Bidirectional relationship between 56 peripheral inflammatory regulators and sleep apnea syndrome: A Mendelian...

Area of Science:

• Genetics
• Immunology
• Neurology

Background:

• Peripheral inflammation is implicated in sleep apnea syndrome (SAS) pathogenesis and outcomes.
• Previous research has not explored the genetic underpinnings of this relationship.

Purpose of the Study:

• To investigate the genetic interaction between 56 peripheral inflammatory regulators and SAS.
• To examine the genetic association of SAS-related inflammatory regulators with neurological disorders like cerebral atherosclerosis and vascular dementia.

Main Methods:

• Utilized genome-wide association study data for SAS, cerebral atherosclerosis, vascular dementia, and peripheral inflammatory markers.
• Employed Two-sample Mendelian randomization for causal inference of exposure and outcome.
• Analyses were conducted using R statistical software.

Main Results:

• Higher IL-25 and lower IL-23, IL-24, IL-36γ, and MIP-1a levels were associated with increased SAS risk.
• SAS was linked to decreased peripheral levels of IL-17A, IL-23, IL-27, IL-36α, and TRAIL.
• Decreased IL-17A and IL-27 were associated with higher cerebral atherosclerosis risk; decreased TRAIL was linked to increased vascular dementia risk.

Conclusions:

• A genetic interaction exists between peripheral inflammation and SAS.
• Peripheral inflammation may play a role in the mechanism by which SAS contributes to neurological diseases.