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.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amyloid beta-Peptides / antagonists & inhibitors
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Amyloid beta-Peptides / blood
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Antibodies, Monoclonal / administration & dosage
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Antifibrinolytic Agents / administration & dosage*
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Cerebral Amyloid Angiopathy / blood
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Cerebral Amyloid Angiopathy / diagnosis
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Cerebral Amyloid Angiopathy / drug therapy*
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Cerebral Hemorrhage / blood
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Cerebral Hemorrhage / diagnosis
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Cerebral Hemorrhage / drug therapy
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Drug Delivery Systems / methods*
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Fibrinolysin / antagonists & inhibitors*
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Fibrinolysin / metabolism
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Humans
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Tranexamic Acid / administration & dosage
Substances
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Amyloid beta-Peptides
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Antibodies, Monoclonal
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Antifibrinolytic Agents
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Tranexamic Acid
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Fibrinolysin