ArticleFrontiers in molecular neuroscience2013
Alzheimer's disease-associated peptide Aβ42 mobilizes ER Ca(2+) via InsP3R-dependent and -independent mechanisms.
Article in Frontiers in molecular neuroscience, 2013. 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
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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
24 citing papers in PubMed, 40 citations in OpenAlex.
- Therapeutic Potentials of the Seaweed-Derived Compounds for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer's disease mice.Journal of neuroinflammation · 2025Article
- The roles of mitochondria in global and local intracellular calcium signalling.Nature reviews. Molecular cell biology · 2025Review
- "Dirty Dancing" of Calcium and Autophagy in Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- Intracellular Injection of Brain Extracts from Alzheimer's Disease Patients Triggers Unregulated CaCells · 2022Article
- Dysregulated CaCells · 2022Review
- Quantifying the dose-dependent impact of intracellular amyloid beta in a mathematical model of calcium regulation in xenopus oocyte.PloS one · 2021Article
- Unraveling Aβ-Mediated Multi-Pathway Calcium Dynamics in Astrocytes: Implications for Alzheimer's Disease Treatment From Simulations.Frontiers in physiology · 2021Article
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- Presenilin 1 increases association with synaptotagmin 1 during normal aging.Neurobiology of aging · 2020Article
- The Link of the Prion Protein with CaInternational journal of molecular sciences · 2019Review
- Data-driven modeling of mitochondrial dysfunction in Alzheimer's disease.Cell calcium · 2018Article
- Dysregulation of Intracellular Calcium Signaling in Alzheimer's Disease.Antioxidants & redox signaling · 2018Review
- Abnormal dendritic calcium activity and synaptic depotentiation occur early in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2017Article
- Determining the Roles of Inositol Trisphosphate Receptors in Neurodegeneration: Interdisciplinary Perspectives on a Complex Topic.Molecular neurobiology · 2017Review
- Amyloid β production is regulated by β2-adrenergic signaling-mediated post-translational modifications of the ryanodine receptor.The Journal of biological chemistry · 2017Article
- Article
- Vitamin D, reactive oxygen species and calcium signalling in ageing and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- The Essential Role of Soluble Aβ Oligomers in Alzheimer's Disease.Molecular neurobiology · 2016Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Dysregulation of Ca(2+) homeostasis is considered to contribute to the toxic action of the Alzheimer's disease (AD)-associated amyloid-β-peptide (Aβ). Ca(2+) fluxes across the plasma membrane and release from intracellular stores have both been reported to underlie the Ca(2+) fluxes induced by Aβ42. Here, we investigated the contribution of Ca(2+) release from the endoplasmic reticulum (ER) to the effects of Aβ42 upon Ca(2+) homeostasis and the mechanism by which Aβ42 elicited these effects. Consistent with previous reports, application of soluble oligomeric forms of Aβ42 induced an elevation in intracellular Ca(2+). The Aβ42-stimulated Ca(2+) signals persisted in the absence of extracellular Ca(2+) indicating a significant contribution of Ca(2+) release from the ER Ca(2+) store to the generation of these signals. Moreover, inositol 1,4,5-trisphosphate (InsP3) signaling contributed to Aβ42-stimulated Ca(2+) release. The Ca(2+) mobilizing effect of Aβ42 was also observed when applied to permeabilized cells deficient in InsP3 receptors, revealing an additional direct effect of Aβ42 upon the ER, and a mechanism for induction of toxicity by intracellular Aβ42.
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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.