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Modeling Alzheimer's disease with human iPS cells: advancements, lessons, and applications.

Authors
  • Essayan-Perez, Sofia1
  • Zhou, Bo2
  • Nabet, Amber M1
  • Wernig, Marius3
  • Huang, Yu-Wen Alvin4
  • 1 Department of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America. , (United States)
  • 2 Department of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America; Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University Medical School, Stanford, CA 94305, United States of America. , (United States)
  • 3 Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University Medical School, Stanford, CA 94305, United States of America. , (United States)
  • 4 Department of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America. Electronic address: [email protected] , (United States)
Type
Published Article
Journal
Neurobiology of Disease
Publisher
Elsevier
Publication Date
Oct 01, 2019
Volume
130
Pages
104503–104503
Identifiers
DOI: 10.1016/j.nbd.2019.104503
PMID: 31202913
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

One in three people will develop Alzheimer's disease (AD) or another dementia and, despite intense research efforts, treatment options remain inadequate. Understanding the mechanisms of AD pathogenesis remains our principal hurdle to developing effective therapeutics to tackle this looming medical crisis. In light of recent discoveries from whole-genome sequencing and technical advances in humanized models, studying disease risk genes with induced human neural cells presents unprecedented advantages. Here, we first review the current knowledge of the proposed mechanisms underlying AD and focus on modern genetic insights to inform future studies. To highlight the utility of human pluripotent stem cell-based innovations, we then present an update on efforts in recapitulating the pathophysiology by induced neuronal, non-neuronal and a collection of brain cell types, departing from the neuron-centric convention. Lastly, we examine the translational potentials of such approaches, and provide our perspectives on the promise they offer to deepen our understanding of AD pathogenesis and to accelerate the development of intervention strategies for patients and risk carriers. Copyright © 2019 Elsevier Inc. All rights reserved.

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