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Fibrinogen and @b-Amyloid Association Alters Thrombosis and Fibrinolysis: A Possible Contributing Factor to Alzheimer's Disease

Marta Cortes-Canteli, Justin Paul, Erin H Norris, Robert Bronstein, Hyung Jin Ahn, Daria Zamolodchikov, Shivaprasad Bhuvanendran, Katherine M Fenz, and Sidney Strickland

Neuron 66(5):15 (2010) PMID 20547128 PMCID PMC2895773

Alzheimer's disease (AD) is a neurodegenerative disorder in which vascular pathology plays an important role. Since the @b-amyloid peptide (A@b) is a critical factor in this disease, we examined its relationship to fibrin clot formation in AD. In vitro and in vivo experiments showed that fibrin clots formed in the presence of A@b are structurally abnormal and resistant to degradation. Fibrin(ogen) was observed in blood vessels positive for amyloid in mouse and human AD samples, and intravital brain imaging of clot formation and dissolution revealed abnormal thrombosis and fibrinolysis in AD mice. Moreover, depletion of fibrinogen lessened cerebral amyloid angiopathy pathology and reduced cognitive impairment in AD mice. These experiments suggest that one important contribution of A@b to AD is via its effects on fibrin clots, implicating fibrin(ogen) as a potential critical factor in this disease.

Copyright © 2010 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.neuron.2010.05.014
Version: za2963e q8za1 q8zb2 q8zc4 q8zd2 q8ze6 q8zf9 q8zgd
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