| First Author | Lin SY | Year | 2019 |
| Journal | Neuroscience | Volume | 418 |
| Pages | 110-121 | PubMed ID | 31349006 |
| Mgi Jnum | J:283001 | Mgi Id | MGI:6384477 |
| Doi | 10.1016/j.neuroscience.2019.07.027 | Citation | Lin SY, et al. (2019) Ozone Inhibits APP/Abeta Production and Improves Cognition in an APP/PS1 Transgenic Mouse Model. Neuroscience 418:110-121 |
| abstractText | Alzheimer's disease (AD) is a progressive neurodegenerative disorder without effective treatment. Accumulating evidence demonstrates the production and deposition of amyloid-beta peptides (Abeta) 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 30mug/ml or 50mug/ml) or abdominocentesis administration daily for 25days, 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-beta 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. |
