ArticlePloS one2018
A mathematical model for the effects of amyloid beta on intracellular calcium.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- CellSwarm-AD: A Multi-Scale Agent-Based Framework for Virtual Alzheimer's Disease Trials.International journal of molecular sciences · 2026Article
- Numerical Simulations and Bifurcation of CaCell biochemistry and biophysics · 2025Article
- The role of IPFrontiers in computational neuroscience · 2025Article
- ACognitive neurodynamics · 2024Article
- Data-driven Stochastic Model for Quantifying the Interplay Between Amyloid-beta and Calcium Levels in Alzheimer's Disease.Statistical analysis and data mining · 2024Article
- Computer-Assisted Proofs of Hopf Bubbles and Degenerate Hopf Bifurcations.Journal of dynamics and differential equations · 2024Article
- Intracellular Injection of Brain Extracts from Alzheimer's Disease Patients Triggers Unregulated CaCells · 2022Article
- Review
- Impact of β-Amyloids Induced Disruption of CaCells · 2022Article
- Calcium Dyshomeostasis in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2021Review
- A Neuron-Glial Model of Exosomal Release in the Onset and Progression of Alzheimer's Disease.Frontiers in computational neuroscience · 2021Article
- Unraveling Aβ-Mediated Multi-Pathway Calcium Dynamics in Astrocytes: Implications for Alzheimer's Disease Treatment From Simulations.Frontiers in physiology · 2021Article
- Quantifying the dose-dependent impact of intracellular amyloid beta in a mathematical model of calcium regulation in xenopus oocyte.PloS one · 2021Article
- Amyloids: Regulators of Metal Homeostasis in the Synapse.Molecules (Basel, Switzerland) · 2020Review
- Current understanding of metal ions in the pathogenesis of Alzheimer's disease.Translational neurodegeneration · 2020Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The accumulation of Alzheimer's disease (AD) associated Amyloid beta (Aβ) oligomers can trigger aberrant intracellular calcium (Ca2+) levels by disrupting the intrinsic Ca2+ regulatory mechanism within cells. These disruptions can cause changes in homeostasis levels that can have detrimental effects on cell function and survival. Although studies have shown that Aβ can interfere with various Ca2+ fluxes, the complexity of these interactions remains elusive. We have constructed a mathematical model that simulates Ca2+ patterns under the influence of Aβ. Our simulations shows that Aβ can increase regions of mixed-mode oscillations leading to aberrant signals under various conditions. We investigate how Aβ affects individual flux contributions through inositol triphosphate (IP3) receptors, ryanodine receptors, and membrane pores. We demonstrate that controlling for the ryanodine receptor's maximal kinetic reaction rate may provide a biophysical way of managing aberrant Ca2+ signals. The influence of a dynamic model for IP3 production is also investigated under various conditions as well as the impact of changes in membrane potential. Our model is one of the first to investigate the effects of Aβ on a variety of cellular mechanisms providing a base modeling scheme from which further studies can draw on to better understand Ca2+ regulation in an AD environment.
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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.