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,eventu...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.展开更多
文摘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.