Obstructive sleep apnea (OSA) is associated with widespread higher-order cognitive consequences, including deficits in memory and executive function. However, the specific cognitive architecture and underlying mechanisms that link the disease’s pathophysiology to these broad cognitive changes remain poorly understood. This study tested the hypothesis that a selective vulnerability of the working memory (WM) executive control system serves as a central hub, mechanistically mediating the relationship between OSA disease burden and memory retention.

Thirty male patients with OSA underwent comprehensive polysomnography and neurocognitive assessment. A data-driven Global Severity Index (GSI) was derived from principal component analysis of the most cognitively-relevant physiological metrics. A multi-task paradigm was used to dissociate performance on tasks of WM maintenance capacity from those requiring executive control. Hierarchical linear regression and mediation analyses were performed, controlling for relevant covariates.

A higher GSI was consistently associated with poorer performance across multiple tasks requiring executive control, but not with measures of WM maintenance capacity or attentional control. Critically, the a priori defined mediation model was supported: the relationship between the GSI and memory retention performance was fully mediated by a latent Executive Control Factor (ECF) derived from the executive tasks.

Our findings delineate a specific mechanistic pathway for the cognitive consequences of OSA. The disease’s pathophysiological burden is selectively associated with executive control performance, and this vulnerability appears to serve as a core mechanism that accounts for the disorder’s downstream impact on memory function. This work identifies executive control as a critical target for mitigating the broader cognitive impact of OSA.