Eur. Phys. J. Plus (2024) 139: 639
https://doi.org/10.1140/epjp/s13360-024-05449-9

Regular Article

Numerical simulation of interacting calcium and buffer dynamics in normal and Alzheimeric neurons

Department of Mathematics, Bioinformatics and Computer Applications, Maulana Azad National Institute of Technology, 462003, Bhopal, Madhya Pradesh, India

^a solankishashiraj0@gmail.com

Received: 5 June 2024
Accepted: 11 July 2024
Published online: 20 July 2024

Abstract

$[{\text{Ca}}^{2+}]$ buffering is the most important part of various divergent mechanisms that are responsible for controlling the free $[{\text{Ca}}^{2+}]$ ions in the cytoplasm. It can regulate the spatiotemporal diffusion of free cytosolic $[{\text{Ca}}^{2+}]$ ions. $[{\text{Ca}}^{2+}]$ buffers and proteins, including pumps, transporters, and channels, are present in every cell and work together to form intracellular $[{\text{Ca}}^{2+}]$ signals. In neuron cells, prior research on buffers’ influence on calcium dynamics treated the buffer’s concentration as a constant. In this study, the effects of the interplay between $[{\text{Ca}}^{2+}]$ and buffers are taken into account with the aim of demonstrating interdependent behavior. The finite element approach, together with the Crank–Nicholson scheme is applied to obtain the numerical results. These numerical results are utilized to examine the spatiotemporal interrelationships of $[{\text{Ca}}^{2+}]$ and buffers in normal and alzheimeric cells. Findings conclude that the homeostasis of $[{\text{Ca}}^{2+}]$ and buffer concentrations in the cells are more effective for dynamic buffers in comparison to constant buffers. Further, the buffer concentration is found to be lower in alzheimeric cells, thereby leading to a rise in their $[{\text{Ca}}^{2+}]$ concentration as compared to normal cells.