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Biomarkers / Alzheimer Disease / Sleep Wake Disorders · Journal article
Sleep Medicine · July 25, 2026
Well-designed and adequately powered for the question it asks.
This longitudinal cohort study identified three sleep disturbance trajectories over 8 years in 774 older adults and found that 'High-peaked' and 'Moderate-increasing' patterns are associated with 3.28-fold and 2.13-fold increased risk of incident AD, respectively, along with faster cognitive decline and CSF Aβ1-42 reduction. The findings support sleep monitoring as a potential stratification tool for AD risk but do not establish sleep disturbance as a causal driver of neuropathology, given the null structural and global PET findings.
Prospective longitudinal cohort study with group-based trajectory modeling. Non-demented participants from the ADNI cohort, ages and specific eligibility criteria not stated in the abstract.. Intervention: Longitudinal observation of sleep disturbance trajectories over 8 years; no active intervention.. Compared with: Reference group: participants without sleep disturbance (Low-stable trajectory).. n = 774. Not stated in the source text..
Three sleep trajectories identified: 'Low-stable' (37.2%), 'High-peaked' (21.0%), 'Moderate-increasing' (41.8%) 'High-peaked' trajectory associated with incident AD risk (HR = 3.28; 95% CI = 1.89–5.70; p < 0.001) 'Moderate-increasing' trajectory associated with incident AD risk (HR = 2.13; 95% CI = 1.28–3.53; p = 0.003)
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Sleep disturbance trajectory patterns, particularly 'High-peaked' and 'Moderate-increasing' patterns, identify older adults at substantially elevated risk for AD and faster cognitive decline. Clinicians should consider longitudinal sleep assessment as part of AD risk stratification in cognitively normal or mildly impaired older adults, though these findings are observational and do not establish causation.
Rigorous longitudinal cohort study with 774 participants, 8-year follow-up, validated trajectory modeling, and multiple biomarker endpoints showing clear associations between sleep disturbance patterns and incident AD risk with strong effect sizes.
As stated by the source record.
Quoted from the source exactly as published.
Sleep disturbance trajectory patterns, particularly 'High-peaked' and 'Moderate-increasing' patterns, identify older adults at substantially elevated risk for AD and faster cognitive decline. Clinicians should consider longitudinal sleep assessment as part of AD risk stratification in cognitively normal or mildly impaired older adults, though these findings are observational and do not establish causation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Background. Sleep disturbance is a core feature of affective and neurodegenerative disorders. This study tracks long-term sleep disturbance trajectories and their links to incident Alzheimer's disease (AD) and longitudinal clinical and pathological changes.Methods. A total of 774 non-demented participants from the ADNI cohort were included. Sleep disturbance (NPI sleep item) trajectories over 8 years were identified via group-based trajectory modeling. Cox proportional hazards regression was used to estimate the risk of incident AD. Linear mixed-effects models were used to assess longitudinal changes in cognition, structural magnetic resonance imaging, amyloid-β positron emission tomography (Aβ-PET), fluorodeoxyglucose (FDG)-PET, and cerebrospinal fluid (CSF) biomarkers.Results. Three trajectories emerged: "Low-stable" (37.2%), "High-peaked" (21.0%), and "Moderate-increasing" (41.8%). Compared to those without sleep disturbance, a significantly elevated risk of incident AD was associated with "High-peaked" (hazard ratio [HR] = 3.28; 95% confidence interval [CI] = 1.89-5.70; p < 0.001) and "Moderate-increasing" trajectories (HR = 2.13; 95% CI = 1.28-3.53; p = 0.003) but not with the "Low-stable" trajectory (p = 0.888). Participants with "High-peaked" trajectory exhibited faster declines in cognition (MMSE, memory, executive function) (p < 0.050) and a steeper reduction in CSF Aβ1-42 levels (p = 0.038) than those with non-sleep disturbance. However, there were no significant differences between groups in the rates of hippocampal, entorhinal, or middle temporal atrophy, global Aβ-PET burden, or FDG-PET changes (p > 0.050).Conclusions. "High-peaked" and "Moderate-increasing" sleep trajectories predict higher AD risk, faster cognitive decline, and faster Aβ1-42 reduction. Long-term monitoring of sleep behaviors is essential for identifying and stratifying individuals at high risk for AD.
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