What can computational modeling offer for studying the Ca²⁺ dysregulation in Alzheimer's disease: Current research and future directions
dc.contributor.author | Liang, J | |
dc.contributor.author | Kulasiri, Don | |
dc.coverage.spatial | India | |
dc.date.accessioned | 2018-10-25T23:37:51Z | |
dc.date.available | 2018-07-13 | |
dc.date.issued | 2018-07-13 | |
dc.date.submitted | 2018-03-07 | |
dc.description.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. | |
dc.format.extent | pp.1156-1158, 3 pages | |
dc.format.medium | ||
dc.identifier | NeuralRegenRes_2018_13_7_1156_235020 | |
dc.identifier | https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=elements_prod&SrcAuth=WosAPI&KeyUT=WOS:000439321600005&DestLinkType=FullRecord&DestApp=WOS_CPL | |
dc.identifier.citation | Liang, 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:10.4103/1673-5374.235020 | |
dc.identifier.doi | 10.4103/1673-5374.235020 | |
dc.identifier.eissn | 1876-7958 | |
dc.identifier.issn | 1673-5374 | |
dc.identifier.other | GN7LJ (isidoc) | |
dc.identifier.other | 30028315 (pubmed) | |
dc.identifier.uri | https://hdl.handle.net/10182/10313 | |
dc.language.iso | en | |
dc.publisher | Medknow Publications | |
dc.relation | The original publication is available from Medknow Publications - https://doi.org/10.4103/1673-5374.235020 - http://dx.doi.org/10.4103/1673-5374.235020 | |
dc.relation.isPartOf | Neural Regeneration Research | |
dc.relation.uri | https://doi.org/10.4103/1673-5374.235020 | |
dc.rights | © The Authors, 2018 | |
dc.rights.ccname | Attribution-NonCommercial-ShareAlike | |
dc.rights.ccuri | https://creativecommons.org/licenses/by-nc-sa/4.0/ | |
dc.subject | Alzheimer's disease | |
dc.subject | amyloid-beta | |
dc.subject | Ca²⁺ hypothesis | |
dc.subject | Ca²⁺ dysregulation | |
dc.subject | computational modeling | |
dc.subject | computational neuroscience | |
dc.subject.anzsrc | ANZSRC::1109 Neurosciences | |
dc.subject.anzsrc | ANZSRC::080108 Neural, Evolutionary and Fuzzy Computation | |
dc.subject.anzsrc2020 | ANZSRC::3209 Neurosciences | |
dc.title | What can computational modeling offer for studying the Ca²⁺ dysregulation in Alzheimer's disease: Current research and future directions | |
dc.type | Journal Article | |
lu.contributor.unit | LU | |
lu.contributor.unit | LU|Agriculture and Life Sciences | |
lu.contributor.unit | LU|Agriculture and Life Sciences|WFMB | |
lu.contributor.unit | LU|Research Management Office | |
lu.contributor.unit | LU|Research Management Office|OLD QE18 | |
lu.identifier.orcid | 0000-0001-8744-1578 | |
pubs.issue | 7 | |
pubs.publication-status | Published | |
pubs.publisher-url | http://dx.doi.org/10.4103/1673-5374.235020 | |
pubs.volume | 13 |
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