ArticleJournal of the American College of Cardiology2019
Long-Term Dabigatran Treatment Delays Alzheimer's Disease Pathogenesis in the TgCRND8 Mouse Model.
Article in Journal of the American College of Cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 90 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
- Advances of therapeutic strategies for Alzheimer's disease.Journal of neurology · 2025Review
- The vascular contribution to cognitive decline in ageing and dementia.Nature reviews. Neuroscience · 2025Review
- Intercellular propagation of RIPK1/RIPK3 amyloid fibrils.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Brain-penetrating peptide and antibody radioligands for proof-of-concept PET imaging of fibrin in Alzheimer's disease.EJNMMI radiopharmacy and chemistry · 2025Article
- Evidence for control of cerebral neurovascular function by circulating platelets in healthy older adults.The Journal of physiology · 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
- Role of Thrombosis in Neurodegenerative Diseases: An Intricate Mechanism of Neurovascular Complications.Molecular neurobiology · 2025Review
- Traumatic Brain Injury and Alzheimer's Disease: A Shared Neurovascular Hypothesis.Neuroscience insights · 2025Review
- Research progress of platelets in neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Atrial Fibrillation and Dementia: Pathophysiological Mechanisms and Clinical Implications.Biomolecules · 2024Review
- Non-coding RNAs and Aquaporin 4: Their Role in the Pathogenesis of Neurological Disorders.Neurochemical research · 2024Review
- Approaches for Increasing Cerebral Efflux of Amyloid-β in Experimental Systems.Journal of Alzheimer's disease : JAD · 2024Review
- Recent Mechanisms of Neurodegeneration and Photobiomodulation in the Context of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?Biomolecules · 2023Review
- Pathophysiological Role of Microglial Activation Induced by Blood-Borne Proteins in Alzheimer's Disease.Biomedicines · 2023Review
- Review
- Vascular Dysfunction in Alzheimer's Disease: Alterations in the Plasma Contact and Fibrinolytic Systems.International journal of molecular sciences · 2023Review
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundAlzheimer's disease (AD) is a multifactorial neurodegenerative disorder with important vascular and hemostatic alterations that should be taken into account during diagnosis and treatment.
objectivesThis study evaluates whether anticoagulation with dabigatran, a clinically approved oral direct thrombin inhibitor with a low risk of intracerebral hemorrhage, ameliorates AD pathogenesis in a transgenic mouse model of AD.
methodsTgCRND8 AD mice and their wild-type littermates were treated for 1 year with dabigatran etexilate or placebo. Cognition was evaluated using the Barnes maze, and cerebral perfusion was examined by arterial spin labeling. At the molecular level, Western blot and histochemical analyses were performed to analyze fibrin content, amyloid burden, neuroinflammatory activity, and blood-brain barrier (BBB) integrity.
resultsAnticoagulation with dabigatran prevented memory decline, cerebral hypoperfusion, and toxic fibrin deposition in the AD mouse brain. In addition, long-term dabigatran treatment significantly reduced the extent of amyloid plaques, oligomers, phagocytic microglia, and infiltrated T cells by 23.7%, 51.8%, 31.3%, and 32.2%, respectively. Dabigatran anticoagulation also prevented AD-related astrogliosis and pericyte alterations, and maintained expression of the water channel aquaporin-4 at astrocytic perivascular endfeet of the BBB.
conclusionsLong-term anticoagulation with dabigatran inhibited thrombin and the formation of occlusive thrombi in AD; preserved cognition, cerebral perfusion, and BBB function; and ameliorated neuroinflammation and amyloid deposition in AD mice. Our results open a field for future investigation on whether the use of direct oral anticoagulants might be of therapeutic value in AD.
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