中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (7): 1156-1158.doi: 10.4103/1673-5374.235020

• 综述:退行性病与再生 • 上一篇    下一篇

什么可以计算建模提供了解阿尔茨海默病的Ca2+失调?当前研究和未来发展方向

  

  • 收稿日期:2018-03-07 出版日期:2018-07-15 发布日期:2018-07-15

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

Jingyi Liang, Don Kulasiri   

  1. Centre for Advanced Computational Solutions (C-fACS), Lincoln University, Christchurch, New Zealand
  • Received:2018-03-07 Online:2018-07-15 Published:2018-07-15
  • Contact: Don Kulasiri, Ph.D., don.kulasiri@lincoln.ac.nz.

摘要:

orcid:0000-0001-8744-1578(Don Kulasiri)

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.

Key words: Alzheimer’s disease, amyloid-beta, Ca2+ hypothesis, Ca2+ dysregulation, computational modeling, computational neuroscience