IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v4y2013i1d10.1038_ncomms3932.html
   My bibliography  Save this article

RETRACTED ARTICLE: Pericyte loss influences Alzheimer-like neurodegeneration in mice

Author

Listed:
  • Abhay P. Sagare

    (Keck School of Medicine, Zilkha Neurogenetic Institute, University of Southern California)

  • Robert D. Bell

    (Center of Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center)

  • Zhen Zhao

    (Keck School of Medicine, Zilkha Neurogenetic Institute, University of Southern California)

  • Qingyi Ma

    (Keck School of Medicine, Zilkha Neurogenetic Institute, University of Southern California)

  • Ethan A. Winkler

    (Center of Neurodegenerative and Vascular Brain Disorders, University of Rochester Medical Center)

  • Anita Ramanathan

    (Keck School of Medicine, Zilkha Neurogenetic Institute, University of Southern California)

  • Berislav V. Zlokovic

    (Keck School of Medicine, Zilkha Neurogenetic Institute, University of Southern California)

Abstract

Pericytes are cells in the blood–brain barrier that degenerate in Alzheimer’s disease (AD), a neurological disorder associated with neurovascular dysfunction, abnormal elevation of amyloid β-peptide (Aβ), tau pathology and neuronal loss. Whether pericyte degeneration can influence AD-like neurodegeneration and contribute to disease pathogenesis remains, however, unknown. Here we show that in mice overexpressing Aβ-precursor protein, pericyte loss elevates brain Aβ40 and Aβ42 levels and accelerates amyloid angiopathy and cerebral β-amyloidosis by diminishing clearance of soluble Aβ40 and Aβ42 from brain interstitial fluid prior to Aβ deposition. We further show that pericyte deficiency leads to the development of tau pathology and an early neuronal loss that is normally absent in Aβ-precursor protein transgenic mice, resulting in cognitive decline. Our data suggest that pericytes control multiple steps of AD-like neurodegeneration pathogenic cascade in Aβ-precursor protein-overexpressing mice. Therefore, pericytes may represent a novel therapeutic target to modify disease progression in AD.

Suggested Citation

  • Abhay P. Sagare & Robert D. Bell & Zhen Zhao & Qingyi Ma & Ethan A. Winkler & Anita Ramanathan & Berislav V. Zlokovic, 2013. "RETRACTED ARTICLE: Pericyte loss influences Alzheimer-like neurodegeneration in mice," Nature Communications, Nature, vol. 4(1), pages 1-14, December.
  • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3932
    DOI: 10.1038/ncomms3932
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms3932
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/ncomms3932?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3932. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.