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Investigating the relationship between sleep disturbances and cortical thickness, brainstem volume, amyloid accumulation, and inflammatory markers in Parkinson's disease patients.

Exp Gerontol · 2025-04-17

DOI: 10.1016/j.exger.2025.112762PMID: 40252714

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BackgroundThis study aimed to explore the relationship between self-reported sleep disturbances (e.g., insomnia, REM sleep behavior disorder [RBD]) and cortical thickness, brainstem volume, amyloid accumulation, and inflammatory markers in Parkinson's disease (PD) patients.MethodsWe conducted a cross-sectional study comparing 100 PD patients (observation group) with 100 age-matched controls. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI), and serum levels of amyloid-beta (Aβ1-42), α-synuclein, and inflammatory markers (CRP, TNF-α, IL-1β) were quantified.ResultsPD patients exhibited significantly poorer sleep quality (PSQI total score: 2.11 ± 0.27 vs. 0.52 ± 0.02, P 3 vs. 3185.16 ± 255.41 mm3, P = 0.007) compared to controls. Biomarker profiling revealed elevated amyloid pathology in PD, with higher serum Aβ1-42 (median [IQR]: 1.98 [1.75-2.22] vs. 1.14 [1.10-1.19], P ConclusionThese findings highlight the interplay between neuroanatomical changes, amyloid pathology, and systemic inflammation in PD-related sleep dysfunction, suggesting potential therapeutic targets.

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