In elderly patients who suffer from depressive symptoms and cognitive impairment the clinical decision between the diagnoses of depression and dementia may be difficult. In addition, patients with dementia and depressed patients frequently show a disturbance of sleep. Sleep EEG registration in depression revealed a characteristic sleep EEG profile concerning distinct alterations of sleep architecture and REM-sleep (reduction of SWS, increase and advance of REM-sleep). In dementia polysomnographic assessment has been done less intensively, mainly in patients with dementia of Alzheimer type (DAT). The most significant polysomnographic finding in DAT is a reduction of REM-sleep, which may reflect impaired cholinergic neurotransmission. Therefore, predominantly REM-sleep variables clearly differ between depressed patients and patients with DAT.

In this presentation polysomnographic data and data of cognitive performance in dementia and depression will be reviewed. In addition, own long term studies in patients with different types of dementia and in depressed patients will be presented. The polysomnographic findings of these studies will be discussed with respect to differential diagnosis, prediction of treatment response and the long term course of both diseases. In addition, the results will be related to the current knowledge of the neurochemical and neuroendocrine regulation of sleep.

The protein brain derived neurotrophic factor (BDNF) is a major contributor to neuronal plasticity. There is numerous evidence that BDNF expression is decreased by experiencing psychological stress and that accordingly a lack of neurotrophic support causes depression. The use of serum BDNF concentration as a potential indicator of brain alteration is justified through extensive evidence. Recently, we reported, for the first time, a relationship between BDNF and insomnia, since we could show that reduced levels of serum BDNF are correlated with sleep impairment in control subjects, while partial sleep deprivation was able to induce a fast increase in serum BDNF levels in depressed patients. Using a bi-directional stress model as an explanation approach, we propose the hypothesis that chronic stress might induce a deregulation of the HPA system leading in the long term to sleep disturbance and decreased BDNF levels, whereas acute sleep deprivation, can be used as therapeutical intervention in some insomniac or depressed patients as compensatory process to normalize BDNF levels. Indeed, partial sleep deprivation (PSD) induced a very fast increase in BDNF serum levels within hours after PSD which is similar to effects seen after ketamine infusion, another fast-acting antidepressant intervention, while traditional antidepressants are characterized by a major delay until treatment response as well as delayed BDNF level increase. Moreover, we revealed that stress experience and subjective sleep perception interact with each other and affect serum BDNF levels. We identified sleep as a mediator of the association between stress experience and serum BDNF levels.