ReviewAntioxidants (Basel, Switzerland)2021
A Leaky Blood-Brain Barrier to Fibrinogen Contributes to Oxidative Damage in Alzheimer's Disease.
Review in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Neuroprotective Effect and Possible Mechanisms of Berberine in Diabetes-Related Cognitive Impairment: A Systematic Review and Meta-Analysis of Animal Studies.Frontiers in pharmacology · 2022Pooled it
- Fibrinogen as a Driver of Oxidative Stress and Apoptosis in the Fetal Brain After Maternal Influenza.Research square · 2026Article
- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
- Photothrombotic and middle cerebral artery occlusion models produce distinct neurovascular injury and sex-dependent outcomes.Scientific reports · 2026Article
- Review
- Endothelialized human umbilical cord mesenchymal stem cell-derived exosomes enhances angiogenesis and stabilizes the blood-spinal cord barrier after spinal cord injury.Journal of nanobiotechnology · 2026Article
- The C3-C3aR axis drives rotenone-induced cognitive damage via synaptic engulfment, dark microglia and PANoptosis.Redox biology · 2026Article
- The Role of MRI in Debunking the Fallacy of "Mild" Traumatic Brain Injury.Journal of magnetic resonance imaging : JMRI · 2026Review
- Computer-aided Drug Design for Alzheimer's Disease: Recent Advancements and Future Perspectives.Current topics in medicinal chemistry · 2026Review
- The immunothrombosis pathway linking pulmonary disease to stroke and neurodegeneration: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Qixian Tongluo Formula promotes the directional differentiation of neural stem cells into neurons via fibrinogen-mediated BMPRI/ID3 signal axis after ischemic stroke.Orphanet journal of rare diseases · 2025Article
- Functionalized Nanoparticles: A Promising Approach for Effective Management of Alzheimer's Disease.Molecular neurobiology · 2025Review
- Revolutionizing brain‒computer interfaces: overcoming biocompatibility challenges in implantable neural interfaces.Journal of nanobiotechnology · 2025Review
- The effect of fibrinogen levels on three-month neurological recovery in acute ischemic stroke patients.Scientific reports · 2025Article
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- Amyloid-β and heart failure in Alzheimer's disease: the new vistas.Frontiers in medicine · 2025Review
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Post-stroke hippocampal neurogenesis is impaired by microvascular dysfunction and PI3K signaling in cerebral amyloid angiopathy.Cell reports · 2024Article
- Proteomic analysis and experimental validation reveal the blood-brain barrier protective of Huanshaodan in the treatment of SAMP8 mouse model of Alzheimer's disease.Chinese medicine · 2024Article
- Identification of Autophagy-Related Candidate Genes in the Early Diagnosis of Alzheimer's Disease and Exploration of Potential Molecular Mechanisms.Molecular neurobiology · 2024Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intactness of blood-brain barrier (BBB) is compromised in Alzheimer's disease (AD). Importantly, evidence suggests that the perturbation and abnormalities appearing in BBB can manifest early in the progression of the disease. The disruption of BBB allows extravasation of the plasma protein, fibrinogen, to enter brain parenchyma, eliciting immune reactivity and response. The presence of amyloid-β (Aβ) peptide leads to the formation of abnormal aggregates of fibrin resistant to degradation. Furthermore, Aβ deposits act on the contact system of blood coagulation, altering levels of thrombin, fibrin clots and neuroinflammation. The neurovascular unit (NVU) comprises an ensemble of brain cells which interact with infiltrating fibrinogen. In particular, interaction of resident immune cell microglia with fibrinogen, fibrin and Aβ results in the production of reactive oxygen species (ROS), a neurotoxic effector in AD brain. Overall, fibrinogen infiltration through a leaky BBB in AD animal models and in human AD tissue is associated with manifold abnormalities including persistent fibrin aggregation and clots, microglial-mediated production of ROS and diminished viability of neurons and synaptic connectivity. An objective of this review is to better understand how processes associated with BBB leakiness to fibrinogen link vascular pathology with neuronal and synaptic damage 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.