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        <datestamp>2026-09-21T04:22:50Z</datestamp>
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          <dc:title>Table 1_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.docx</dc:title>
          <dc:creator>Jing Wang (6206297)</dc:creator>
          <dc:creator>Ligeer Che (22518114)</dc:creator>
          <dc:creator>Rina Su (520454)</dc:creator>
          <dc:creator>Xianbin Wang (3336642)</dc:creator>
          <dc:subject>Neurology and Neuromuscular Diseases</dc:subject>
          <dc:subject>Alzheimer's disease</dc:subject>
          <dc:subject>blood biomarkers</dc:subject>
          <dc:subject>cerebrospinal fluid biomarkers</dc:subject>
          <dc:subject>meta-analysis</dc:subject>
          <dc:subject>obstructive sleep apnea</dc:subject>
          <dc:subject>systematic review</dc:subject>
          <dc:description>Purpose&lt;p&gt;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.&lt;/p&gt;Methods&lt;p&gt;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.&lt;/p&gt;Results&lt;p&gt;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&lt;sup&gt;2&lt;/sup&gt; = 0%, p &lt; 0.01) and T-tau (SMD = 1.48, 95% CI [0.33, 2.62], I&lt;sup&gt;2&lt;/sup&gt; = 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&lt;sup&gt;2&lt;/sup&gt; = 0%, p &lt; 0.01) and Aβ42 (SMD = −1.23, 95% CI [−1.84, −0.63], I&lt;sup&gt;2&lt;/sup&gt; = 77.3%, p &lt; 0.01), but no differences in Aβ42/Aβ40 ratio, T-tau, or P-tau.&lt;/p&gt;Limitations&lt;p&gt;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.&lt;/p&gt;Conclusions&lt;p&gt;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.&lt;/p&gt;&lt;p&gt;Systematic review registration:https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=1148709, identifier CRD420251148709.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-21T04:22:50Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fneur.2026.1817426.s001</dc:identifier>
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