Effect of regular exercise on ocular inflammation and mitochondrial biogenesis in experimental Alzheimer's disease model.

Abstract

This study investigates the effects of regular exercise on inflammation and mitochondrial biogenesis in the eye using a controlled experimental Alzheimer's disease (AD) model. Twenty-four male Wistar rats were divided into four groups: control, Alzheimer, exercise, and Alzheimer with exercise. Molecular markers, including Nuclear Factor Kappa B (NF-κB), Fibronectin Type III Domain-Containing Protein 5 (FNDC5), Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-Alpha (PGC-1α), Sirtuin 1 (SIRT1) were analyzed through real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) Matrix Metalloproteinase 2 (MMP-2), and Interleukin-1 Beta (IL-1β) were analyzed enzyme-linked immunosorbent assay (ELISA)  to evaluate exercise-induced changes in inflammation and mitochondrial function. NF-κB levels were significantly elevated in the Alzheimer group, reflecting neuroinflammation, while exercise partially mitigated these effects. Exercise increased FNDC5, PGC-1α, and SIRT1 levels, suggesting a role in promoting neuroprotection and mitochondrial biogenesis. However, MMP-2 and IL-1β effects were primarily observed at the gene expression level, without substantial changes in protein levels. The use of an Alzheimer-specific model reduced confounding factors, such as age-related pathologies, providing a clearer perspective on Alzheimer-associated ocular changes. These findings highlight the potential of exercise in modulating key molecular pathways involved in AD.