title: 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 (PrP (C) ) 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-PrP (C) antibody or PrP (C) peptide was able to block oligomeric Aβ-induced neurotoxicity. These findings demonstrate that PrP (C) may be involved in neuropathologic conditions other than conventional prion diseases, i.e., Creutzfeldt-Jakob disease.
authors.affiliation: Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
authors.forename: Wataru
authors.initials: W
authors.lastname: Kudo
authors.forename: Robert B
authors.initials: RB
authors.lastname: Petersen
authors.forename: Hyoung-Gon
authors.initials: HG
authors.lastname: Lee
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D016923:Cell Death; D006801:Humans; D051379:Mice; D009474:Neurons / Q000378:metabolism* / Q000473:pathology; D017096:Prion Diseases / Q000378:metabolism* / Q000473:pathology; D011328:Prions / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D011328:Prions