Rescue of cognitive deficits in APP/PS1 mice by accelerating the aggregation of β-amyloid peptide.

ABSTRACT:

Background

Brain amyloid deposition is one of the main pathological characteristics of Alzheimer's disease (AD). Soluble oligomers formed during the process that causes β-amyloid (Aβ) to aggregate into plaques are considered to have major neurotoxicity. Currently, drug development for the treatment of Alzheimer's disease has encountered serious difficulties. Our newly proposed solution is to accelerate the aggregation of Aβ to reduce the amount of cytotoxic Aβ oligomers in brain tissue. This strategy differs from the existing strategy of reducing the total Aβ content and the number of amyloid plaques.

Method

In this study, we screened a small library and found that a flavonoid compound (ZGM1) promoted the aggregation of β-amyloid (Aβ). We further verified the binding of ZGM1

SUBMITTER: Zhang JX 

PROVIDER: S-EPMC6918606 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature