ArticleFrontiers in neuroscience2024
Slow-wave sleep dysfunction in mild parkinsonism is associated with excessive beta and reduced delta oscillations in motor cortex.
Article in Frontiers in neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Enhancing sleep slow waves with auditory stimulation in people with Parkinson's disease: a randomized proof-of-concept trial.Scientific reports · 2026Trial
- Slow wave canonical activity deviation concept: Toward a slow wave-based EEG-fMRI reference map for health-associated network function.iScience · 2026Article
- Progress in the study of ion channel function, mechanisms, and mathematical modeling in Parkinson's disease.iScience · 2026Review
- Sleep firing rate homeostasis is disrupted in mild parkinsonism.NPJ Parkinson's disease · 2026Article
- Excessive daytime sleepiness in parkinsonism is associated with cortical and basal ganglia beta oscillatory activity.Communications biology · 2026Article
- A Wireless Cortical Surface Implant for Diagnosing and Alleviating Parkinson's Disease Symptoms in Freely Moving Animals.Advanced healthcare materials · 2025Article
- Alterations in non-REM sleep and EEG spectra precede REM-sleep deficits in a model of synucleinopathy.Journal of Parkinson's disease · 2025Article
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12 authors at 1 institution in 1 country.
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Abstract
Increasing evidence suggests slow-wave sleep (SWS) dysfunction in Parkinson's disease (PD) is associated with faster disease progression, cognitive impairment, and excessive daytime sleepiness. Beta oscillations (8-35 Hz) in the basal ganglia thalamocortical (BGTC) network are thought to play a role in the development of cardinal motor signs of PD. The role cortical beta oscillations play in SWS dysfunction in the early stage of parkinsonism is not understood, however. To address this question, we used a within-subject design in a nonhuman primate (NHP) model of PD to record local field potentials from the primary motor cortex (MC) during sleep across normal and mild parkinsonian states. The MC is a critical node in the BGTC network, exhibits pathological oscillations with depletion in dopamine tone, and displays high amplitude slow oscillations during SWS. The MC is therefore an appropriate recording site to understand the neurophysiology of SWS dysfunction in parkinsonism. We observed a reduction in SWS quantity (
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