ArticleFrontiers in cellular neuroscience2021
Beta-Secretase 1 Underlies Reactive Astrocytes and Endothelial Disruption in Neurodegeneration.
Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Identifying Potential BACE1 Inhibitors from the ChEMBL Database Using Machine Learning and Atomistic Simulation Approaches.ACS omega · 2026Article
- Modeling Alzheimer's disease with brain organoids: mechanisms, applications, and future directions.Frontiers in cell and developmental biology · 2026Review
- The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer's disease: a narrative review.Neural regeneration research · 2023Review
- Potential drugs for the treatment of Alzheimer's disease.Pharmacological reports : PR · 2023Review
- BACE1 regulates expression of Clusterin in astrocytes for enhancing clearance of β-amyloid peptides.Molecular neurodegeneration · 2023Article
- BACE1 and SCD1 are associated with neurodegeneration.Frontiers in aging neuroscience · 2023Article
- Blood-brain barrier dysfunction and reduced cerebrospinal fluid levels of soluble amyloid precursor protein-β in patients with subcortical small-vessel disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- Cholesterol Dysmetabolism in Alzheimer's Disease: A Starring Role for Astrocytes?Antioxidants (Basel, Switzerland) · 2021Review
- Blood-Brain Barrier Breakdown: An Emerging Biomarker of Cognitive Impairment in Normal Aging and Dementia.Frontiers in neuroscience · 2021Review
- Neurovascular Alterations in Vascular Dementia: Emphasis on Risk Factors.Frontiers in aging neuroscience · 2021Article
- Obesity in Late-Life as a Protective Factor Against Dementia and Dementia-Related Mortality.American journal of Alzheimer's disease and other dementiasArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunction in the neurovascular unit (NVU) is a key component in the progressive deterioration of Alzheimer's disease (AD) and is critical in vascular dementia. Recent studies have shown that inflammation plays early and perhaps causal roles in the pathogenesis of AD related to NVU damage, possibly in part by overactivating the aspartic acid protease activity of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1), which until now has almost solely been studied in the context of the β-amyloid cascade. In this study, we analyzed the relationship of BACE1 with astrocytes and blood vessels in human brains with sporadic and familial dementia [Autosomal dominant cerebral arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), sporadic Alzheimer's disease (SAD), and familial Alzheimer's disease (FAD)] and how BACE1 inhibition affects astrocytes and endothelial cells under conditions of glutamate toxicity. Our results show increased BACE1, PHF (Paired helical filaments)-tau and GFAP (Glial Fibrillary Acid Protein) immunoreactivity (IR) in the CA1 hippocampal regions of FAD and SAD brains. Furthermore, BACE1 immunoprecipitated with GFAP in tissue samples from all study cases, but their immunofluorescence close to (10 μm
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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.