Multi-omics delineate growth factor network underlying exercise effects in an Alzheimer's mouse model.

ABSTRACT:

Introduction

Physical exercise is a primary defense against age-related cognitive decline and Alzheimer's disease (AD).

Methods

We conducted single-nucleus transcriptomic and chromatin accessibility analyses (snRNA-seq and snATAC-seq) on the hippocampus of mice carrying mutations in the amyloid precursor protein gene (APP^NL-G-F) following prolonged voluntary wheel-running exercise.

Results

Exercise mitigates amyloid-induced changes in transcriptome and chromatin accessibility through cell type-specific regulatory networks converging on growth factor signaling, particularly the epidermal growth factor receptor (EGFR) signaling. The beneficial effects of exercise on neurocognition can be blocked by pharmacological inhibition of EGFR and its downstream PI3K si

SUBMITTER: Li X 

PROVIDER: S-EPMC11953571 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature