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Cognitive function in prepubertal children with obstructive sleep apnea: a modifying role for NADPH oxidase p22
David Gozal1, Abdelnaby Khalyfa, Oscar Sans Capdevila
1Section of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, University of Chicago, Illinois, USA. dgozal@peds.bsd.uchicago.edu
Antioxidants & Redox Signaling
|September 10, 2011
Summary
Genetic variations in NADPH oxidase (NOX) genes may influence cognitive deficits in children with obstructive sleep apnea (OSA). Specific NOX polymorphisms, like rs4673, were linked to better neurocognitive outcomes in children with OSA.
Area of Science:
- Genetics
- Pediatric Sleep Medicine
- Neuroscience
Background:
- Pediatric obstructive sleep apnea (OSA) is linked to neurocognitive dysfunction in some children.
- The underlying genetic and molecular mechanisms contributing to this variability are not fully understood.
Purpose of the Study:
- To investigate the association between NADPH oxidase (NOX) gene polymorphisms and neurocognitive function in children with OSA.
- To explore the role of oxidative stress markers in relation to NOX polymorphisms and cognitive outcomes.
Main Methods:
- Genotyping for NOX p22phox subunit polymorphisms (rs6520785, rs4673) in children with and without OSA.
- Assessment of neurocognitive deficits in the study cohort.
- Measurement of urinary 8-hydroxydeoxyguanine levels and NOX activity as markers of oxidative stress.
Main Results:
- Frequencies of most NOX polymorphisms were similar between OSA and control groups.
- The rs4673 polymorphism was significantly more frequent in OSA children without cognitive deficits compared to those with deficits (p<0.02).
- Lower urinary 8-hydroxydeoxyguanine levels and NOX activity were observed in children without cognitive deficits, especially those with the rs4673 polymorphism.
Conclusions:
- Polymorphisms in the NOX gene, particularly rs4673, may contribute to the variability in cognitive deficits observed in pediatric OSA.
- These findings suggest a potential role for NOX-related oxidative stress pathways in the neurocognitive impact of OSA in children.
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