What can computational modeling offer for studying the Ca2+ dysregulation in Alzheimer's disease: current research and future directions

Neural Regeneration Research
Jingyi Liang, Don Kulasiri

Abstract

Ca2+ dysregulation is an early event observed in Alzheimer's disease (AD) patients preceding the presence of its clinical symptoms. Dysregulation of neuronal Ca2+ will cause synaptic loss and neuronal death, eventually leading to memory impairments and cognitive decline. Treatments targeting Ca2+ signaling pathways are potential therapeutic strategies against AD. The complicated interactions make it challenging and expensive to study the underlying mechanisms as to how Ca2+ signaling contributes to the pathogenesis of AD. Computational modeling offers new opportunities to study the signaling pathway and test proposed mechanisms. In this mini-review, we present some computational approaches that have been used to study Ca2+ dysregulation of AD by simulating Ca2+ signaling at various levels. We also pointed out the future directions that computational modeling can be done in studying the Ca2+ dysregulation in AD.

References

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Methods Mentioned

BETA
transgenic

Software Mentioned

COPASI
Mathematica
NEURON
CellDesigner
GENESIS
MATLAB
Python
R
MCell

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