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

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 

作者机构:Centre for Advanced Computational Solutions(C-fACS)Lincoln University 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2018年第13卷第7期

页      面:1156-1158页

核心收录:

学科分类:1002[医学-临床医学] 100203[医学-老年医学] 10[医学] 

主  题:Alzheimer's disease amyloid-beta Ca^2+ hypothesis Ca^2+ dysregulation computational modeling computational neuroscience 

摘      要:Ca^2+ dysregulation is an early event observed in Alzheimer's disease(AD) patients preceding the presence of its clinical *** of neuronalCa^2+ will cause synaptic loss and neuronal death,eventually leading to memory impairments and cognitive *** targetingCa^2+ signaling pathways are potential therapeutic strategies against *** complicated interactions make it challenging and expensive to study the underlying mechanisms as to how Ca^2+ signaling contributes to the pathogenesis of *** modeling offers new opportunities to study the signaling pathway and test proposed *** 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 *** also pointed out the future directions that computational modeling can be done in studying the Ca^2+ dysregulation in AD.

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