Inhibition of formyl peptide receptors improves the outcome in a mouse model of Alzheimer disease.

ABSTRACT:

Background

An important hallmark of Alzheimer's disease (AD) is the increase of Aβ1-42 burden and its accumulation to senile plaques, leading the reactive gliosis and neurodegeneration. The modulation of glia cell function represents an attractive therapeutic strategy, but is currently limited by an incomplete understanding of its relevance for AD. The chemotactic G-protein coupled formyl peptide receptor (FPR), which is known to modulate Aβ1-42 uptake and signal transduction, might be one candidate molecule regulating glia function in AD. Here, we investigate whether the modulation of FPR exerts beneficial effects in an AD preclinical model.

Methods

To address this question, APP/PS1 double-transgenic AD mice were treated for 20 weeks with either the pro-inflammatory FPR ago

SUBMITTER: Schroder N 

PROVIDER: S-EPMC7181500 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature