What can computational modeling offer for studying the Ca^(2+) dysregulation in Alzheimer's disease:current research and future directions  

作　　者：Jingyi Liang Don Kulasiri 

机构地区：[1]Centre for Advanced Computational Solutions(C-fACS),Lincoln University

出　　处：《Neural Regeneration Research》2018年第7期1156-1158,共3页中国神经再生研究（英文版）

摘　　要：Ca^2＋ dysregulation is an early event observed in Alzheimer＇s disease（AD） patients preceding the presence of its clinical symptoms.Dysregulation of neuronalCa^2＋ will cause synaptic loss and neuronal death,eventually leading to memory impairments and cognitive decline.Treatments targetingCa^2＋ signaling pathways are potential therapeutic strategies against AD.The complicated interactions make it challenging and expensive to study the underlying mechanisms as to how Ca^2＋ 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 Ca^2＋ dysregulation of AD by simulating Ca^2＋signaling at various levels.We also pointed out the future directions that computational modeling can be done in studying the Ca^2＋ dysregulation in AD.Ca^2＋ dysregulation is an early event observed in Alzheimer＇s disease（AD） patients preceding the presence of its clinical symptoms.Dysregulation of neuronalCa^2＋ will cause synaptic loss and neuronal death,eventually leading to memory impairments and cognitive decline.Treatments targetingCa^2＋ signaling pathways are potential therapeutic strategies against AD.The complicated interactions make it challenging and expensive to study the underlying mechanisms as to how Ca^2＋ 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 Ca^2＋ dysregulation of AD by simulating Ca^2＋signaling at various levels.We also pointed out the future directions that computational modeling can be done in studying the Ca^2＋ dysregulation in AD.

关 键 词：Alzheimer＇s disease amyloid-beta Ca^2＋ hypothesis Ca^2＋ dysregulation computational modeling computational neuroscience 

分 类 号：R749.16[医药卫生—神经病学与精神病学]