ArticleThe Journal of biological chemistry2013
Ca2+ influx through store-operated Ca2+ channels reduces Alzheimer disease β-amyloid peptide secretion.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- Ginsenosides Decrease β-Amyloid Production via Potentiating Capacitative Calcium Entry.Biomolecules & therapeutics · 2024Article
- Store-Operated Calcium Entry Inhibition and Plasma Membrane Calcium Pump Upregulation Contribute to the Maintenance of Resting Cytosolic Calcium Concentration in A1-like Astrocytes.Molecules (Basel, Switzerland) · 2023Article
- Dysfunctional Glucose Metabolism in Alzheimer's Disease Onset and Potential Pharmacological Interventions.International journal of molecular sciences · 2022Review
- Elevating the Levels of Calcium Ions Exacerbate Alzheimer's Disease via Inducing the Production and Aggregation of β-Amyloid Protein and Phosphorylated Tau.International journal of molecular sciences · 2021Review
- The Relevance of Amyloid β-Calmodulin Complexation in Neurons and Brain Degeneration in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Alterations of the Endoplasmic Reticulum (ER) Calcium Signaling Molecular Components in Alzheimer's Disease.Cells · 2020Review
- Review
- ORAI2 Down-Regulation Potentiates SOCE and Decreases Aβ42 Accumulation in Human Neuroglioma Cells.International journal of molecular sciences · 2020Article
- Article
- Calcium Sensors STIM1 and STIM2 Regulate Different Calcium Functions in Cultured Hippocampal Neurons.Frontiers in synaptic neuroscience · 2020Article
- Role of STIM1 in neurodegeneration.World journal of biological chemistry · 2018Review
- Oleanolic Acid Ameliorates Aβ25-35 Injection-induced Memory Deficit in Alzheimer's Disease Model Rats by Maintaining Synaptic Plasticity.CNS & neurological disorders drug targets · 2018Article
- On the Role of Store-Operated Calcium Entry in Acute and Chronic Neurodegenerative Diseases.Frontiers in molecular neuroscience · 2018Review
- Abnormal dendritic calcium activity and synaptic depotentiation occur early in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2017Article
- Endoplasmic Reticulum Malfunction in the Nervous System.Frontiers in neuroscience · 2017Article
- Amyloid-beta disrupts calcium and redox homeostasis in brain endothelial cells.Molecular neurobiology · 2015Article
- Stim and Orai proteins in neuronal Ca(2+) signaling and excitability.Frontiers in cellular neuroscience · 2015Review
- Tau acts as a mediator for Alzheimer's disease-related synaptic deficits.The European journal of neuroscience · 2014Review
- Our "energy-Ca(2+) signaling deficits" hypothesis and its explanatory potential for key features of Alzheimer's disease.Frontiers in aging neuroscience · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer disease (AD), the leading cause of dementia, is characterized by the accumulation of β-amyloid peptides (Aβ) in senile plaques in the brains of affected patients. Many cellular mechanisms are thought to play important roles in the development and progression of AD. Several lines of evidence point to the dysregulation of Ca(2+) homeostasis as underlying aspects of AD pathogenesis. Moreover, direct roles in the regulation of Ca(2+) homeostasis have been demonstrated for proteins encoded by familial AD-linked genes such as PSEN1, PSEN2, and APP, as well as Aβ peptides. Whereas these studies support the hypothesis that disruption of Ca(2+) homeostasis contributes to AD, it is difficult to disentangle the effects of familial AD-linked genes on Aβ production from their effects on Ca(2+) homeostasis. Here, we developed a system in which cellular Ca(2+) homeostasis could be directly manipulated to study the effects on amyloid precursor protein metabolism and Aβ production. We overexpressed stromal interaction molecule 1 (STIM1) and Orai1, the components of the store-operated Ca(2+) entry pathway, to generate cells with constitutive and store depletion-induced Ca(2+) entry. We found striking effects of Ca(2+) entry induced by overexpression of the constitutively active STIM1(D76A) mutant on amyloid precursor protein metabolism. Specifically, constitutive activation of Ca(2+) entry by expression of STIM1(D76A) significantly reduced Aβ secretion. Our results suggest that disruptions in Ca(2+) homeostasis may influence AD pathogenesis directly through the modulation of Aβ production.
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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.