ArticleAdvances in experimental medicine and biology2013
Considering the vascular hypothesis of Alzheimer's disease: effect of copper associated amyloid on red blood cells.
Article in Advances in experimental medicine and biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- Monoclonal immunoglobulins on red blood cells: a potential supplementary diagnostic indicator for monoclonal gammopathies.Frontiers in immunology · 2025Article
- Three-dimensional organotypic mouse brain slices to study Alzheimer's disease pathologies: a review.Frontiers in dementia · 2025Review
- Components of the Glutathione Cycle as Markers of Biological Age: An Approach to Clinical Application in Aging.Antioxidants (Basel, Switzerland) · 2023Article
- Sensing red blood cell nano-mechanics: Toward a novel blood biomarker for Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Clearance of amyloid-beta in Alzheimer's disease: shifting the action site from center to periphery.Molecular neurobiology · 2015Review
- Dietary methanol regulates human gene activity.PloS one · 2014Article
- Death by a thousand cuts in Alzheimer's disease: hypoxia--the prodrome.Neurotoxicity research · 2013Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The vascular hypothesis of Alzheimer's disease (AD) considers cerebral hypoperfusion as a primary trigger for neuronal dysfunction. We have previously reported that red blood cells (RBCs) bind amyloid, which are the characteristic deposits found in AD brains, and interact with amyloid on the vasculature [1-3]. Oxidative stress triggered by these RBC/amyloid interactions could impair oxygen delivery. Recent literature has implicated copper bound amyloid-β peptide (CuAβ) and the associated production of reactive oxygen species (ROS) as one of the primary factors contributing to AD pathology. In this work, we have investigated CuAβ generated RBC oxidative stress. Aβ(1-40) peptide with a stoichiometric amount of copper bound was produced and compared to the metal-free form of the peptide. Different aggregation states of the peptides were isolated and incubated with RBCs for 15 h. Interestingly, CuAβ stimulated a pronounced increase in red cell oxidative stress as indicated by increased hemoglobin (Hb) oxidation, increased formation of fluorescent heme degradation products, and a decrease in RBC deformability. These findings demonstrate a potential role for CuAβ in promoting vascular oxidative stress leading to impaired cerebral oxygen delivery, which may contribute to neurodegeneration associated with AD.
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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.