ArticleAlzheimer's research & therapy2026
Surrogates of glymphatic metrics decline and coupled sleep rhythms disruption in Alzheimer's disease.
Article in Alzheimer's research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Central nervous system lymphatic network: from the maintenance of brain homeostasis to emerging therapeutic perspectives in neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Modifiable Physiological Factors Associated With Human Glymphatic and Interstitial Fluid Dynamics-Related Measures: A Scoping Review.The European journal of neuroscience · 2026Article
- Objective Sleep Architecture Alterations and Sleep-Dependent Brain Clearance Dysfunction Across the Early Alzheimer's Disease Continuum: A Systematic Review.Journal of clinical medicine · 2026Review
- Relationship between insomnia and cognitive function in elderly Chinese cerebral small vessel disease patients: mediating effect of neutrophil-to-lymphocyte ratio.Frontiers in psychiatry · 2026Article
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6 authors.
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Abstract
backgroundSleep is essential for brain homeostasis, in part by supporting glymphatic clearance through sleep-related oscillations. However, the relationship between putative glymphatic metrics and coupled sleep rhythm disruption, and their combined role in Alzheimer's disease (AD) progression, remains poorly understood.
methodsWe analyzed data from 75 individuals, 54 with AD and 21 cognitively normal (CN) controls, including sleep electroencephalography (EEG), magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) AD biomarkers, and two-year longitudinal cognitive assessments. Putative glymphatic metrics was evaluated using choroid plexus (CP) volume, perivascular spaces (PVSs), diffusion tensor imaging along the perivascular space (DTI-ALPS) index, and blood oxygen level-dependent signal coupled to CSF signal (BOLD-CSF coupling). Coupled sleep rhythm was assessed via slow oscillation (SO)-theta and SO-spindle couplings. Correlation and mediation analyses explored associations between these MRI-derived indices and coupled sleep oscillations, and least absolute shrinkage and selection operator (LASSO) regression was used to predict AD progression.
resultsCompared to CN controls, individuals with AD had reduced DTI-ALPS index and BOLD-CSF coupling (p < 0.05), along with disrupted SO-spindle coupling (p = 0.029). Across all participants, lower global BOLD-CSF coupling correlated with misaligned SO-theta burst coupling (r = 0.311, p = 0.018), and reduced DTI-ALPS was associated with misaligned SO-spindle coupling (r = 0.370, p = 0.008). In the AD group, DTI-ALPS remained correlated with SO-spindle misalignment (r = 0.376, p = 0.028). Mediation analysis revealed that SO-spindle misalignment contributed to cognitive decline through its effect on DTI-ALPS. Importantly, combining putative glymphatic and sleep EEG metrics effectively predicted AD progression.
conclusionsOur findings suggest that disruptions in surrogates marker of glymphatic clearance and coupled sleep rhythms are jointly associated with AD-related cognitive decline. These metrics offer a promising framework for predicting disease progression and understanding neurodegenerative mechanisms in AD.
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