ArticleNature communications2024
Endothelial leakiness elicited by amyloid protein aggregation.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Peptide-Functionalized Hydroxypropyl Cellulose Mitigates Amyloid-β Protein Induced Endothelial Leakiness and Enhances Cognitive Function in Alzheimer's Disease.Angewandte Chemie (International ed. in English) · 2026Article
- Pathogenic landscape shaped by cerebral amyloid oligomers.Neural regeneration research · 2026Article
- A Question of Origins: Non-neuronal Sources of Amyloid-β.Neuroscience bulletin · 2026Review
- Dysfunction of the neurovascular unit as a temporal driver in Alzheimer's pathogenesis.Translational neurodegeneration · 2026Review
- Pathology-directed drug delivery strategies: How to overcome blood-brain barrier for the treatment of brain diseases.Acta pharmaceutica Sinica. B · 2026Review
- Endothelial NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Nanomaterial strategies for mitigating protein misfolding and neuroinflammation in neurodegenerative diseases.Zoological research · 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
- Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics.Environment & health (Washington, D.C.) · 2025Article
- The Evolution of Functional Amyloids and Their Impact on Host-Microbe Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Aging microvasculature: Effects on immune cell trafficking and inflammatory diseases.The Journal of experimental medicine · 2025Review
- Microglial Clearance of Alzheimer's Amyloid-Beta Obstructed by Nanoplastics.Environmental science. Nano · 2025Article
- Emerging biophysical origins and pathogenic implications of amyloid oligomers.Nature communications · 2025Review
- Programmable production of bioactive extracellular vesicles in vivo to treat myocardial infarction.Nature communications · 2025Article
- Mapping cellular stress and lipid dysregulation in Alzheimer-related progressive neurodegeneration using label-free Raman microscopy.Communications biology · 2024Article
- Deciphering the Morphological Difference of Amyloid-β Fibrils in Familial and Sporadic Alzheimer's Diseases.Journal of chemical information and modeling · 2024Article
- Biomaterials Mimicking Mechanobiology: A Specific Design for a Specific Biological Application.International journal of molecular sciences · 2024Review
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 7 institutions in 4 countries.
Funding
Abstract
Alzheimer's disease (AD) is a major cause of dementia debilitating the global ageing population. Current understanding of the AD pathophysiology implicates the aggregation of amyloid beta (Aβ) as causative to neurodegeneration, with tauopathies, apolipoprotein E and neuroinflammation considered as other major culprits. Curiously, vascular endothelial barrier dysfunction is strongly associated with Aβ deposition and 80-90% AD subjects also experience cerebral amyloid angiopathy. Here we show amyloid protein-induced endothelial leakiness (APEL) in human microvascular endothelial monolayers as well as in mouse cerebral vasculature. Using signaling pathway assays and discrete molecular dynamics, we revealed that the angiopathy first arose from a disruption to vascular endothelial (VE)-cadherin junctions exposed to the nanoparticulates of Aβ oligomers and seeds, preceding the earlier implicated proinflammatory and pro-oxidative stressors to endothelial leakiness. These findings were analogous to nanomaterials-induced endothelial leakiness (NanoEL), a major phenomenon in nanomedicine depicting the paracellular transport of anionic inorganic nanoparticles in the vasculature. As APEL also occurred in vitro with the oligomers and seeds of alpha synuclein, this study proposes a paradigm for elucidating the vascular permeation, systemic spread, and cross-seeding of amyloid proteins that underlie the pathogeneses of AD and Parkinson's disease.
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What OpenQuestion holds
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.