Circadian rhythms of melatonin and peripheral clock gene expression in idiopathic REM sleep behavior disorder
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30195196
DOI
10.1016/j.sleep.2018.07.019
PII: S1389-9457(18)30519-7
Knihovny.cz E-resources
- Keywords
- Clock genes expression, Idiopathic rapid eye movement sleep (REM) sleep behavior disorder, Melatonin,
- MeSH
- Period Circadian Proteins genetics MeSH
- Circadian Rhythm genetics MeSH
- Gene Expression * MeSH
- Nuclear Receptor Subfamily 1, Group D, Member 1 genetics MeSH
- Humans MeSH
- Melatonin blood metabolism MeSH
- Polysomnography MeSH
- REM Sleep Behavior Disorder genetics MeSH
- CLOCK Proteins genetics MeSH
- Surveys and Questionnaires MeSH
- Aged MeSH
- Sleep Stages genetics MeSH
- ARNTL Transcription Factors genetics MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Aged MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- BMAL1 protein, human MeSH Browser
- Period Circadian Proteins MeSH
- Nuclear Receptor Subfamily 1, Group D, Member 1 MeSH
- Melatonin MeSH
- NR1D1 protein, human MeSH Browser
- PER1 protein, human MeSH Browser
- PER2 protein, human MeSH Browser
- CLOCK Proteins MeSH
- ARNTL Transcription Factors MeSH
OBJECTIVE: To evaluate changes in the expression of clock genes and melatonin levels in patients with idiopathic REM sleep behavior disorder (RBD) as a potential early stage of synucleinopathies. METHODS: We assessed the rhythmicity of circadian clock genes using real time-quantitative polymerase chain reaction and 24-h blood melatonin profiles using radio-immunoassay in 10 RBD patients and nine age-matched controls. RESULTS: The RBD patients did not show circadian rhythmicity for clock genes Per2, Bmal1, and Nr1d1 but the rhythmicity of Per 1 remained, and the amplitude of Per3 was diminished. The 24-h melatonin rhythm did not differ between RBD patients and healthy control subjects. Melatonin profile in RBD patients was delayed by 2 h compared to controls, the habitual sleep phases were phase delayed by about 1 h, however no phase shift occurred in any of the clock genes studied. The control group had stable acrophases of melatonin rhythms of approximately 5 h whereas the RBD patients had a more dispersed range over 11 h. CONCLUSIONS: Our results suggest that RBD could be associated with altered expression of clock genes and delayed melatonin secretion. Thus, we argue that circadian system dysregulation could play a role in RBD.
Department of Physiology Faculty of Science Charles University Prague Czech Republic
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