Journal Article

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 and Hyoung-gon Lee

in Human Molecular Genetics

Volume 21, issue 5, pages 1138-1144
Published in print March 2012 | ISSN: 0964-6906
Published online November 2011 | e-ISSN: 1460-2083 | DOI: http://dx.doi.org/10.1093/hmg/ddr542
Cellular prion protein is essential for oligomeric amyloid-β-induced neuronal cell death

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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 (PrPC) 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 PrPC and no study to date has reported whether PrPC 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-PrPC antibody or PrPC peptide prevents Aβ oligomer-induced neurotoxicity. These findings are the first to demonstrate that PrPC is required for Aβ oligomer-induced neuronal cell death, the pathology essential to cognitive loss.

Journal Article.  3033 words.  Illustrated.

Subjects: Genetics and Genomics

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