Cerebral Amyloid Angiopathy and the Fibrinolytic System: Is Plasmin a Therapeutic Target?
Chloe A. Mutimer, Charithani B. Keragala, Hugh S. Markus, David J. Werring, Geoffrey Cloud, Robert L. Medcalf
Abstract
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.
Topics & Concepts
Cerebral amyloid angiopathyMedicinePlasminStroke (engine)Intracerebral hemorrhageAngiopathyAmyloid (mycology)PathophysiologyPathologyInternal medicineDiabetes mellitusEndocrinologyDementiaDiseaseBiochemistryChemistrySubarachnoid hemorrhageEngineeringMechanical engineeringEnzymeIntracerebral and Subarachnoid Hemorrhage ResearchAlzheimer's disease research and treatmentsAcute Ischemic Stroke Management