Back to Search
Start Over
Ozone Inhibits APP/Aβ Production and Improves Cognition in an APP/PS1 Transgenic Mouse Model.
- Source :
-
Neuroscience [Neuroscience] 2019 Oct 15; Vol. 418, pp. 110-121. Date of Electronic Publication: 2019 Jul 23. - Publication Year :
- 2019
-
Abstract
- 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.<br /> (Copyright © 2019. Published by Elsevier Ltd.)
- Subjects :
- Alzheimer Disease drug therapy
Alzheimer Disease pathology
Amyloid beta-Peptides drug effects
Amyloid beta-Peptides metabolism
Amyloid beta-Protein Precursor drug effects
Animals
Brain metabolism
Cognition Disorders drug therapy
Cognition Disorders pathology
Disease Models, Animal
Memory, Short-Term drug effects
Mice, Transgenic
Amyloid beta-Protein Precursor metabolism
Brain drug effects
Cognition drug effects
Ozone pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1873-7544
- Volume :
- 418
- Database :
- MEDLINE
- Journal :
- Neuroscience
- Publication Type :
- Academic Journal
- Accession number :
- 31349006
- Full Text :
- https://doi.org/10.1016/j.neuroscience.2019.07.027