Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression
Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression
About this item
Full title
Author / Creator
Publisher
England: BioMed Central
Journal title
Language
English
Formats
Publication information
Publisher
England: BioMed Central
Subjects
More information
Scope and Contents
Contents
The amyloid cascade hypothesis posits that the initiating event in Alzheimer's disease (AD) is the aggregation and deposition of the β-amyloid (Aβ) peptide, which is a proteolytic cleavage product of the amyloid precursor protein (APP). Mounting evidence suggests that the formation and spread of prion-like Aβ aggregates during AD may contribute to...
Alternative Titles
Full title
Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression
Authors, Artists and Contributors
Identifiers
Primary Identifiers
Record Identifier
TN_cdi_doaj_primary_oai_doaj_org_article_e8779bde378d4e898068a96d4935bbd0
Permalink
https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_e8779bde378d4e898068a96d4935bbd0
Other Identifiers
ISSN
2051-5960
E-ISSN
2051-5960
DOI
10.1186/s40478-018-0529-x