β-淀粉样肽与纤维蛋白原和凝血因子XII的相互作用可能与阿尔茨海默病有关。
Interactions of β-amyloid peptide with fibrinogen and coagulation factor XII may contribute to Alzheimer's disease.
作者信息
Ahn Hyung J, Chen Zu-Lin, Zamolodchikov Daria, Norris Erin H, Strickland Sidney
机构信息
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.
出版信息
Curr Opin Hematol. 2017 Sep;24(5):427-431. doi: 10.1097/MOH.0000000000000368.
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.
摘要
综述目的
综述关于阿尔茨海默病肽β-淀粉样蛋白与血液凝固系统相互作用并影响该疾病病理生理学的证据。
最新发现
β-淀粉样蛋白可与纤维蛋白原和血液凝固因子XII相互作用，并引发缺血和炎症。
总结
β-淀粉样蛋白与纤维蛋白原和因子XII相互作用。这些相互作用可导致凝血增加、异常凝块形成、持续性纤维蛋白沉积以及促炎分子的产生。这些事件可损害神经元，并可能导致阿尔茨海默病患者的认知衰退。
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