Kruppel-like factor 5 accelerates the pathogenesis of Alzheimer's disease via BACE1-mediated APP processing.

ABSTRACT:

Background

The deposition of β-amyloid (Aβ) in the brain plays a major role in the pathogenesis of Alzheimer's disease (AD). Aβ is generated via amyloid precursor protein (APP) cleavage through the amyloidogenic pathway. In this pathway, β-secretase (BACE1) is the first and rate-limiting enzyme. Its expression increases through an unknown mechanism in patients with AD. Thus, the key regulatory mechanism of BACE1 in the AD process should be revealed to understand the pathogenesis of AD and explore the key treatment targets of AD.

Methods

Here, APPswe/PS1dE9 (APP/PS1) mice were employed to observe the Krüppel-like factor 5 (KLF5) and BACE1 levels in the serum and brain tissues. HT22 cells were used to explore the relationship between KLF5 and BACE1.

Results

In this stud

SUBMITTER: Wang Y 

PROVIDER: S-EPMC9316766 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature