"Dual Disease" TgAD/GSS mice exhibit enhanced Alzheimer's disease pathology and reveal PrP^C-dependent secretion of Aβ.

ABSTRACT: To address the question of cross-talk between prion protein (PrP) and Alzheimer's disease (AD), we generated TgAD/GSS mice that develop amyloid-β (Aβ) plaques of AD and PrP (specifically mutated PrP^A116V) plaques of Gerstmann-Sträussler-Scheinker disease (GSS) and compared plaque-related features in these mice to AD mice that express normal (TgAD), high (TgAD/HuPrP), or no (TgAD/PrP^-/-) PrP^C. In contrast to PrP^C, PrP^A116V weakly co-localized to Aβ plaques, did not co-immunoprecipitate with Aβ, and poorly bound to Aβ in an ELISA-based binding assay. Despite the reduced association of PrP^A116V with Aβ, TgAD/GSS and TgAD/HuPrP mice that express comparable levels of PrP^A116V and PrP^C respectively, displayed

SUBMITTER: Qin K 

PROVIDER: S-EPMC6562043 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature