• Users Online: 2021
  • Home
  • Print this page
  • Email this page
Year : 2018  |  Volume : 13  |  Issue : 7  |  Page : 1156-1158

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

Centre for Advanced Computational Solutions (C-fACS), Lincoln University, Christchurch, New Zealand

Correspondence Address:
Don Kulasiri
Centre for Advanced Computational Solutions (C-fACS), Lincoln University, Christchurch
New Zealand
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1673-5374.235020

Rights and Permissions

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.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded222    
    Comments [Add]    

Recommend this journal