ArticleMolecular neurobiology2015
Amyloid-beta disrupts calcium and redox homeostasis in brain endothelial cells.
Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Homocysteine-induced endothelial dysfunction through mediating endoplasmic reticulum stress.The Journal of international medical research · 2026Article
- Role of Mitochondrial Calcium Dysregulation in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2025Review
- The microcirculation, the blood-brain barrier, and the neurovascular unit in health and Alzheimer disease: The aberrant pericyte is a central player.Pharmacological reviews · 2025Review
- Pathological Mechanisms and Molecular Imaging Advances in Alzheimer's Disease.Clinical interventions in aging · 2025Review
- Restoring Brain Pathways Involved in Diabetes-Associated Neurocognitive Disorders: The Potential of Dipeptidyl Peptidase 4 Inhibitors as a Therapeutic Strategy.Current neuropharmacology · 2025Article
- Exercise-mediated cerebrovascular repair in Alzheimer's disease: from pathophysiology to therapeutic precision.Frontiers in aging neuroscience · 2025Review
- Amyloid beta peptides (Aβ) from Alzheimer's disease neuronal secretome induce endothelial activation in a human cerebral microvessel model.Neurobiology of disease · 2023Article
- INPP5A/HLA-G1/IL-10/MMP-21 Axis in Progression of Esophageal Squamous Cell CarcinomaIranian biomedical journal · 2022Article
- Extracellular Calcium Receptor as a Target for Glutathione and Its Derivatives.International journal of molecular sciences · 2022Review
- Calcium Dyshomeostasis in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2021Review
- Targeting Mitochondrial Dysfunction for Bipolar Disorder.Current topics in behavioral neurosciences · 2021Review
- Genistein and Galantamine Combinations Decrease β-Amyloid PeptideNeurotoxicity research · 2020Article
- Partial loss of endothelial nitric oxide leads to increased cerebrovascular beta amyloid.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- A multipredictor model to predict the conversion of mild cognitive impairment to Alzheimer's disease by using a predictive nomogram.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Target Molecules of STIM Proteins in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- Type 2 Diabetes Alters Intracellular CaInternational journal of molecular sciences · 2019Article
- Azelnidipine Attenuates the Oxidative and NFκB Pathways in Amyloid-β-Stimulated Cerebral Endothelial Cells.ACS chemical neuroscience · 2019Article
- Endothelial Mitochondrial Dysfunction in Cerebral Amyloid Angiopathy and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Alzheimer's Disease as a Membrane Disorder: Spatial Cross-Talk Among Beta-Amyloid Peptides, Nicotinic Acetylcholine Receptors and Lipid Rafts.Frontiers in cellular neuroscience · 2019Review
- Sub-Toxic Human Amylin Fragment Concentrations Promote the Survival and Proliferation of SH-SY5Y Cells via the Release of VEGF and HspB5 from Endothelial RBE4 Cells.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
In Alzheimer's disease, the accumulation of amyloid-beta (Aβ) in the brain occurs in the parenchyma and cerebrovasculature. Several evidences support that the neuronal demise is potentiated by vascular alterations in the early stages of the disease, but the mechanisms responsible for the dysfunction of brain endothelial cells that underlie these cerebrovascular changes are unknown. Using rat brain microvascular endothelial cells, we found that short-term treatment with a toxic dose of Aβ1-40 inhibits the Ca(2+) refill and retention ability of the endoplasmic reticulum and enhances the mitochondrial and cytosolic response to adenosine triphosphate (ATP)-stimulated endoplasmic reticulum Ca(2+) release. Upon prolonged Aβ1-40 exposure, Ca(2+) homeostasis was restored concomitantly with a decrease in the levels of proteins involved in its regulation operating at the plasma membrane, endoplasmic reticulum, and mitochondria. Along with perturbations in Ca(2+) regulation, an early increase in the levels of oxidants and a decrease in the ratio between reduced and oxidized glutathione were observed in Aβ1-40-treated endothelial cells. Under these conditions, the nuclear levels of oxidative stress-related transcription factors, namely, hypoxia-inducible factor 1α and nuclear factor (erythroid-derived 2)-related factor 2, were enhanced as well as the protein levels of target genes. In conclusion, Aβ1-40 affects several mechanisms involved in Ca(2+) homeostasis and impairs the redox homeostasis simultaneously with stimulation of protective stress responses in brain endothelial cells. However, the imbalance between cell death and survival pathways leads to endothelial dysfunction that in turn contributes to cerebrovascular impairment in Alzheimer's disease.
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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.