The influence of the amyloid β-protein and its precursor in modulating cerebral hemostasis

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1862

Review

Van Nostrand, William E.^1,2 

[1] SUNY Stony Brook, Dept Neurosurg, HSC T12-086, Stony Brook, NY 11794 USA

[2] SUNY Stony Brook, Dept Med, HSC T12-086, Stony Brook, NY 11794 USA

关键词: Ischemia;    Hemorrhage;    Cerebral hemostasis;    Amyloid beta-protein;    Cerebral amyloid angiopathy;    Amyloid beta-protein precursor;    Proteinase inhibition;   

DOI  :  10.1016/j.bbadis.2015.10.020

来源: Elsevier

【 摘 要 】

Ischemic and hemorrhagic strokes are a significant cause of brain injury leading to vascular cognitive impairment and dementia (VCID). These deleterious events largely result from disruption of cerebral hemostasis, a well-controlled and delicate balance between thrombotic and fibrinolytic pathways in cerebral blood vessels and surrounding brain tissue. Ischemia and hemorrhage are both commonly associated with cerebrovascular deposition of amyloid beta-protein (A beta). In this regard, A beta directly and indirectly modulates cerebral thrombosis and fibrinolysis. Further, major isoforms of the A beta precursor protein (A beta PP) function as a potent inhibitor of pro-thrombotic proteinases. The purpose of this review article is to summarize recent research on how cerebral vascular A beta and A beta PP influence cerebral hemostasis. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia, edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock. (c) 2015 Elsevier B.V. All rights reserved.

【 授权许可】

Free