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Mathematical Modeling of Calcium Oscillatory Patterns in a Neuron
Devanshi D Dave1, Brajesh Kumar Jha2
1Department of Mathematics, School of Technology, PDPU, Gandhinagar, 382007, Gujarat, India. ddave1822@gmail.com.
Interdisciplinary Sciences, Computational Life Sciences
|November 10, 2020
Summary
High neuronal calcium levels, influenced by channels and buffers, may cause Alzheimer's Disease (AD). Replenishing buffers can restore calcium balance and potentially aid AD-affected cells.
Area of Science:
- Neuroscience
- Computational Biology
- Biophysics
Background:
- Calcium oscillations are crucial signaling events involving complex interactions between cellular components.
- Elevated intracellular calcium concentrations in neurons are implicated in the pathogenesis of Alzheimer's Disease (AD).
Purpose of the Study:
- To investigate the role of cellular calcium dynamics in neuronal function and its connection to Alzheimer's Disease.
- To develop and analyze a mathematical model simulating calcium handling in a three-dimensional neuronal environment.
Main Methods:
- Formulation of a three-dimensional mathematical model using differential equations to represent cytosolic, ER, and mitochondrial calcium.
- Application of the finite element technique in Comsol Multiphysics 5.4 to solve the model within a neuronal structure.
- Implementation of in-situ boundary conditions to accurately reflect physiological conditions.
Main Results:
- Demonstrated that reduced buffer concentration and heightened activity of voltage-gated calcium channels (VGCC), sodium-calcium exchanger (NCX), endoplasmic reticulum (ER), and mitochondria significantly impact neuronal calcium profiles.
- Identified these altered calcium dynamics as potential contributors to Alzheimer's Disease.
- Showcased that introducing exogenous buffers can help normalize cellular calcium levels.
Conclusions:
- Neuronal calcium dysregulation, driven by specific ion channels, exchangers, and organelles, is a key factor in Alzheimer's Disease.
- Buffer replenishment emerges as a promising therapeutic strategy to restore calcium homeostasis and mitigate AD-related cellular damage.
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