University of Texas at San Antonio

Publication Detail

The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.

Cellular prion protein is essential for oligomeric amyloid-β-induced neuronal cell death.

Wataru Kudo; Hyun-Pil Lee; Wen-Quan Zou; Xinglong Wang; George Perry; Xiongwei Zhu; Mark A Smith; Robert B Petersen; Hyoung-gon Lee (Profiled Authors: Zhu, Xiongwei; Perry, George)

Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Human molecular genetics 2012;21(5):1138-44.

In Alzheimer disease (AD), amyloid-β (Aβ) oligomer is suggested to play a critical role in imitating neurodegeneration, although its pathogenic mechanism remains to be determined. Recently, the cellular prion protein (PrP(C)) has been reported to be an essential co-factor in mediating the neurotoxic effect of Aβ oligomer. However, these previous studies focused on the synaptic plasticity in either the presence or the absence of PrP(C) and no study to date has reported whether PrP(C) is required for the neuronal cell death, the most critical element of neurodegeneration in AD. Here, we show that Prnp(-/-) mice are resistant to the neurotoxic effect of Aβ oligomer in vivo and in vitro. Furthermore, application of an anti-PrP(C) antibody or PrP(C) peptide prevents Aβ oligomer-induced neurotoxicity. These findings are the first to demonstrate that PrP(C) is required for Aβ oligomer-induced neuronal cell death, the pathology essential to cognitive loss.

1 Originating Grant

• 1.

  SMITH, MARK A

  Role of Cell Cycle in Neurodegeneration

  1 March 2008 - 28 February 2013

  NATIONAL INSTITUTE ON AGING

  Total Funding: $ 960,623

Scientific Context

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