Hyung J Ahn1, Zu-Lin Chen, Daria Zamolodchikov, Erin H Norris, Sidney Strickland. 1. aPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York City bRegeneron Pharmaceuticals, Tarrytown, New York, USA *Hyung J. Ahn, Zu-Lin Chen, and Daria Zamolodchikov contributed equally to this article.
Abstract
PURPOSE OF REVIEW: To review the evidence that the Alzheimer peptide β-amyloid interacts with the blood coagulation system and influences the pathophysiology of the disease. RECENT FINDINGS: β-amyloid can interact with fibrinogen and blood coagulation factor XII and trigger ischemia and inflammation. SUMMARY: β-amyloid interacts with fibrinogen and factor XII. These interactions can lead to increased clotting, abnormal clot formation, persistent fibrin deposition, and generation of proinflammatory molecules. These events can damage neurons and could contribute to the cognitive decline in Alzheimer's disease patients.
PURPOSE OF REVIEW: To review the evidence that the Alzheimer peptide β-amyloid interacts with the blood coagulation system and influences the pathophysiology of the disease. RECENT FINDINGS: β-amyloid can interact with fibrinogen and blood coagulation factor XII and trigger ischemia and inflammation. SUMMARY: β-amyloid interacts with fibrinogen and factor XII. These interactions can lead to increased clotting, abnormal clot formation, persistent fibrin deposition, and generation of proinflammatory molecules. These events can damage neurons and could contribute to the cognitive decline in Alzheimer's diseasepatients.
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