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World J Stem Cells. May 26, 2019; 11(5): 236-253
Published online May 26, 2019. doi: 10.4252/wjsc.v11.i5.236
Modelling mitochondrial dysfunction in Alzheimer’s disease using human induced pluripotent stem cells
Kate Elizabeth Hawkins, Michael Duchen
Kate Elizabeth Hawkins, Michael Duchen, Cell and Developmental Biology, Division of Biosciences, University College London, London WC1E 6BT, United Kingdom
Author contributions: Hawkins KE wrote this manuscript and Duchen M edited the manuscript and provided feedback.
Conflict-of-interest statement: The author has no conflict of interest to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Corresponding author: Kate Elizabeth Hawkins, PhD, Postdoc, Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, United Kingdom.
Telephone: +44-207-1507119
Received: January 16, 2019
Peer-review started: January 16, 2019
First decision: January 29, 2019
Revised: February 22, 2018
Accepted: March 26, 2019
Article in press: March 26, 2019
Published online: May 26, 2019
Core Tip

Core tip: Alzheimer’s disease (AD) is a huge burden on the healthcare system and on society. At present, there are no therapeutic approaches that address the underlying causes of this devastating disease, largely because we lack understanding of the underlying molecular mechanisms. Induced pluripotent stem cells (iPSCs) from AD or Down syndrome patients can be used to elucidate these molecular mechanisms, therefore presenting a novel approach to this problem. In this review, we focus on the ability of iPSC models to gain insight into the mitochondrial dysfunction that occurs during AD and therefore identify novel drug targets.