ReviewFrontiers in neuroscience2023
Blood-brain barrier endothelial cells in neurodegenerative diseases: Signals from the "barrier".
Review in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Article
- Amyloid-β aggregates induce vasculopathy via ferroptosis in brain endothelial cells.Brain pathology (Zurich, Switzerland) · 2026Article
- Dysfunction of the neurovascular unit as a temporal driver in Alzheimer's pathogenesis.Translational neurodegeneration · 2026Review
- Neurovascular Uncoupling in Alzheimer's and Parkinson's Diseases: Mechanisms and Therapeutic Strategies.Brain sciences · 2026Review
- Angiotensin II impairs the remyelination mediated by brain endothelial cell-derived exosomes.Acta neuropathologica communications · 2026Article
- BBB-Permeable PROTACs: Where Do We Stand?ACS medicinal chemistry letters · 2026Review
- Neurovascular Unit-Derived Extracellular Vesicles as Regulators of Post-Stroke Pathology and Neurorestoration.Biomolecules · 2026Review
- Potential Neuroprotective Role of GLP-2 in Alzheimer's Disease: Clinical Observations, Mechanistic Insights, and Comparison with GLP-1.International journal of molecular sciences · 2026Article
- Adiponectin deficiency drives cerebrovascular dysfunction and synergizes with amyloid-β to exacerbate alzheimer's pathology.Alzheimer's research & therapy · 2026Article
- Ferroptosis in Parkinson's disease: a review of molecular mechanisms and emerging therapeutic strategies.Frontiers in neuroscience · 2026Review
- The process of angiogenesis in neurodegeneration-pathomechanisms and new therapeutic interventions.Psychopharmacology · 2026Review
- Predicting low premorbid cognitive ability with social determinants: A machine learning approach.JAR life · 2026Article
- Chronic stress, cortisol dysregulation, and neurodegenerative vulnerability: mechanistic pathways linking HPA-axis dysfunction to Alzheimer's disease risk.Frontiers in aging neuroscience · 2026Review
- Neurovascular dysfunction in the development and progression of neuroinflammatory diseases.Frontiers in cellular neuroscience · 2026Review
- Attenuation of blood-brain barrier dysfunction by functionalized gold nanoparticles against amyloid-β peptide in an Alzheimer's disease-on-a-chip model.Materials today. Bio · 2025Article
- The effects of doxorubicin on blood-brain barrier integrity in hCMEC/D3.Neurotoxicology · 2025Article
- Bridging regional neurovascular unit heterogeneity and cognitive function: a review.Fluids and barriers of the CNS · 2025Review
- Tirzepatide mitigates Stroke-Induced Blood-Brain barrier disruption by modulating Claudin-1 and C/EBP-α pathways.Molecular medicine (Cambridge, Mass.) · 2025Article
- Active Transport of Therapeutic Triblock Amphiphilic Polymer Poloxamer 188 in Brain Endothelial Cells for Cellular Repair.Journal of biomedical science and engineering · 2025Article
- Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As blood-brain barrier (BBB) disruption emerges as a common problem in the early stages of neurodegenerative diseases, the crucial roles of barrier-type brain endothelial cells (BECs), the primary part of the BBB, have been reported in the pathophysiology of neurodegenerative diseases. The mechanisms of how early vascular dysfunction contributes to the progress of neurodegeneration are still unclear, and understanding BEC functions is a promising start. Our understanding of the BBB has gone through different stages, from a passive diffusion barrier to a mediator of central-peripheral interactions. BECs serve two seemingly paradoxical roles: as a barrier to protect the delicate brain from toxins and as an interface to constantly receive and release signals, thus maintaining and regulating the homeostasis of the brain. Most previous studies about neurodegenerative diseases focus on the loss of barrier functions, and far too little attention has been paid to the active regulations of BECs. In this review, we present the current evidence of BEC dysfunction in neurodegenerative diseases and explore how BEC signals participate in the pathogenesis of neurodegenerative diseases.
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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 Socratic graph.