deposition contribute to an impaired brain tissue plasminogen activator activity by different mechanisms — Mathias Cacquevel (2007) | RDL Network
Back
Cite
Save
Save for later
Share
Home
Publications
Ageing and amyloid-beta peptide deposition contribute to an impaired brain tissue plasminogen activator activity by different mechanisms
Shared by
Peter Carmeliet
Aarhus University
Ageing and amyloid-beta peptide deposition contribute to an impaired brain tissue plasminogen activator activity by different mechanisms
Article
2007
en
Authors
+7 more
MC
Mathias Cacquevel
SL
Séverine Launay
HC
Hervé Castel
Discussion
(0)
Sign in
to like and join the discussion.
No comments yet. Be the first to comment.
Related publications
Article
1999
Tissue Plasminogen Activator (tPA) Deficiency Exacerbates Cerebrovascular Fibrin Deposition and Brain Injury in a Murine Stroke Model
Peyman Tabrizi
,
Liang Wang
,
Nicholas W. Seeds
,
J. Gordon McComb
,
Shinya Yamada
,
John H. Griffin
,
Peter Carmeliet
,
Martin Weiß
,
Berislav V. Zloković
Article
1998
Coordinated induction of plasminogen activator inhibitor-1 (PAI-1) and inhibition of plasminogen activator gene expression by hypoxia promotes pulmonary vascular fibrin deposition.
David J. Pinsky
,
Hui Liao
,
Charles A. Lawson
,
Shi Fang Yan
,
J Chen
,
Peter Carmeliet
,
David J. Loskutoff
,
D Stern
Article
2016
Tau, Amyloid Beta and Deep Brain Stimulation: Aiming to Restore Cognitive Deficit in Alzheimer's Disease
Siddhartha Mondragón‐Rodríguez
,
George Perry
,
Fernando Peña‐Ortega
,
Sylvain Williams
Article
2004
Ontogenic study of the influence of tissue plasminogen activator (t-PA) in neonatal excitotoxic brain insult and the subsequent microglia/macrophage activation
Olivier Hennebert
,
Vincent Laudenbach
,
A. Laquérrière
,
Catherine Verney
,
Peter Carmeliet
,
Stéphane Marret
,
Philippe Leroux
Dataset
Faculty Opinions recommendation of The fetal basis of amyloidogenesis: exposure to lead and latent overexpression of amyloid precursor protein and beta-amyloid in the aging brain.
George Perry
Discussion(0)
No comments yet. Be the first to comment.