Cellular prion protein and Alzheimer disease: Link to oligomeric amyloid-β and neuronal cell death

 Abstract

Soluble oligomeric amyloid-β (Aβ) has been suggested to impair synaptic and neuronal function, leading to neurodegeneration that is clinically observed as the memory and cognitive dysfunction characteristic of Alzheimer disease, while the precise mechanism(s) whereby oligomeric Aβ causes neurotoxicity remains unknown. Recently, the cellular prion protein (PrPC) was reported to be an essential co-factor in mediating the neurotoxic effect of oligomeric Aβ. Our recent study showed that Prnp−/− mice are resistant to the neurotoxic effect of oligomeric Aβ in vivo and in vitro. Furthermore, application of an anti-PrPC antibody or PrPC peptide was able to block oligomeric Aβ-induced neurotoxicity. These findings demonstrate that PrPC may be involved in neuropathologic conditions other than conventional prion diseases, i.e., Creutzfeldt-Jakob disease.

 Related Article:

W Kudo, HP Lee, WQ Zou, X Wang, G Perry, X Zhu, MA Smith, RB Petersen, HG Lee. Cellular prion protein is essential for oligomeric amyloid-β-induced neuronal cell death. Hum Mol Genet 2012; 21: 1138- 44.
PMID: 22100763 DOI: 10.1093/hmg/ddr542

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114 - 116
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10.4161/pri.22848
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Cellular prion protein and Alzheimer disease: Link to oligomeric amyloid-β and neuronal cell death