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Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells

Author

Listed:
  • Mason A. Israel

    (University of California, San Diego, La Jolla, California 92093, USA
    Biomedical Sciences Graduate Program, University of California, San Diego, La Jolla, California 92093, USA)

  • Shauna H. Yuan

    (University of California, San Diego, La Jolla, California 92093, USA
    University of California, San Diego, La Jolla, California, USA)

  • Cedric Bardy

    (The Salk Institute for Biological Studies)

  • Sol M. Reyna

    (University of California, San Diego, La Jolla, California 92093, USA
    Biomedical Sciences Graduate Program, University of California, San Diego, La Jolla, California 92093, USA)

  • Yangling Mu

    (The Salk Institute for Biological Studies)

  • Cheryl Herrera

    (University of California, San Diego, La Jolla, California 92093, USA)

  • Michael P. Hefferan

    (University of California, San Diego, La Jolla, California 92093, USA)

  • Sebastiaan Van Gorp

    (Maastricht University Medical Center)

  • Kristopher L. Nazor

    (The Scripps Research Institute)

  • Francesca S. Boscolo

    (University of California, San Diego, La Jolla, California 92093, USA)

  • Christian T. Carson

    (BD Biosciences)

  • Louise C. Laurent

    (University of California, San Diego, La Jolla, California 92093, USA)

  • Martin Marsala

    (University of California, San Diego, La Jolla, California 92093, USA
    Institute of Neurobiology, Slovak Academy of Sciences, Kosice SK-04001, Slovakia)

  • Fred H. Gage

    (The Salk Institute for Biological Studies)

  • Anne M. Remes

    (Neurology and Clinical Research Center, University of Oulu, Oulu FIN-90015, Finland)

  • Edward H. Koo

    (University of California, San Diego, La Jolla, California, USA)

  • Lawrence S. B. Goldstein

    (University of California, San Diego, La Jolla, California 92093, USA
    University of California, San Diego, La Jolla, California, USA)

Abstract

Induced pluripotent stem cells are shown to be useful for studying phenotypes relevant to familial and sporadic Alzheimer’s disease, even though it can take decades for the disease to manifest in patients.

Suggested Citation

  • Mason A. Israel & Shauna H. Yuan & Cedric Bardy & Sol M. Reyna & Yangling Mu & Cheryl Herrera & Michael P. Hefferan & Sebastiaan Van Gorp & Kristopher L. Nazor & Francesca S. Boscolo & Christian T. Ca, 2012. "Probing sporadic and familial Alzheimer’s disease using induced pluripotent stem cells," Nature, Nature, vol. 482(7384), pages 216-220, February.
    • Handle: RePEc:nat:nature:v:482:y:2012:i:7384:d:10.1038_nature10821
    DOI: 10.1038/nature10821
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    Cited by:

    1. Zoë P. Van Acker & Anika Perdok & Ruben Hellemans & Katherine North & Inge Vorsters & Cedric Cappel & Jonas Dehairs & Johannes V. Swinnen & Ragna Sannerud & Marine Bretou & Markus Damme & Wim Annaert, 2023. "Phospholipase D3 degrades mitochondrial DNA to regulate nucleotide signaling and APP metabolism," Nature Communications, Nature, vol. 14(1), pages 1-21, December.
    2. Jennifer P. Nguyen & Timothy D. Arthur & Kyohei Fujita & Bianca M. Salgado & Margaret K. R. Donovan & Hiroko Matsui & Ji Hyun Kim & Agnieszka D’Antonio-Chronowska & Matteo D’Antonio & Kelly A. Frazer, 2023. "eQTL mapping in fetal-like pancreatic progenitor cells reveals early developmental insights into diabetes risk," Nature Communications, Nature, vol. 14(1), pages 1-22, December.
    3. Hannah Drew Rickner & Lulu Jiang & Rui Hong & Nicholas K. O’Neill & Chromewell A. Mojica & Benjamin J. Snyder & Lushuang Zhang & Dipan Shaw & Maria Medalla & Benjamin Wolozin & Christine S. Cheng, 2022. "Single cell transcriptomic profiling of a neuron-astrocyte assembloid tauopathy model," Nature Communications, Nature, vol. 13(1), pages 1-22, December.
    4. Chiara Scopa & Samantha M. Barnada & Maria E. Cicardi & Mo Singer & Davide Trotti & Marco Trizzino, 2023. "JUN upregulation drives aberrant transposable element mobilization, associated innate immune response, and impaired neurogenesis in Alzheimer’s disease," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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