Sleep and circadian disturbances in Alzheimer’s disease: clinical assessment, treatable syndromes, and limits of biomarker inference
- 1Department of Geriatrics, Chongming Hospital Affiliated to Shanghai University of Medicine & Health Sciences
- 2The Second School of Clinical Medicine, Southern Medical University
- 3Neurosurgery Center, National Key Clinical Specialty, Engineering Research Center of Diagnostic and Therapeutic Technology and Devices for Cerebrovascular Diseases in Ministry of Education, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, Zhujiang Hospital Institute for Brain Science and Intelligence, Zhujiang Hospital, Southern Medical University
Abstract
Sleep and circadian disturbances in Alzheimer’s disease (AD) affect patients and caregivers, but clinical action depends on the syndrome, measurement, and outcome under consideration. This narrative review links sleep assessment to indication-based care while distinguishing symptomatic benefit, physiological target engagement, and disease modification. A purposive literature search was supplemented by targeted checks of PubMed-indexed and original publisher records through 4 October 2026. Selected studies are described by population, AD ascertainment, comparator, and measured endpoint rather than assigned formal evidence-certainty grades. Actigraphy characterizes behavioral rest–activity patterns; melatonin timing and temperature rhythms address endogenous circadian physiology under controlled conditions. Polysomnography and quantitative electroencephalography characterize respiratory events, sleep architecture, and oscillatory activity. These measurements inform different questions and do not independently assign AD etiology or cognitive-functional stage. Clinical priorities include confirmed obstructive sleep apnea, cognition-adapted insomnia care, irregular sleep timing, medication-related effects, parasomnias, limb symptoms, and excessive daytime sleepiness. Interpretation incorporates hypoxemia, treatment exposure, comorbidity, caregiver support, and competing diagnoses. Randomized sleep benefits remain distinct from observational cognitive associations or exploratory imaging and cerebrospinal fluid changes. Human and animal studies of arousal circuits, protein dynamics, inflammation, and fluid transport provide mechanistic context, with conflicting results interpreted according to the actual experimental endpoint. The review provides a clinically organized account of selected evidence, not a comprehensive treatment ranking. Sleep care and cognitive-etiologic assessment should proceed in parallel, with follow-up matched to patient function, safety, and the specific treatment goal.
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BibTeX
@article{gan2026sleep,
title = {{Sleep and circadian disturbances in Alzheimer’s disease: clinical assessment, treatable syndromes, and limits of biomarker inference}},
author = {Xuying Gan and Xilin Zhou and Shuolan Yan and Simin Yang and Zhihua Li},
journal = {Frontiers in Neurology},
year = {2026},
month = oct,
doi = {10.3389/fneur.2026.1998439},
url = {https://www.frontiersin.org/articles/10.3389/fneur.2026.1998439/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Sleep and circadian disturbances in Alzheimer’s disease: clinical assessment, treatable syndromes, and limits of biomarker inference
AU - Xuying Gan
AU - Xilin Zhou
AU - Shuolan Yan
AU - Simin Yang
AU - Zhihua Li
PY - 2026
DA - 2026/10/28
JO - Frontiers in Neurology
DO - 10.3389/fneur.2026.1998439
UR - https://www.frontiersin.org/articles/10.3389/fneur.2026.1998439/full
AB - Sleep and circadian disturbances in Alzheimer’s disease (AD) affect patients and caregivers, but clinical action depends on the syndrome, measurement, and outcome under consideration. This narrative review links sleep assessment to indication-based care while distinguishing symptomatic benefit, physiological target engagement, and disease modification. A purposive literature search was supplemented by targeted checks of PubMed-indexed and original publisher records through 4 October 2026. Selected studies are described by population, AD ascertainment, comparator, and measured endpoint rather than assigned formal evidence-certainty grades. Actigraphy characterizes behavioral rest–activity patterns; melatonin timing and temperature rhythms address endogenous circadian physiology under controlled conditions. Polysomnography and quantitative electroencephalography characterize respiratory events, sleep architecture, and oscillatory activity. These measurements inform different questions and do not independently assign AD etiology or cognitive-functional stage. Clinical priorities include confirmed obstructive sleep apnea, cognition-adapted insomnia care, irregular sleep timing, medication-related effects, parasomnias, limb symptoms, and excessive daytime sleepiness. Interpretation incorporates hypoxemia, treatment exposure, comorbidity, caregiver support, and competing diagnoses. Randomized sleep benefits remain distinct from observational cognitive associations or exploratory imaging and cerebrospinal fluid changes. Human and animal studies of arousal circuits, protein dynamics, inflammation, and fluid transport provide mechanistic context, with conflicting results interpreted according to the actual experimental endpoint. The review provides a clinically organized account of selected evidence, not a comprehensive treatment ranking. Sleep care and cognitive-etiologic assessment should proceed in parallel, with follow-up matched to patient function, safety, and the specific treatment goal.
SN - 1664-2295
ER -