Parkinsonism & related disorders · 2026
Impaired sleep microarchitecture is associated with locus coeruleus degeneration in Parkinson's disease.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Doppler Christopher E J, Sembowski Nora, Plottka Dean, Hommelsen Maximilian, Röttgen Sinah, Schwabedal Justus T C, Schreiner Simon J, Fink Gereon R, Borghammer Per, Bialonski Stephan, Sommerauer Michael
Аннотация
STUDY OBJECTIVES: Sleep disorders are common non-motor symptoms of Parkinson's disease (PD) that significantly impact patients' quality of life. Specifically, alterations in sleep microstructure - such as reduced slow-wave activity and sleep spindles - are prevalent in PD. The locus coeruleus (LC), the brain's primary source of noradrenaline, plays a pivotal role in regulating sleep and wakefulness and is highly vulnerable to neurodegeneration in PD. This study explores whether disruptions in sleep microarchitecture in PD are linked to LC degeneration.
METHODS: We assessed polysomnography for sleep macroarchitecture, EEG spectral power, and spindle density in 32 PD patients and 24 age- and sex-matched controls. In a sample subset (n = 42), neuromelanin-sensitive MRI was performed, and LC neuromelanin contrast was correlated to sleep metrics.
RESULTS: PD patients exhibited reduced slow-wave activity (p < 0.01), slow-to-fast frequency ratio (p < 0.01), and spindle density (p < 0.05) compared to HC subjects. LC neuromelanin contrast was diminished in PD patients (p < 0.05). Even though group differences were detected for slow-wave activity, a positive correlation between LC contrast and spindle density but not slow-wave activity was observed in the entire sample.
CONCLUSIONS: The findings indicate that spindle density, but not slow-wave activity, is associated with LC degeneration. Further research is needed to determine whether, besides this association, noradrenergic dysfunction is causal for impaired sleep microarchitecture and whether this connection also contributes to cognitive decline in PD and other neurodegenerative diseases, such as Alzheimer's disease.
METHODS: We assessed polysomnography for sleep macroarchitecture, EEG spectral power, and spindle density in 32 PD patients and 24 age- and sex-matched controls. In a sample subset (n = 42), neuromelanin-sensitive MRI was performed, and LC neuromelanin contrast was correlated to sleep metrics.
RESULTS: PD patients exhibited reduced slow-wave activity (p < 0.01), slow-to-fast frequency ratio (p < 0.01), and spindle density (p < 0.05) compared to HC subjects. LC neuromelanin contrast was diminished in PD patients (p < 0.05). Even though group differences were detected for slow-wave activity, a positive correlation between LC contrast and spindle density but not slow-wave activity was observed in the entire sample.
CONCLUSIONS: The findings indicate that spindle density, but not slow-wave activity, is associated with LC degeneration. Further research is needed to determine whether, besides this association, noradrenergic dysfunction is causal for impaired sleep microarchitecture and whether this connection also contributes to cognitive decline in PD and other neurodegenerative diseases, such as Alzheimer's disease.