Cerebral Amyloid Angiopathy and the Fibrinolytic System: Is Plasmin a Therapeutic Target?
Amyloid beta-Peptides
/ antagonists & inhibitors
Antibodies, Monoclonal
/ administration & dosage
Antifibrinolytic Agents
/ administration & dosage
Cerebral Amyloid Angiopathy
/ blood
Cerebral Hemorrhage
/ blood
Drug Delivery Systems
/ methods
Fibrinolysin
/ antagonists & inhibitors
Humans
Tranexamic Acid
/ administration & dosage
cerebral amyloid angiopathy
cerebral hemorrhage
fibrinolysis
thrombolytic therapy
tranexamic acid
Journal
Stroke
ISSN: 1524-4628
Titre abrégé: Stroke
Pays: United States
ID NLM: 0235266
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
pubmed:
16
6
2021
medline:
5
1
2022
entrez:
15
6
2021
Statut:
ppublish
Résumé
Cerebral amyloid angiopathy is a devastating cause of intracerebral hemorrhage for which there is no specific secondary stroke prevention treatment. Here we review the current literature regarding cerebral amyloid angiopathy pathophysiology and treatment, as well as what is known of the fibrinolytic pathway and its interaction with amyloid. We postulate that tranexamic acid is a potential secondary stroke prevention treatment agent in sporadic cerebral amyloid angiopathy, although further research is required.
Identifiants
pubmed: 34126761
doi: 10.1161/STROKEAHA.120.033107
doi:
Substances chimiques
Amyloid beta-Peptides
0
Antibodies, Monoclonal
0
Antifibrinolytic Agents
0
Tranexamic Acid
6T84R30KC1
Fibrinolysin
EC 3.4.21.7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM