# CPAP Treatment Exposure, but Not Daytime Sleepiness or Neurofilament Light Chain, Is Associated with Cognitive Performance in Obstructive Sleep Apnea

**Authors:** Sofia Tagini, Stefania Cattaldo, Federica Scarpina, Erica Sabattini, Giulia Chirchio, Elisa Prina, Paolo Piterà, Clara Paschino, Riccardo Cremascoli, Mirna Solange Barrio Lower Daniele, Mauro Cornacchia, Theodore Tsaras, Amelia Brunani, Massimo Scacchi, Paolo Fanari, Alessandro Mauro, Lorenzo Priano

PMC · DOI: 10.3390/jcm15041588 · 2026-02-18

## TL;DR

This study finds that cognitive performance in obstructive sleep apnea is more linked to age, education, and CPAP treatment than to disease severity or sleepiness.

## Contribution

The study shows that CPAP treatment duration, not disease severity or neurofilament levels, is associated with cognitive performance in obstructive sleep apnea.

## Key findings

- Neither apnea severity nor daytime sleepiness significantly predicted cognitive performance.
- Longer CPAP treatment was positively correlated with better verbal memory and problem-solving speed.
- Age and lower education were significant predictors of worse verbal memory.

## Abstract

Background: The mechanisms underlying cognitive impairment in obstructive sleep apnea syndrome (OSAS) remain incompletely understood. In particular, the relative contribution of daytime sleepiness versus the direct effects of hypoxia on the brain requires clarification. Objectives: This study aims to explore the association between verbal memory and problem-solving abilities, OSAS severity, self-reported daytime sleepiness, and neurofilament light chain (NfL) serum concentration, as marker of neuroaxonal injury possibly related to chronic hypoxia. Methods: In this cross-sectional study, cognitive performance was assessed in 72 patients with mild to severe OSAS using the Selective Reminding Test (SRT) and the Tower of London (ToL). The apnea–hypopnea index (AHI), the Epworth Sleepiness Scale (ESS) and serum NfL concentrations were collected. Hierarchical multiple linear regression analyses adjusting for age, years of education, body mass index, and duration of continuous positive airway pressure (CPAP) treatment, were conducted for each cognitive outcome. Results. Neither AHI, ESS scores nor serum NfL concentrations were significantly associated with verbal memory or problem-solving performance. Higher age and lower education were significant predictors of lower verbal memory indices, whereas longer CPAP treatment duration was positively correlated with verbal memory performance and problem-solving speed. Conclusions: In this sample, cognitive performance was more strongly related to demographic factors and CPAP exposure compared to disease severity, subjective sleepiness, or peripheral markers of neuroaxonal injury. These findings suggest that AHI, subjective measures of sleepiness and NfL may inadequately capture neurocognitive vulnerability in OSAS. Moreover, they underscore the imperative for longitudinal and larger studies to clarify mechanisms linking OSAS and cognitive impairments.

## Linked entities

- **Diseases:** obstructive sleep apnea syndrome (MONDO:0007147), obstructive sleep apnea (MONDO:0007147)

## Full-text entities

- **Genes:** NEFL (neurofilament light chain) [NCBI Gene 4747] {aka CMT1F, CMT2E, CMTDIG, NF-L, NF68, NFL}
- **Diseases:** Chronic intermittent hypoxia (MESH:D000860), axonal injury (MESH:D001480), cognitive decline (MESH:D003072), breathing disorder (MESH:D012891), Sleepiness (MESH:D000077260), neuroaxonal damage (MESH:D019150), deficits in (MESH:D009461), upper airway obstruction (MESH:D000402), executive dysfunction (MESH:D006331), functions (MESH:D003291), renal dysfunction (MESH:D007674), hypoxic (MESH:D002534), obese (MESH:D009765), neurological disease (MESH:D020271), white-matter abnormalities (MESH:D056784), AHI (MESH:D020181), sleep fragmentation (MESH:D012892), respiratory dysfunction (MESH:D012131), neuronal damage (MESH:D009410), neuroinflammation (MESH:D000090862), weight (MESH:D015431), attentional and memory deficits (MESH:D001289), Impairment in attention and vigilance, memory, visuospatial abilities, and (OMIM:313000), sensory deficits (MESH:D012678), neurotoxic (MESH:D020258), cardiovascular, metabolic disease (MESH:D002318), neural damage (MESH:D015441), alcohol or substance abuse (MESH:D019966), psychiatric or neurological disorders (MESH:D001523), ToL (MESH:C563785), brain (MESH:D001927), Daytime Sleepiness (MESH:D012893), cerebral hypoperfusion (MESH:D002547), inflammation (MESH:D007249), neurodegeneration (MESH:D019636), Excessive daytime sleepiness (MESH:D006970), injury to (MESH:D014947)
- **Chemicals:** oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

---
Source: https://tomesphere.com/paper/PMC12942159