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 C. Cloud; Robert L. Medcalf

doi:10.1161/STROKEAHA.120.033107

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 C. Cloud, Robert L. Medcalf

Research output: Contribution to journal › Review Article › Other › peer-review

10 Citations (Scopus)

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

Original language	English
Pages (from-to)	2707-2714
Number of pages	8
Journal	Stroke
Volume	52
Issue number	8
DOIs	https://doi.org/10.1161/STROKEAHA.120.033107
Publication status	Published - Aug 2021

Keywords

cerebral amyloid angiopathy
cerebral hemorrhage
fibrinolysis
thrombolytic therapy
tranexamic acid

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10.1161/STROKEAHA.120.033107

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title = "Cerebral Amyloid Angiopathy and the Fibrinolytic System: Is Plasmin a Therapeutic Target?",

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 ",

keywords = "cerebral amyloid angiopathy, cerebral hemorrhage, fibrinolysis, thrombolytic therapy, tranexamic acid",

author = "Mutimer, {Chloe A.} and Keragala, {Charithani B.} and Markus, {Hugh S.} and Werring, {David J.} and Cloud, {Geoffrey C.} and Medcalf, {Robert L.}",

year = "2021",

month = aug,

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T1 - Cerebral Amyloid Angiopathy and the Fibrinolytic System

T2 - Is Plasmin a Therapeutic Target?

AU - Mutimer, Chloe A.

AU - Keragala, Charithani B.

AU - Markus, Hugh S.

AU - Werring, David J.

AU - Cloud, Geoffrey C.

AU - Medcalf, Robert L.

PY - 2021/8

Y1 - 2021/8

N2 - 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

AB - 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

KW - cerebral amyloid angiopathy

KW - cerebral hemorrhage

KW - fibrinolysis

KW - thrombolytic therapy

KW - tranexamic acid

UR - http://www.scopus.com/inward/record.url?scp=85111419634&partnerID=8YFLogxK

U2 - 10.1161/STROKEAHA.120.033107

DO - 10.1161/STROKEAHA.120.033107

M3 - Review Article

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AN - SCOPUS:85111419634

SN - 0039-2499

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SP - 2707

EP - 2714

JO - Stroke

JF - Stroke

IS - 8

ER -

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

Abstract

Keywords

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