Regulation of PPARα by APP in Alzheimer disease affects the pharmacological modulation of synaptic activity.

ABSTRACT: Among genetic susceptibility loci associated with late-onset Alzheimer disease (LOAD), genetic polymorphisms identified in genes encoding lipid carriers led to the hypothesis that a disruption of lipid metabolism could promote disease progression. We previously reported that amyloid precursor protein (APP) involved in Alzheimer disease (AD) physiopathology impairs lipid synthesis needed for cortical networks' activity and that activation of peroxisome proliferator-activated receptor α (PPARα), a metabolic regulator involved in lipid metabolism, improves synaptic plasticity in an AD mouse model. These observations led us to investigate a possible correlation between PPARα function and full-length APP expression. Here, we report that PPARα expression and activation were inversely related to

SUBMITTER: Saez-Orellana F 

PROVIDER: S-EPMC8410016 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature