ArticleJournal of thrombosis and haemostasis : JTH2016
The Alzheimer's disease peptide β-amyloid promotes thrombin generation through activation of coagulation factor XII.
Article in Journal of thrombosis and haemostasis : JTH, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Distinct ocular microvascular alterations in Alzheimer's disease and cerebral small vessel disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Review
- A Snail Galactosed Glycosaminoglycan Inhibits Thrombosis without Affecting Hemostasis via Disrupting FIXa-FVIIIa Complex Generation.ACS central science · 2026Article
- Article
- Identification of Six Potential Therapeutic Targets Common to Ischemic Stroke and Vascular Dementia: Genetic Insights From an Integrated Bioinformatics Analysis.Brain and behavior · 2025Article
- Association of Platelet Aggregation With Markers of Alzheimer Disease Pathology in Middle-Aged Participants of the Framingham Heart Study.Neurology · 2025Article
- Blood-based biomarkers of Alzheimer's disease and incident dementia in the community.Nature medicine · 2025Article
- Amyloid-beta metabolism in age-related neurocardiovascular diseases.European heart journal · 2025Review
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
- Bat-derived oligopeptide LE6 inhibits the contact-kinin pathway and harbors anti-thromboinflammation and stroke potential.Zoological research · 2024Article
- Elevated protease-activated receptor 4 (PAR4) gene expression in Alzheimer's disease predicts cognitive decline.Neurobiology of aging · 2024Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Recurrence of macular edema in patients with branch retinal vein occlusion: a proteomic study.BMC ophthalmology · 2024Article
- Correlation of Plasmatic Amyloid Beta Peptides (Aβ-40, Aβ-42) with Myocardial Injury and Inflammatory Biomarkers in Acute Coronary Syndrome.Journal of clinical medicine · 2024Article
- Penalized Regression Based Proteome-Wide Association Study Reveals Potential Population-Specific Drug Targets for Alzheimer's Disease in European and African American Cohorts.AMIA ... Annual Symposium proceedings. AMIA Symposium · 2024Article
- Tauroursodeoxycholic acid: a bile acid that may be used for the prevention and treatment of Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Blood Coagulation and Beyond: Position Paper from the Fourth Maastricht Consensus Conference on Thrombosis.Thrombosis and haemostasis · 2023Article
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
- Vascular Dysfunction in Alzheimer's Disease: Alterations in the Plasma Contact and Fibrinolytic Systems.International journal of molecular sciences · 2023Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
unlabelledEssentials How the Alzheimer's disease (AD) peptide β-amyloid (Aβ) disrupts neuronal function in the disease is unclear. Factor (F) XII initiates blood clotting via FXI, and thrombosis has been implicated in AD. Aβ triggers FXII-dependent FXI and thrombin activation, evidence of which is seen in AD plasma. Aβ-triggered clotting could contribute to neuronal dysfunction in AD and be a novel therapeutic target. SUMMARY: Background β-Amyloid (Aβ) is a key pathologic element in Alzheimer's disease (AD), but the mechanisms by which it disrupts neuronal function in vivo are not completely understood. AD is characterized by a prothrombotic state, which could contribute to neuronal dysfunction by affecting cerebral blood flow and inducing inflammation. The plasma protein factor XII triggers clot formation via the intrinsic coagulation cascade, and has been implicated in thrombosis. Objectives To investigate the potential for Aβ to contribute to a prothrombotic state. Methods and results We show that Aβ activates FXII, resulting in FXI activation and thrombin generation in human plasma, thereby establishing Aβ as a possible driver of prothrombotic states. We provide evidence for this process in AD by demonstrating decreased levels of FXI and its inhibitor C1 esterase inhibitor in AD patient plasma, suggesting chronic activation, inhibition and clearance of FXI in AD. Activation of the intrinsic coagulation pathway in AD is further supported by elevated fibrin levels in AD patient plasma. Conclusions The ability of Aβ to promote coagulation via the FXII-driven contact system identifies new mechanisms by which it could contribute to neuronal dysfunction and suggests potential new therapeutic targets in AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.