Sleep medicine · 2026
Obstructive sleep apnea, biomarker profiles, and clinical progression in Parkinson's disease: Longitudinal effects of CPAP therapy.
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Zhu Shasha, An Di, Liu Xiaoxi
Аннотация
BACKGROUND: Obstructive sleep apnea (OSA) is common in Parkinson's disease (PD) and may exacerbate neurodegeneration via inflammatory and glial mechanisms, yet longitudinal biomarker data are scarce. We aimed to compare inflammatory, glial, and neurodegenerative biomarkers in PD patients with and without OSA, assess associations between OSA severity and biomarker levels, evaluate biomarker-symptom relationships, and determine the longitudinal effects of continuous positive airway pressure (CPAP) therapy on clinical and biomarker outcomes.
METHODS: In this 12-month prospective cohort study, 140 PD patients (PD + OSA n = 72; PD-OSA n = 68) underwent polysomnography, clinical evaluations, and blood/CSF sampling. Biomarkers included IL-1β, IL-18, IL-6, TNF-α, CRP, CHI3L1, S100B, GFAP, and NfL. Cross-sectional and longitudinal associations were analyzed using multivariable regression and linear mixed-effects models. CPAP-treated participants were stratified by adherence. Mediation analyses (5000 bootstraps) assessed pathways linking biomarker changes to clinical improvement.
RESULTS: Among 140 patients with Parkinson's disease (PD), 72 (51.4 %) had obstructive sleep apnea (OSA). PD + OSA showed higher BMI (27.41 vs 25.92 kg/m2; P = 0.018), worse ESS (10.91 vs 8.42; P < 0.001), and lower MoCA (24.41 vs 25.82; P = 0.009). Sleep studies confirmed markedly elevated AHI (24.82 vs 4.82/h; P < 0.001) and deeper desaturation. PD + OSA displayed higher inflammatory (IL-1β, IL-6, TNF-α), glial (CHI3L1, GFAP, S100B), and neurodegeneration markers (NfL; 1584 vs 1291 pg/mL; P = 0.001). OSA severity correlated strongly with biomarker levels, especially ODI (e.g., IL-6 β = 0.40; P < 0.001; NfL β = 0.34; P = 0.001). Biomarkers predicted symptoms: IL-6 with UPDRS III, CHI3L1 with ESS, and NfL with MoCA decline. Longitudinally, PD + OSA worsened faster in motor (UPDRS III +2.34 vs + 1.12/year; P < 0.001), non-motor, and cognitive outcomes (MoCA -1.01 vs -0.42/year; P = 0.003). Among 58 PD + OSA initiating CPAP, 29 were adherent. Adherence reduced AHI (-12.60; P < 0.001), slowed motor decline (UPDRS III -0.62 vs + 2.41/year; P < 0.001), preserved cognition, and lowered IL-6, TNF-α, CRP, CHI3L1, and S100B. Reductions in IL-6 and NfL mediated ∼40 % of CPAP's motor benefits, and CHI3L1 mediated improvements in daytime sleepiness.
CONCLUSIONS: OSA substantially enhances inflammatory, glial, and neuroaxonal injury pathways in PD and contributes to worse motor, non-motor, and cognitive outcomes. CPAP therapy attenuates these pathological processes and improves clinical symptoms, suggesting a mechanistic basis for incorporating OSA screening and treatment into comprehensive PD management.
METHODS: In this 12-month prospective cohort study, 140 PD patients (PD + OSA n = 72; PD-OSA n = 68) underwent polysomnography, clinical evaluations, and blood/CSF sampling. Biomarkers included IL-1β, IL-18, IL-6, TNF-α, CRP, CHI3L1, S100B, GFAP, and NfL. Cross-sectional and longitudinal associations were analyzed using multivariable regression and linear mixed-effects models. CPAP-treated participants were stratified by adherence. Mediation analyses (5000 bootstraps) assessed pathways linking biomarker changes to clinical improvement.
RESULTS: Among 140 patients with Parkinson's disease (PD), 72 (51.4 %) had obstructive sleep apnea (OSA). PD + OSA showed higher BMI (27.41 vs 25.92 kg/m2; P = 0.018), worse ESS (10.91 vs 8.42; P < 0.001), and lower MoCA (24.41 vs 25.82; P = 0.009). Sleep studies confirmed markedly elevated AHI (24.82 vs 4.82/h; P < 0.001) and deeper desaturation. PD + OSA displayed higher inflammatory (IL-1β, IL-6, TNF-α), glial (CHI3L1, GFAP, S100B), and neurodegeneration markers (NfL; 1584 vs 1291 pg/mL; P = 0.001). OSA severity correlated strongly with biomarker levels, especially ODI (e.g., IL-6 β = 0.40; P < 0.001; NfL β = 0.34; P = 0.001). Biomarkers predicted symptoms: IL-6 with UPDRS III, CHI3L1 with ESS, and NfL with MoCA decline. Longitudinally, PD + OSA worsened faster in motor (UPDRS III +2.34 vs + 1.12/year; P < 0.001), non-motor, and cognitive outcomes (MoCA -1.01 vs -0.42/year; P = 0.003). Among 58 PD + OSA initiating CPAP, 29 were adherent. Adherence reduced AHI (-12.60; P < 0.001), slowed motor decline (UPDRS III -0.62 vs + 2.41/year; P < 0.001), preserved cognition, and lowered IL-6, TNF-α, CRP, CHI3L1, and S100B. Reductions in IL-6 and NfL mediated ∼40 % of CPAP's motor benefits, and CHI3L1 mediated improvements in daytime sleepiness.
CONCLUSIONS: OSA substantially enhances inflammatory, glial, and neuroaxonal injury pathways in PD and contributes to worse motor, non-motor, and cognitive outcomes. CPAP therapy attenuates these pathological processes and improves clinical symptoms, suggesting a mechanistic basis for incorporating OSA screening and treatment into comprehensive PD management.
Предметные рубрики MeSH
HumansSleep Apnea, ObstructiveContinuous Positive Airway PressureBiomarkersParkinson DiseaseMaleFemaleMiddle AgedAgedProspective StudiesDisease ProgressionPolysomnographyLongitudinal StudiesS100 Calcium Binding Protein beta SubunitInterleukin-6Glial Fibrillary Acidic ProteinInterleukin-1betaCross-Sectional StudiesTumor Necrosis Factor-alphaChitinase-3-Like Protein 1Neurofilament ProteinsInterleukin-18