Cerebral Amyloid Angiopathy and the Fibrinolytic System: Is Plasmin a Therapeutic Target? | Zendy

Chloe A. Mutimer | Zendy; Charithani B. Keragala | Zendy; Hugh S. Markus | Zendy; David J. Werring | Zendy; Geoffrey Cloud | Zendy; Robert L. Medcalf | Zendy

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Cerebral Amyloid Angiopathy and the Fibrinolytic System: Is Plasmin a Therapeutic Target?

Author(s) -

Chloe A. Mutimer,

Charithani B. Keragala,

Hugh S. Markus,

David J. Werring,

Geoffrey Cloud,

Robert L. Medcalf

Publication year - 2021

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.120.033107

Subject(s) - cerebral amyloid angiopathy , medicine , plasmin , stroke (engine) , intracerebral hemorrhage , angiopathy , amyloid (mycology) , pathophysiology , pathology , diabetes mellitus , endocrinology , dementia , disease , biochemistry , chemistry , mechanical engineering , subarachnoid hemorrhage , engineering , enzyme

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.

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