A novel mechanism of synaptic and cognitive impairments mediated via microRNA-30b in Alzheimer's disease.

ABSTRACT:

Background

It is widely accepted that cognitive and memory deficits in Alzheimer's disease (AD) primarily result from synaptic failure. However, the mechanisms that underlie synaptic and cognitive dysfunction remain unclear.

Methods

We utilized molecular biology techniques, electrophysiological recordings, fluorescence in situ hybridization (FISH), immuno- and Golgi-staining, chromatin immunoprecipitation (CHIP); lentivirus (LV)-based microRNA overexpression and 'sponging', and behavioral tests to assess upregulated miR-30b causing synaptic and cognitive declines in APP transgenic (TG) mice.

Findings

We provide evidence that expression of miR-30b, which targets molecules important for maintaining synaptic integrity, including ephrin type-B receptor 2 (ephB2), sirtuin1

SUBMITTER: Song Y 

PROVIDER: S-EPMC6354659 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature