کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
4321939 1291669 2010 15 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Fibrinogen and β-Amyloid Association Alters Thrombosis and Fibrinolysis: A Possible Contributing Factor to Alzheimer's Disease
موضوعات مرتبط
علوم زیستی و بیوفناوری علم عصب شناسی علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
Fibrinogen and β-Amyloid Association Alters Thrombosis and Fibrinolysis: A Possible Contributing Factor to Alzheimer's Disease
چکیده انگلیسی

SummaryAlzheimer's disease (AD) is a neurodegenerative disorder in which vascular pathology plays an important role. Since the β-amyloid peptide (Aβ) 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 Aβ 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 Aβ to AD is via its effects on fibrin clots, implicating fibrin(ogen) as a potential critical factor in this disease.


► Altered hemostasis in Alzheimer's disease
► Aβ42 affects clot formation and degradation in vitro and in vivo
► A possible role for Aβ and fibrinogen in Alzheimer's disease
► Decreasing fibrin(ogen) levels lessens CAA pathology

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 66, Issue 5, 10 June 2010, Pages 695–709
نویسندگان
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