Ozone Inhibits APP/Aβ Production and Improves Cognition in an APP/PS1 Transgenic Mouse Model

Alzheimer's disease (AD) is a progressive neurodegenerative disorder without effective treatment. Accumulating evidence demonstrates the production and deposition of amyloid-β peptides (Aβ) in the pathological mechanism of this disease. In our study, we investigated the effect of an ozone intraperitoneal injection on AD pathology in APP/PS1 transgenic mouse model. The male mice (5-months-old) received either ozone intraperitoneal injection (at 30 μg/ml or 50 μg/ml) or abdominocentesis administration daily for 25 days, and they were evaluated in the Morris water maze and the open field test for improvements in spatial learning-memory and working memory and anxious. Prefrontal cortex and hippocampus amyloid-β precursor protein (APP), along with other relevant biomarkers for AD, were measured through ELISA, western blot and immunohistochemistry. Results showed that ozone ameliorated the behavioral and pathological deterioration of APP/PS1 transgenic mice, and reduced the level of APP, which supports the therapeutic potential of administration of ozone in APP/PS1 mice.