ArticleBlood2017
Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice.
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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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
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Factor XII-A New Therapeutic Target? A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Serum proteomic analysis in esophagectomy patients with postoperative delirium: A case-control study.Heart & lung : the journal of critical careTrial
- Article
- Advancements in research on the thrombo-inflammation mechanisms mediated by factor XII in ischemic stroke.Journal of thrombosis and thrombolysis · 2025Review
- A Bibliometric Analysis of Macrophage Research Associated with Periodontitis Over the Past Two Decades.International dental journal · 2025Article
- Discovery of a new lead molecule to develop a novel class of human factor XIIa inhibitors.Journal of thrombosis and thrombolysis · 2024Article
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Proteomics of human platelet lysates and insight from animal studies on platelet protein diffusion to hippocampus upon intranasal administration.APL bioengineering · 2024Article
- Article
- Sex-Specific and Traumatic Brain Injury Effects on Dopamine Receptor Expression in the Hippocampus.International journal of molecular sciences · 2023Article
- The Venular Side of Cerebral Amyloid Angiopathy: Proof of Concept of a Neglected Issue.Biomedicines · 2023Review
- A possible mechanism for the enhanced toxicity of beta-amyloid protofibrils in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- 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
- Triazol-1-yl Benzamides Promote Anticoagulant ActivityCardiovascular & hematological agents in medicinal chemistry · 2023Article
- Cellular mechanisms of fibrin (ogen): insight from neurodegenerative diseases.Frontiers in neuroscience · 2023Review
- Dysregulated haemostasis in thrombo-inflammatory disease.Clinical science (London, England : 1979) · 2022Review
- Blocking domain 6 of high molecular weight kininogen to understand intrinsic clotting mechanisms.Research and practice in thrombosis and haemostasis · 2022Article
- Direct Oral Anticoagulants (DOACs) for Therapeutic Targeting of Thrombin, a Key Mediator of Cerebrovascular and Neuronal Dysfunction in Alzheimer's Disease.Biomedicines · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) -initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment.
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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.