Background: Obstructive sleep apnea (OSA) is highly prevalent in the early stages of Alzheimer’s disease (AD), and its hallmark, sleep fragmentation, may accelerate cognitive decline. Continuous positive airway pressure (CPAP) improves OSA-related hypoxia during slow-wave sleep, but its cognitive benefits in AD remain unclear. Methods: We performed a 12-month sub-analysis of a prospective, longitudinal pilot study that enrolled 21 adults (median age = 77 yr; 71% women) with Mild Cognitive Impairment (MCI) with AD confirmed biomarkers and polysomnography-diagnosed OSA. All participants underwent baseline overnight polysomnography (PSG) and neuropsychological testing (Clinical Dementia Rating (CDR), Mini-Mental State Examination (MMSE), Repeatable Battery for the Assessment of Neuropsychological Status (RBANS)) that were repeated after 12 months. Twelve participants were CPAP-compliant (moderate/severe OSA) and nine were non-users (mild OSA/intolerance). Cognitive change scores (Δ = 12 months -baseline) were compared with Generalized Linear Models (GLM) adjusted for baseline cognition and Apnea–Hypopnea Index (AHI); associations between baseline sleep parameters and cognitive trajectories were examined. And the association of sleep variables with the use of CPAP was also evaluated. Results: Compared with non-users, CPAP users showed significantly slower global decline (Δ MMSE: p = 0.016) and improvements in overall cognition (Δ RBANS Total: p = 0.028) and RBANS sub-domains (Δ RBANS FC: p = 0.010; Δ RBANS SF: p = 0.045). Longer baseline non-rapid eye movement (NREM) stage 3 and rapid eye movement (REM) sleep, greater total sleep time and sleep efficiency, and right-side sleeping were each linked to better cognitive outcomes, whereas extended NREM stage 2, wakefulness, and supine sleeping were associated with poorer trajectories. Conclusions: Twelve months of CPAP use was associated with attenuated cognitive decline and domain-specific gains in AD-related MCI with OSA. Sleep architecture and body position during sleep predicted cognitive outcomes, underscoring the therapeutic relevance of optimizing breathing and sleep quality. Larger, longer-term trials are warranted to confirm CPAP’s disease-modifying potential and to clarify the mechanistic role of sleep in AD progression.

Background Obstructive sleep apnea (OSA) is highly prevalent in the early stages of Alzheimer’s disease (AD), and its hallmark, sleep fragmentation, may accelerate cognitive decline. Continuous positive airway pressure (CPAP) improves OSA-related hypoxia during slow-wave sleep, but its cognitive benefits in AD remain unclear. Methods We performed a 12-month sub-analysis of a prospective, longitudinal pilot study that enrolled 21 adults (median age = 77 yr; 71% women) with MCI with AD confirmed biomarkers and polysomnography-diagnosed OSA. All participants underwent baseline overnight PSG and neuropsychological testing (CDR, MMSE, RBANS) that were repeated after 12 months. Twelve participants were CPAP-compliant (moderate/severe OSA) and nine were non-users (mild OSA/intolerance). Cognitive change scores (Δ = 12 months – baseline) were compared with generalized linear models adjusted for baseline cognition and apnea-hypopnea index; associations between baseline sleep parameters and cognitive trajectories were examined. And the association of sleep variables with the use of CPAP was also evaluated. Results Compared with non-users, CPAP users showed significantly slower global decline (Δ MMSE: p = 1.60e-02) and improvements in overall cognition (Δ RBANS Total: p = 2.80e-02), and RBANS subdomains (Δ RBANS FC: p = 1.06e-02; Δ RBANS SF: p = 4.53e-02). Longer baseline NREM stage 3 and REM sleep, greater total sleep time and sleep efficiency, and right-side sleeping were each linked to better cognitive outcomes, whereas extended NREM stage 2, wakefulness, and supine sleeping were associated with poorer trajectories. Conclusions Twelve months of CPAP use was associated with attenuated cognitive decline and domain-specific gains in AD-related MCI with OSA. Sleep architecture and body position during sleep predicted cognitive outcomes, underscoring the therapeutic relevance of optimizing breathing and sleep quality. Larger, longer-term trials are warranted to confirm CPAP’s disease-modifying potential and to clarify the mechanistic role of sleep in AD progression.

Background/Objectives: Obesity is associated with cognitive decline, and metabolic bariatric surgery (MBS) can improve both physical and cognitive outcomes. However, cognitive improvements post-surgery are variable. This study explores the role of skeletal muscle health, specifically muscle strength and mass, in cognitive performance after MBS, aiming to identify factors that influence cognitive recovery. Methods: In this prospective study, 55 patients scheduled for MBS were assessed 1 month before and 12 months after surgery. Body composition, including appendicular lean mass (ALM) and fat mass, was measured using dual-energy X-ray absorptiometry (DXA). Handgrip strength (HGS) was assessed via dynamometry, and neurocognitive performance was evaluated using a standardized test battery. Results: Significant improvements in cognitive performance were observed at 12 months post-surgery in attention, memory, language, executive functions and overall cognitive performance. Regarding body composition, significant reductions were observed in fat mass and body mass index (BMI). A decrease in ALM and no changes in HGS were observed; however, when adjusted for body size, both showed an increase. Regression analysis identified baseline HGS, but not muscle mass, as a significant predictor of cognitive performance at 12 months post-surgery. Conclusions: MBS leads to significant improvements in cognitive function. Our results suggest that baseline HGS may play a role in predicting cognitive outcomes post-surgery, highlighting the need for comprehensive assessments of both physical and cognitive health in patients undergoing MBS. Further longitudinal studies are needed to explore causal relationships and the potential reversibility of cognitive deficits post-surgery.