SynthesisFluids and barriers of the CNS2026
The impact of chronic and acute sleep deprivation on key Alzheimer's disease biomarkers: a systematic review and meta-analysis.
Synthesis in Fluids and barriers of the CNS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Harnessing Brain Age-Specific Effects on the Associations Between Sleep Quality, Glymphatic Function, and Cognition in Normal Ageing Adults: Insights for Gerotherapeutics.Neurology and therapy · 2026Article
- Sleep-Dependent Clearance of Brain Metabolites via the Glymphatic System: Implications for Alzheimer's Pathophysiology.Brain and behavior · 2026Review
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundSleep disruption is recognized as a risk factor for Alzheimer’s disease (AD). Both chronic and acute sleep deprivation (SD) may increase cerebrospinal fluid (CSF) levels of amyloid-beta (Aβ) and tau, potentially complicating early AD diagnoses. Some studies also suggest an inverse relationship in plasma biomarker levels, although these effects remain poorly characterized.
methodsWe conducted a systematic review and meta-analysis to examine whether SD elevates CSF concentrations of key AD biomarkers (Aβ40, Aβ42, total tau [t-tau], phosphorylated tau [p-tau]) in individuals without established AD.
resultsSix studies (n = 169 participants) were included. Pooled results showed that SD significantly raised CSF Aβ40 (mean difference [MD]: 31.88, 95% CI: 25.61–38.15) and Aβ42 (MD: 37.32, 95% CI: 32.67–41.97 after sensitivity analysis). While initial analyses suggested inconsistent findings for t-tau and p-tau, excluding outlier data consistently revealed elevated levels in both (t-tau MD: 37.81, 95% CI: 23.27–52.35; p-tau MD: 1.01, 95% CI: 0.26–1.77). Possible publication bias was noted, but overall findings indicate that SD may cause meaningful biomarker fluctuations.
conclusionShort- or long-term SD may transiently elevate CSF Aβ and tau, underscoring the importance of assessing recent sleep history when interpreting AD biomarkers. Although not directly evaluated here, preliminary data suggest plasma biomarkers might move in the opposite direction, warranting further investigation. Clinically, these results highlight the potential impact of sleep patterns on biomarker-driven AD risk assessments. Addressing SD could thus be a valuable target for both optimizing diagnostic accuracy and potentially slowing early neurodegenerative processes.
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