Toxic amyloid-β oligomers induced self-replication in astrocytes triggering neuronal injury.

ABSTRACT:

Background

Soluble amyloid-β oligomer (AβO) induced deleterious cascades have recently been considered to be the initiating pathologic agents of Alzheimer's disease (AD). However, little is known about the neurotoxicity and production of different AβOs. Understanding the production and spread of toxic AβOs within the brain is important to improving understanding of AD pathogenesis and treatment.

Methods

Here, PS1V97L transgenic mice, a useful tool for studying the role of AβOs in AD, were used to identify the specific AβO assembly that contributes to neuronal injury and cognitive deficits. Then, we investigated the production and spread of toxic Aβ assemblies in astrocyte and neuron cultures, and further tested the results following intracerebroventricular injection of AβOs

SUBMITTER: Wang W 

PROVIDER: S-EPMC6491655 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature