Neurobiology of aging · 2025
Persistent blood-brain barrier dysregulation in patients with obstructive sleep apnea following long-term continuous positive airway pressure treatment.
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Fernandes Mariana, Placidi Fabio, Izzi Francesca, Nuccetelli Marzia, Bernardini Sergio, Mercuri Nicola Biagio, Liguori Claudio
Аннотация
INTRODUCTION: Blood-brain barrier (BBB) dysfunction has been hypothesized to be a triggering factor in neurodegeneration. This study compared moderate-severe obstructive sleep apnea (OSA) patients with controls to evaluate the effects of this sleep disorder on BBB integrity, as well as explore the impact of continuous positive airway pressure (CPAP) treatment on BBB.
METHODS: This study included moderate-severe OSA patients, OSA patients being treated with CPAP for at least 12 months (OSA-CPAP), and a control group with no neurological or psychiatric diseases. Participants underwent neurological examination, cognitive assessment (to exclude cognitive impairment) and lumbar puncture for cerebrospinal-fluid (CSF) biomarkers analysis [β-amyloid42 (Aβ42), total-tau, phosphorylated tau, ratio between CSF and serum albumin levels (Qalb)].
RESULTS: 38 moderate-severe OSA patients (mean age 65.50 ± 9.16), 12 patients with OSA treated with CPAP (OSA-CPAP, mean age 65.42 ± 6.45) and 25 controls (mean age 65.64 ± 8.10) were included. Moderate-severe OSA patients showed higher Qalb than controls (p = 0.026); also OSA-CPAP patients presented higher Qalb than controls (p = 0.044). Qalb did not differ comparing moderate-severe OSA and OSA-CPAP groups. OSA patients showed lower CSF Aβ42 levels compared to both controls (p < 0.001) and the OSA-CPAP patients (p < 0.001).
CONCLUSIONS: These findings confirmed CSF Aβ42 alteration and documented BBB dysfunction, as indicated by the higher Qalb, in OSA patients. The metabolic and oxidative damage caused by hypoxia could account for these phenomenona; however, the BBB impairment seems to be not reversible, as OSA-CPAP patients presented the BBB alteration although normal CSF Aβ42 levels. Further studies exploring BBB function and its clinical implication for neurodegeneration in OSA are needed.
METHODS: This study included moderate-severe OSA patients, OSA patients being treated with CPAP for at least 12 months (OSA-CPAP), and a control group with no neurological or psychiatric diseases. Participants underwent neurological examination, cognitive assessment (to exclude cognitive impairment) and lumbar puncture for cerebrospinal-fluid (CSF) biomarkers analysis [β-amyloid42 (Aβ42), total-tau, phosphorylated tau, ratio between CSF and serum albumin levels (Qalb)].
RESULTS: 38 moderate-severe OSA patients (mean age 65.50 ± 9.16), 12 patients with OSA treated with CPAP (OSA-CPAP, mean age 65.42 ± 6.45) and 25 controls (mean age 65.64 ± 8.10) were included. Moderate-severe OSA patients showed higher Qalb than controls (p = 0.026); also OSA-CPAP patients presented higher Qalb than controls (p = 0.044). Qalb did not differ comparing moderate-severe OSA and OSA-CPAP groups. OSA patients showed lower CSF Aβ42 levels compared to both controls (p < 0.001) and the OSA-CPAP patients (p < 0.001).
CONCLUSIONS: These findings confirmed CSF Aβ42 alteration and documented BBB dysfunction, as indicated by the higher Qalb, in OSA patients. The metabolic and oxidative damage caused by hypoxia could account for these phenomenona; however, the BBB impairment seems to be not reversible, as OSA-CPAP patients presented the BBB alteration although normal CSF Aβ42 levels. Further studies exploring BBB function and its clinical implication for neurodegeneration in OSA are needed.