Liang, JingyiKulasiri, Don2018-10-252018-07-132018-07-132018-03-07Liang, J., Kulasiri, G.D. (2018). What can computational modeling offer for studying the Ca2+ dysregulation in Alzheimer’s disease: Current research and future directions. Neural Regeneration Research 13(7), 1156-8. doi:10.4103/1673-5374.2350201673-5374GN7LJ (isidoc)30028315 (pubmed)https://hdl.handle.net/10182/10313Ca²⁺ 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.pp.1156-1158, 3 pagesPrinten© The Authors, 2018Alzheimer's diseaseamyloid-betaCa²⁺ hypothesisCa²⁺ dysregulationcomputational modelingcomputational neuroscienceJournal Article10.4103/1673-5374.235020ANZSRC::1109 NeurosciencesANZSRC::080108 Neural, Evolutionary and Fuzzy Computation1876-7958ANZSRC::3209 Neuroscienceshttps://creativecommons.org/licenses/by-nc-sa/4.0/Attribution-NonCommercial-ShareAlike