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Introduction: Sleep is increasingly recognized as a major risk factor for neurodegenerative disorders such as Alzheimer's disease (AD).
Methods: Using an magnetic resonance imaging (MRI)-based AD score based on clinical data from the Alzheimer's Disease Neuroimaging Initiative 1 (ADNI1) case-control cohort, we investigated the associations between polysomnography-based sleep macro-architecture and AD-related brain atrophy patterns in 712 pre-symptomatic, healthy subjects from the population-based Study of Health in Pomerania.
Results: We identified a robust inverse association between slow-wave sleep and the AD marker (estimate: -0.019; 95% confidence interval: -0.03 to -0.0076; false discovery rate [FDR] = 0.0041), as well as with gray matter (GM) thicknesses in typical individual cortical AD-signature regions. No effects were identified regarding rapid eye movement or non-rapid eye movement (NREM) stage 2 sleep, and NREM stage 1 was positively associated with GM thickness, mainly in the prefrontal cortical regions.
Discussion: There is a cross-sectional relationship between AD-related neurodegenerative patterns and the proportion of sleep spent in slow-wave sleep.
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http://dx.doi.org/10.1002/dad2.12371 | DOI Listing |
Alzheimers Dement
September 2025
Department of Neurology, Beijing TianTan Hospital, Capital Medical University, Beijing, China.
Cognitive impairment and dementia, including Alzheimer's disease (AD), pose a global health crisis, necessitating non-invasive biomarkers for early detection. This review highlights the retina, an accessible extension of the central nervous system (CNS), as a window to cerebral pathology through structural, functional, and molecular alterations. By synthesizing interdisciplinary evidence, we identify retinal biomarkers as promising tools for early diagnosis and risk stratification.
View Article and Find Full Text PDFBrain Res Bull
September 2025
Department of Neurology, The Second Affiliated Hospital of Anhui Medical University, 230601, He Fei, China; Collaborative Innovation Center of Neuropsychiatric Disorders and Mental Health, 230032, Hefei, China; Anhui Province Key Laboratory of Cognition and Neuropsychiatric Disorders, 230032, Hefei,
Background: The relationships between white matter microstructure, cortical atrophy, and cognitive function in cerebral small vessel disease (CSVD)-related white matter hyperintensities (WMHs) patients are unclear.
Methods: 71 right-handed WMHs patients (mild, n=23; moderate, n=27; severe, n=21) and 35 healthy controls were included. Tract-based spatial statistics (TBSS) assessed microstructure via fractional anisotropy (FA) and mean diffusivity (MD).
Neurol Neuroimmunol Neuroinflamm
November 2025
Departments of Neurology and Ophthalmology, NYU Grossman School of Medicine, NY; and.
Background And Objectives: While reductions in optical coherence tomography (OCT) pRNFL and ganglion cell-inner plexiform layer thicknesses have been shown to be associated with brain atrophy in adult-onset MS (AOMS) cohorts, the relationship between OCT and brain MRI measures is less established in pediatric-onset MS (POMS). Our aim was to examine the associations of OCT measures with volumetric MRI in a cohort of patients with POMS to determine whether OCT measures reflect CNS neurodegeneration in this patient population, as is seen in AOMS cohorts.
Methods: This was a cross-sectional study with retrospective ascertainment of patients with POMS evaluated at a single center with expertise in POMS and neuro-ophthalmology.
J Alzheimers Dis
September 2025
Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Compared with more typical late-onset Alzheimer's disease (AD), the mechanisms of young-onset AD (YOAD; age of symptom onset <65 years) remain less understood. Using resting-state functional MRI data and dynamic causal modeling techniques, Sacu et al. demonstrate that individuals with YOAD (amnestic AD or posterior cortical atrophy) exhibit alterations in effective (i.
View Article and Find Full Text PDFJCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
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