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Journal Article

Brain-derived neurotrophic factor is a biomarker for subjective insomnia but not objectively assessable poor sleep continuity


Mikoteit,  Thorsten
Max Planck Institute of Psychiatry, Max Planck Society;

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Mikoteit, T., Brand, S., Eckert, A., Holsboer-Trachsler, E., & Beck, J. (2019). Brain-derived neurotrophic factor is a biomarker for subjective insomnia but not objectively assessable poor sleep continuity. JOURNAL OF PSYCHIATRIC RESEARCH, 110, 103-109. doi:10.1016/j.jpsychires.2018.12.020.

Cite as: http://hdl.handle.net/21.11116/0000-0009-61B5-D
Objectives: Brain-derived neurotrophic factor (BDNF) is a central mediator of the effects of stress on neuronal plasticity. Patients with subjective insomnia have significantly lower serum BDNF (sBDNF) levels. The aims of the present study were to investigate the associations of sBDNF with, 1) subjective and 2) objective sleep; 3) to investigate the associations between dimensions of psychopathology, subjective sleep and sBDNF, and 4) to investigate the associations between insomnia, sBDNF and cortisol. Methods: 60 patients with insomnia (IG; mean age: 40.4 years; 48.3% females) and 30 healthy, age and gender matched controls (CG) took part in the study. Subjective sleep was assessed using the Insomnia Severity Index (ISI), objective sleep was assessed once via sleep-EEG recordings. Both sBDNF and salivary cortisol were sampled once the following morning. Last, experts rated participants' symptoms of depression and anxiety. Results: sBDNF was significantly lower in the IG than in the CG (large effect size; Hedge's g = 1.75), while higher insomnia scores, but not depression or anxiety ratings, predicted lower sBDNF levels. Concerning objective sleep, low sBDNF did not correlate with sleep continuity measures, but with decreased REM-sleep; the latter was also characteristic of the IG. sBDNF and salivary morning cortisol were unrelated. Conclusions: Independently of symptoms of depression or anxiety, sBDNF appears to be a biomarker for the clinical diagnosis of insomnia, but not for objectively assessed poor sleep continuity. A possible link between sBDNF and insomnia seems to be via regulation of REM-sleep, but not salivary morning cortisol.