Associations between obstructive sleep apnea and Alzheimer's disease-related biomarkers (amyloid-β and tau) in blood and cerebrospinal fluid: a systematic review and meta-analysis.
- 1Baotou Medical College, Inner Mongolia University of Science & Technology, Baotou, China.
- 2The Second Affiliated Hospital of Baotou Medical College, Inner Mongolia University of Science & Technology, Baotou, China.
Abstract
Purpose
This study aimed to clarify the relationship between obstructive sleep apnea (OSA) and Alzheimer's disease (AD)-related biomarkers-specifically amyloid β (Aβ) and tau proteins-in blood and cerebrospinal fluid (CSF) through a systematic review and meta-analysis.Methods
PubMed, Web of Science (WOS), Embase, and Cochrane Library were searched from database inception to December 30, 2024 (PROSPERO registration: CRD420251148709). Studies reporting blood or CSF levels of Aβ40, Aβ42, total Aβ (T-Aβ), total tau (T-tau), or phosphorylated tau (P-tau) in patients with OSA vs. non-OSA controls were included. A random-effects model was employed for all meta-analyses. The risk of bias was assessed using appropriate validated tools.Results
Thirteen studies (seven blood, six CSF) were included. In blood, OSA patients showed significantly higher T-Aβ (SMD = 0.66, 95% CI [0.34, 0.97], I ² = 0%, p < 0.01) and T-tau (SMD = 1.48, 95% CI [0.33, 2.62], I ² = 93.6%, p = 0.011). No significant differences were found for blood Aβ40, Aβ42, Aβ42/Aβ40 ratio, or P-tau. In CSF, patients with OSA had significantly lower Aβ40 (SMD = -1.13, 95% CI [-1.65, -0.60], I ² = 0%, p < 0.01) and Aβ42 (SMD = -1.23, 95% CI [-1.84, -0.63], I ² = 77.3%, p < 0.01), but no differences in Aβ42/Aβ40 ratio, T-tau, or P-tau.Limitations
High heterogeneity, pre-dominantly cross-sectional designs, low-to-very-low GRADE certainty for most outcomes, retrospective registration, and limited study numbers preclude causal inference and warrant cautious interpretation.Conclusions
This exploratory meta-analysis revealed compartment-specific associations between certain AD-related biomarkers and OSA. However, given the low-to-very-low certainty of the available evidence and the substantial uncertainty reflected by prediction intervals that frequently crossed the null value, these findings should be regarded as hypothesis-generating rather than conclusive. Notably, the absence of consistent alterations in P-tau or the CSF Aβ42/Aβ40 ratio argues against a direct signature of established AD neuropathology. Future rigorously designed, large-scale prospective studies are warranted to determine whether these biomarker changes reflect early AD pathology or reversible physiological responses to OSA-related hypoxia and sleep fragmentation.Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=1148709, identifier CRD420251148709.
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BibTeX
@article{wang2026associations,
title = {{Associations between obstructive sleep apnea and Alzheimer's disease-related biomarkers (amyloid-β and tau) in blood and cerebrospinal fluid: a systematic review and meta-analysis.}},
author = {Jing Wang and Ligeer Che and Rina Su and Xianbin Wang},
journal = {Frontiers in neurology},
year = {2026},
month = sep,
doi = {10.3389/fneur.2026.1817426},
url = {https://europepmc.org/article/MED/42834920},
note = {CC BY},
}
RIS
TY - JOUR
TI - Associations between obstructive sleep apnea and Alzheimer's disease-related biomarkers (amyloid-β and tau) in blood and cerebrospinal fluid: a systematic review and meta-analysis.
AU - Jing Wang
AU - Ligeer Che
AU - Rina Su
AU - Xianbin Wang
PY - 2026
DA - 2026/09/21
JO - Frontiers in neurology
DO - 10.3389/fneur.2026.1817426
UR - https://europepmc.org/article/MED/42834920
AB - Purpose This study aimed to clarify the relationship between obstructive sleep apnea (OSA) and Alzheimer's disease (AD)-related biomarkers-specifically amyloid β (Aβ) and tau proteins-in blood and cerebrospinal fluid (CSF) through a systematic review and meta-analysis.Methods PubMed, Web of Science (WOS), Embase, and Cochrane Library were searched from database inception to December 30, 2024 (PROSPERO registration: CRD420251148709). Studies reporting blood or CSF levels of Aβ40, Aβ42, total Aβ (T-Aβ), total tau (T-tau), or phosphorylated tau (P-tau) in patients with OSA vs. non-OSA controls were included. A random-effects model was employed for all meta-analyses. The risk of bias was assessed using appropriate validated tools.Results Thirteen studies (seven blood, six CSF) were included. In blood, OSA patients showed significantly higher T-Aβ (SMD = 0.66, 95% CI [0.34, 0.97], I ² = 0%, p < 0.01) and T-tau (SMD = 1.48, 95% CI [0.33, 2.62], I ² = 93.6%, p = 0.011). No significant differences were found for blood Aβ40, Aβ42, Aβ42/Aβ40 ratio, or P-tau. In CSF, patients with OSA had significantly lower Aβ40 (SMD = -1.13, 95% CI [-1.65, -0.60], I ² = 0%, p < 0.01) and Aβ42 (SMD = -1.23, 95% CI [-1.84, -0.63], I ² = 77.3%, p < 0.01), but no differences in Aβ42/Aβ40 ratio, T-tau, or P-tau.Limitations High heterogeneity, pre-dominantly cross-sectional designs, low-to-very-low GRADE certainty for most outcomes, retrospective registration, and limited study numbers preclude causal inference and warrant cautious interpretation.Conclusions This exploratory meta-analysis revealed compartment-specific associations between certain AD-related biomarkers and OSA. However, given the low-to-very-low certainty of the available evidence and the substantial uncertainty reflected by prediction intervals that frequently crossed the null value, these findings should be regarded as hypothesis-generating rather than conclusive. Notably, the absence of consistent alterations in P-tau or the CSF Aβ42/Aβ40 ratio argues against a direct signature of established AD neuropathology. Future rigorously designed, large-scale prospective studies are warranted to determine whether these biomarker changes reflect early AD pathology or reversible physiological responses to OSA-related hypoxia and sleep fragmentation.Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=1148709, identifier CRD420251148709.
SN - 1664-2295
ER -