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Review
. 2018 Jul;13(7):1156-1158.
doi: 10.4103/1673-5374.235020.

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

Affiliations
Review

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

Jingyi Liang et al. Neural Regen Res. 2018 Jul.

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.

Keywords: Alzheimer's disease; Ca2+ dysregulation; Ca2+ hypothesis; amyloid-beta; computational modeling; computational neuroscience.

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Conflict of interest statement

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