NADPH Oxidase Activity and Cognitive Deficits in Sleep Apnea
Author Information
Author(s): Nair Deepti, Dayyat Ehab A., Zhang Shelley X., Wang Yang, Gozal David
Primary Institution: Department of Pediatrics, Pritzker School of Medicine, University of Chicago, Chicago, Illinois, United States of America
Hypothesis
Excessive NADPH oxidase activity mediates cognitive deficits induced by intermittent hypoxia in a murine model of sleep apnea.
Conclusion
The study found that NADPH oxidase activity contributes to cognitive and behavioral impairments caused by intermittent hypoxia during sleep.
Supporting Evidence
- Wild-type mice exposed to intermittent hypoxia showed significant deficits in spatial learning compared to controls.
- Anxiety levels were increased in wild-type mice exposed to intermittent hypoxia.
- gp91phox-/Y mice did not exhibit the same cognitive deficits as wild-type mice when exposed to intermittent hypoxia.
Takeaway
Mice exposed to low oxygen levels during sleep had trouble learning and remembering things, but those without a specific enzyme (NADPH oxidase) did much better.
Methodology
Mice were exposed to intermittent hypoxia and tested in the Morris water maze and elevated plus maze to assess learning, memory, and anxiety.
Limitations
The study was conducted in a murine model, which may not fully replicate human conditions.
Participant Demographics
Male hemizygous gp91phox-/Y and C57BL/6J mice, aged 20-22 grams.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.001
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website