PPARgamma agonists rescue increased phosphorylation of FGF14 at S226 in the Tg2576 mouse model of Alzheimer's disease.

ABSTRACT:

Background

Cognitive impairment in humans with Alzheimer's disease (AD) and in animal models of Aβ-pathology can be ameliorated by treatments with the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARγ) agonists, such as rosiglitazone (RSG). Previously, we demonstrated that in the Tg2576 animal model of AD, RSG treatment rescued cognitive deficits and reduced aberrant activity of granule neurons in the dentate gyrus (DG), an area critical for memory formation.

Methods

We used a combination of mass spectrometry, confocal imaging, electrophysiology and split-luciferase assay and in vitro phosphorylation and Ingenuity Pathway Analysis.

Results

Using an unbiased, quantitative nano-LC-MS/MS screening, we searched for potential molecular targets of the

SUBMITTER: Hsu WJ 

PROVIDER: S-EPMC5762202 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature