Document Detail

Cellular prion protein and Alzheimer disease: link to oligomeric amyloid-β and neuronal cell death.
MedLine Citation:
PMID:  23154635     Owner:  NLM     Status:  MEDLINE    
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.
Wataru Kudo; Robert B Petersen; Hyoung-Gon Lee
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-11-15
Journal Detail:
Title:  Prion     Volume:  7     ISSN:  1933-690X     ISO Abbreviation:  Prion     Publication Date:    2013 Mar-Apr
Date Detail:
Created Date:  2013-03-08     Completed Date:  2013-12-30     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  101472305     Medline TA:  Prion     Country:  United States    
Other Details:
Languages:  eng     Pagination:  114-6     Citation Subset:  IM    
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MeSH Terms
Alzheimer Disease / metabolism*,  pathology
Amyloid beta-Peptides / metabolism*
Cell Death
Neurons / metabolism*,  pathology
Prion Diseases / metabolism*,  pathology
Prions / metabolism*
Grant Support
Reg. No./Substance:
0/Amyloid beta-Peptides; 0/Prions

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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