ReviewJournal of clinical medicine2020
Interactions between Amyloid-Β Proteins and Human Brain Pericytes: Implications for the Pathobiology of Alzheimer's Disease.
Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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
27 citing papers in PubMed, 44 citations in OpenAlex.
- Review
- Emerging roles of circular RNAs and enhancer RNAs: new insights into the development and management of neurodegenerative disorders.Biomarker research · 2026Review
- CSF markers of vascular injury correlate with tau and cognitive decline in early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Histological and Functional Breakdown of the Blood-Brain Barrier in Alzheimer's Disease: A Multifactorial Intersection.Neurology international · 2025Review
- Review
- Emerging biophysical origins and pathogenic implications of amyloid oligomers.Nature communications · 2025Review
- iPSC-derived blood-brain barrier modeling reveals APOE isoform-dependent interactions with amyloid beta.Fluids and barriers of the CNS · 2024Article
- Assessing blood-brain barrier dysfunction and its association with Alzheimer's pathology, cognitive impairment and neuroinflammation.Alzheimer's research & therapy · 2024Article
- The Role ofJournal of clinical medicine · 2024Review
- Amyloid β oligomer induces cerebral vasculopathy via pericyte-mediated endothelial dysfunction.Alzheimer's research & therapy · 2024Article
- Amyloid Beta-Mediated Neurovascular Toxicity in Alzheimer's Disease.Methods in molecular biology (Clifton, N.J.) · 2024Article
- The clinical perspective of circular RNAs in neurodegenerative diseases: potential diagnostic tools and therapeutic targets.Frontiers in cellular neuroscience · 2024Review
- Blood-Brain Barrier Breakdown in Alzheimer's Disease: Mechanisms and Targeted Strategies.International journal of molecular sciences · 2023Review
- Microglia and the Blood-Brain Barrier: An External Player in Acute and Chronic Neuroinflammatory Conditions.International journal of molecular sciences · 2023Review
- Microvascular Contributions to Alzheimer Disease Pathogenesis: Is Alzheimer Disease Primarily an Endotheliopathy?Biomolecules · 2023Review
- Vascular contributions to Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Cooperation between neurovascular dysfunction and Aβ in Alzheimer's disease.Frontiers in molecular neuroscience · 2023Review
- Circular RNAs: New players involved in the regulation of cognition and cognitive diseases.Frontiers in neuroscience · 2023Review
- Brain pericyte biology: from physiopathological mechanisms to potential therapeutic applications in ischemic stroke.Frontiers in cellular neuroscience · 2023Review
- Chronic effects of blast injury on the microvasculature in a transgenic mouse model of Alzheimer's disease related Aβ amyloidosis.Fluids and barriers of the CNS · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disease that is the most common cause of dementia, especially among aging populations. Despite advances in AD research, the underlying cause and the discovery of disease-modifying treatments have remained elusive. Two key features of AD pathology are the aberrant deposition of amyloid beta (amyloid-β or Aβ) proteins in the brain parenchyma and Aβ toxicity in brain pericytes of the neurovascular unit/blood-brain barrier (NVU/BBB). This toxicity induces oxidative stress in pericytes and leads to capillary constriction. The interaction between pericytes and Aβ proteins results in the release of endothelin-1 in the pericytes. Endothelin-1 interacts with ET
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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.