Mutations in the β-amyloid precursor protein in familial Alzheimer's disease increase Aβ oligomer production in cellular models.

ABSTRACT: Soluble oligomers of amyloid-β (Aβ) peptides (AβOs) contribute to neurotoxicity in Alzheimer's disease (AD). However, it currently remains unknown whether an increase in AβOs is the common phenotype in cellular and animal models. Furthermore, it has not yet been established whether experimental studies conducted using models overexpressing mutant genes of the amyloid precursor protein (APP) are suitable for investigating the underlying molecular mechanism of AD. We herein employed the Flp-In™ T-REx™-293 (T-REx 293) cellular system transfected with a single copy of wild-type, Swedish-, Dutch-, or London-type APP, and quantified the levels of Aβ monomers (Aβ1-40 and Aβ1-42) and AβOs using an enzyme-linked immunosorbent assay (ELISA). The levels of extracellular AβOs were significantly higher

SUBMITTER: Ohshima Y 

PROVIDER: S-EPMC5857613 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature