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REVIEW
Year : 2018  |  Volume : 13  |  Issue : 7  |  Page : 1156-1158

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


Centre for Advanced Computational Solutions (C-fACS), Lincoln University, Christchurch, New Zealand

Correspondence Address:
Don Kulasiri
Centre for Advanced Computational Solutions (C-fACS), Lincoln University, Christchurch
New Zealand
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1673-5374.235020

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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.


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