Article
Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression.
Acta neuropathologica communications - 3 Apr 2018
Ruiz-Riquelme Alejandro, Lau Heather H C, Stuart Erica, Goczi Adrienn N, Wang Zhilan, Schmitt-Ulms Gerold, Watts Joel C
Abstract excerpt
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 disease progression. Inoculation of transgenic mice that...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.