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

• Main Authors: Jingyi Liang, Don Kulasiri
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2018-01-01
• Series: Neural Regeneration Research
• Subjects: Alzheimer′s disease; amyloid-beta; Ca2+ hypothesis; Ca2+ dysregulation; computational modeling; computational neuroscience
• Online Access: http://www.nrronline.org/article.asp?issn=1673-5374;year=2018;volume=13;issue=7;spage=1156;epage=1158;aulast=Liang

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.