Journal Article

FZJ-2026-02564

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Impaired sleep microarchitecture is associated with locus coeruleus degeneration in Parkinson's disease

Doppler, C. E. J. (Corresponding author)FZJ* ; Sembowski, N. ; Plottka, D. ; Hommelsen, M. ; Röttgen, S.FZJ* ; Schwabedal, J. T. C. ; Schreiner, S. J. ; Fink, G. R.FZJ* ; Borghammer, P. ; Bialonski, S. ; Sommerauer, M.FZJ*

2026
Elsevier Science Amsterdam [u.a.]

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Please use a persistent id in citations: doi:10.1016/j.parkreldis.2026.108339  doi:10.34734/FZJ-2026-02564

Abstract: Abstract: 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.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.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.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.

Note: C. E. J. Doppler received grants from the Clinician Scientist Program (CCSP), funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) - FI 773/15-1.M. Sommerauer received grants from the Else Kröner-Fresenius­ Stiftung (grant number 2019_EKES.02), and funding from the program "Netzwe rke 2021", an initiative of the Ministry of Culture and Science of the State of North Rhine Westphalia. The Federal Ministry of Education and Research (BMBF) is funding the project within the framework of the funding programme ACCENT (funding code 01EO2107).G.R.F. is funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) - Project-ID 431549029 - SFB 1451.Open access publication funded by the Deutsche For­ schungsgemeinschaft (DFG, German Research Foundation) 491111487.

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Contributing Institute(s):

1. Kognitive Neurowissenschaften (INM-3)

Research Program(s):

1. 5252 - Brain Dysfunction and Plasticity (POF4-525) (POF4-525)
2. DFG project G:(GEPRIS)491111487 - Open-Access-Publikationskosten / 2025 - 2027 / Forschungszentrum Jülich (OAPKFZJ) (491111487) (491111487)
3. DFG project G:(GEPRIS)431549029 - SFB 1451: Schlüsselmechanismen normaler und krankheitsbedingt gestörter motorischer Kontrolle (431549029) (431549029)

Appears in the scientific report 2026

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Database coverage:
; ; ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Ebsco Academic Search ; Essential Science Indicators ; IF < 5 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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