Impact of sleep disruptions on gray matter structural covariance networks across the Alzheimer's disease continuum
Abstract BACKGROUND This study explores the impact of sleep disturbances on gray matter structural covariance networks (SCNs) across the Alzheimer's disease (AD) continuum. METHODS Amyloid‐negative participants served as controls, whereas amyloid positive (A+) individuals were categorized into...
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| Main Authors: | , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2025-01-01
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| Series: | Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/dad2.70077 |
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| Summary: | Abstract BACKGROUND This study explores the impact of sleep disturbances on gray matter structural covariance networks (SCNs) across the Alzheimer's disease (AD) continuum. METHODS Amyloid‐negative participants served as controls, whereas amyloid positive (A+) individuals were categorized into six groups based on cognitive status and sleep quality. SCNs for the default mode network (DMN), salience network (SN), and executive control network (ECN) were derived from T1‐weighted magnetic resonance images. RESULTS In the DMN, increased structural associations were observed in cognitive unimpaired (CU) A+ and mild cognitive impairment (MCI) groups regardless of sleep quality, whereas AD with poor sleep (PS) showed a decrease and AD with normal sleep (NS) an increase. For the ECN, AD‐NS showed increased and AD‐PS showed reduced associations. In the SN, reduced associations were observed in CU A+ NS and MCI‐NS, whereas AD‐NS displayed increased associations; only AD‐PS had decreased associations. CONCLUSION Distinct SCN damage patterns between normal and poor sleepers provide insights into sleep disturbances in AD. Highlights We delineated distinct patterns of structural covariance networks (SCN) impairment across the Alzheimer's disease (AD) continuum, uncovering significant disparities between individuals with normal sleep architecture and those afflicted by sleep disturbances. These observations underscore the pivotal importance of addressing sleep disruptions in AD therapeutics, providing a refined understanding of their detrimental impact on brain networks implicated in the disease. Our investigation epitomizes methodological precision by constructing an AD continuum using amyloid positron emission tomography (PET) and cerebrospinal fluid (CSF) biomarkers to minimize diagnostic heterogeneity, further enhanced by a substantial cohort size that bolsters the robustness and generalizability of our findings. |
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| ISSN: | 2352-8729 |