ArticleBlood2012
Aβ delays fibrin clot lysis by altering fibrin structure and attenuating plasminogen binding to fibrin.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
74 citing papers in PubMed, 109 citations in OpenAlex.
- Molecular Pathogenesis of Cerebral Amyloid Angiopathy in Alzheimer's Disease: The Role of the Central Fibrinolytic Cascade at the Neurovascular Unit.Molecular neurobiology · 2026Review
- Unveiling the procoagulant state in Alzheimer's disease: A novel PET imaging strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Ultrasound-Mediated Thrombolysis: From Mechanistic Insights to Advanced Nanoplatforms and Clinical Translation.Advanced healthcare materials · 2026Review
- AmyloGram reveals amyloidogenic potential in stroke thrombus proteomes.The Biochemical journal · 2025Article
- Synergistic effects of the Aβ/fibrinogen complex on synaptotoxicity, neuroinflammation, and blood-brain barrier damage in Alzheimer's disease models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Fibrinogen Oxidation and Thrombosis: Shaping Structure and Function.Antioxidants (Basel, Switzerland) · 2025Review
- The Gut Microbiota-Brain Axis: A New Frontier in Alzheimer's Disease Pathology.CNS & neurological disorders drug targets · 2025Review
- Fibrinaloid Microclots and Atrial Fibrillation.Biomedicines · 2024Review
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Elucidating the Mechanisms of Sodium Benzoate in Alzheimer Disease: Insights from Quantitative Proteomics Analysis of Serum Samples.The international journal of neuropsychopharmacology · 2023Article
- Vascular Dysfunction in Alzheimer's Disease: Alterations in the Plasma Contact and Fibrinolytic Systems.International journal of molecular sciences · 2023Review
- Vascular Effects on Cerebrovascular Permeability and Neurodegeneration.Biomolecules · 2023Review
- Clot Imaging Using Photostable Nanodiamond.Nanomaterials (Basel, Switzerland) · 2023Article
- Fibrin-Targeting Immunotherapy for Dementia.The journal of prevention of Alzheimer's disease · 2023Article
- Cellular mechanisms of fibrin (ogen): insight from neurodegenerative diseases.Frontiers in neuroscience · 2023Review
- Fibrin-targeting molecular MRI in inflammatory CNS disorders.European journal of nuclear medicine and molecular imaging · 2022Article
- Neurovascular coupling mechanisms in health and neurovascular uncoupling in Alzheimer's disease.Brain : a journal of neurology · 2022Article
- Microscale structural changes of individual fibrin fibers during fibrinolysis.Acta biomaterialia · 2022Article
- Targeting hypercoagulation to alleviate Alzheimer's disease progression in metabolic syndrome.International journal of obesity (2005) · 2022Review
- Fibrinogen, Fibrin, and Fibrin Degradation Products in COVID-19.Current drug targets · 2022Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer disease is characterized by the presence of increased levels of the β-amyloid peptide (Aβ) in the brain parenchyma and cerebral blood vessels. This accumulated Aβ can bind to fibrin(ogen) and render fibrin clots more resistant to degradation. Here, we demonstrate that Aβ(42) specifically binds to fibrin and induces a tighter fibrin network characterized by thinner fibers and increased resistance to lysis. However, Aβ(42)-induced structural changes cannot be the sole mechanism of delayed lysis because Aβ overlaid on normal preformed clots also binds to fibrin and delays lysis without altering clot structure. In this regard, we show that Aβ interferes with the binding of plasminogen to fibrin, which could impair plasmin generation and fibrin degradation. Indeed, plasmin generation by tissue plasminogen activator (tPA), but not streptokinase, is slowed in fibrin clots containing Aβ(42), and clot lysis by plasmin, but not trypsin, is delayed. Notably, plasmin and tPA activities, as well as tPA-dependent generation of plasmin in solution, are not decreased in the presence of Aβ(42). Our results indicate the existence of 2 mechanisms of Aβ(42) involvement in delayed fibrinolysis: (1) through the induction of a tighter fibrin network composed of thinner fibers, and (2) through inhibition of plasmin(ogen)-fibrin binding.
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Registered trials
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.