LAUSR

Calcium oscillations are an imperative mode of signaling phenomenon. These oscillations are due to the active interactions taking place between some of the parameters like voltage gated calcium channels (VGCC), sodium calcium exchanger (NCX), calcium binding buffers, endoplasmic reticulum (ER) and mitochondria. The present paper focuses on the problem of higher level of calcium concentration in neurons which may further result into Alzheimer's Disease (AD). For this, a three-dimensional mathematical model having a system of differential equations depicting the changes in cytosolic calcium (in presence of buffers, VGCC and NCX), ER calcium and mitochondrial calcium, is formulated. A three-dimensional neuronal structure is targeted as the domain which is further discussed and solved using finite element technique in Comsol Multiphysics 5.4. Apposite boundary conditions matching well with the in-situ conditions are assumed. The obtained results clearly show the significance of the lower amount of the buffer and higher calcium mediated activities of VGCC, NCX, ER and mitochondria on calcium profile. These changes may lead to AD. To transit from AD condition to normal, exogenous buffers are added to check their significance. The results thus show that the replenishment of buffer may balance the amount of cell calcium and hence can affect positively on Alzheimer's affected cells.