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43 Publications visible to you, out of a total of 43
Sleep disturbances and upregulation of brain arousal during daytime in depressed versus non-depressed elderly subjects.
LIFE Adult

Abstract (Expand)

OBJECTIVES: Although patients with depression often suffer from sleep disturbances, most of them are not sleepy. Upregulation of brain arousal has been proposed as pathophysiological mechanism explaining … sleep disturbances, inner tension, autonomic hyperarousal and anhedonia in depression. The aim of the current study was to examine the association between night-time sleep disturbances and brain arousal regulation the next day in depressed versus non-depressed subjects. METHODS: Twenty-eight elderly subjects (21 female; age = 70.5 +/- 4.4 years) with depressive syndromes without psychotropic medication, and 28 controls (22 female; age = 70.9 +/- 4.5 years), underwent a 15-min resting electroencephalogram; the Vigilance Algorithm Leipzig (VIGALL 2.1) provided an objective measure of brain arousal regulation. Sleep disturbances were assessed by a validated and self-rated sleep questionnaire. RESULTS: In the depressive group, but not in controls, more sleep disturbances were associated with a higher brain arousal stability score (high score corresponds to upregulation) the next day (sleep onset latency: rs = 0.69, P < .0001; sleep quality: rs = -0.59, P < .001). CONCLUSIONS: The data confirm the hypothesis that in persons with depressive syndromes sleep disturbances are related to upregulation of brain arousal the next day. This finding is in line with the concept that dysregulation of brain arousal is a central pathophysiological aspect in depression.

Authors: C. Ulke, C. Sander, P. Jawinski, N. Mauche, J. Huang, J. Spada, D. Wittekind, R. Mergl, T. Luck, S. Riedel-Heller, T. Hensch, U. Hegerl

Date Published: 25th Aug 2016

Publication Type: Journal article

Human Diseases: mental depression

Education as protector against dementia, but what exactly do we mean by education?
LIFE Adult

Abstract (Expand)

OBJECTIVES: even though a great number of research studies have shown that high education has protective effects against dementia, some studies did not observe such a significant effect. In that respect, … the aim of our study was to investigate and compare various operationalisation approaches of education and how they impact dementia risk within one sample. METHODS: data were derived from the Leipzig longitudinal study of the aged (LEILA75+). Individuals aged 75 and older underwent six cognitive assessments at an interval of 1.5 years and a final follow-up 15 years after the baseline assessment. We operationalised education according to different approaches used in previous studies and analysed the impact on dementia incidence via multivariate cox regression modelling. RESULTS: the results showed that whether education is identified as significant protector against dementia strongly depends on the operationalisation of education. Whereas the pure number of years of education showed statistically significant protective effects on dementia risk, other more complex categorical classification approaches did not. Moreover, completing >10 years of education or a tertiary level seems to be an important threshold to significantly reduce dementia risk. CONCLUSION: findings suggest a protective effect of more years of education on a lower dementia risk with a particular critical threshold of completing >10 years of education. Further, the findings highlight that, when examining risks and protective factors of dementia, a careful consideration of the underlying definitions and operationalisation approaches is required.

Authors: F. S. Then, T. Luck, M. C. Angermeyer, S. G. Riedel-Heller

Date Published: 9th Apr 2016

Publication Type: Journal article

Human Diseases: dementia

Compression of dementia morbidity by higher education
LIFE - Leipzig Research Center for Civilization Diseases

Abstract (Expand)

Objectives: The concept of compression of morbidity suggests that compressing cognitive morbidity into a shorter lifetime period would result in a better cumulative lifetime cognitive functioning. Some … lifestyle factors, like higher education, that are known to protect cognitive functioning in old age and lower dementia risk, could compress cognitive morbidity. Therefore the aim of our study was to investigate whether higher education leads to a better cumulative lifetime cognitive functioning and, hence, the compression of cognitive morbidity. Methods: Data were derived from the population-based Leipzig longitudinal study of the aged (LEILA75+). From 1998-2005, individuals aged 75 years and older underwent up to seven assessments at a 1.5-year interval and a long-term follow-up assessment after 15 years (2013). Analyses on the impact of higher education on compression of cognitive morbidity were carried out via multilevel logistic mixed-models and tobit analyses using the participants’ age as time scale (n=742). Results: The results revealed that more years of education were significantly associated with a better cognitive functioning but not with the age at dementia onset or the age at death. Computation of cumulative lifetime cognitive functioning was weighted for survival probability and indicated a gain of 21 MMSE points during the lifetime period 75 through 100 years of age by having more than 12 years of education compared to having less than 9 years of education. Conclusion: Overall, the findings suggest a compression of cognitive morbidity by higher education prior to dementia onset. More years of education could therefore contribute to a better cognitive functioning even under consideration of survival probability. Hence, efforts to ensure access to higher education for as many people in a population as possible might compress disease burden due to cognitive morbidity.

Authors: F. S. Then, T. Luck, H. Matschinger, M. C. Angermeyer, S. G. Riedel-Heller

Date Published: 1st Mar 2016

Publication Type: Not specified

Human Diseases: dementia

Serum BDNF correlates with connectivity in the (pre)motor hub in the aging human brain--a resting-state fMRI pilot study.
LIFE Adult

Abstract (Expand)

Brain-derived neurotrophic factor (BDNF) has been discussed to be involved in plasticity processes in the human brain, in particular during aging. Recently, aging and its (neurodegenerative) diseases … have increasingly been conceptualized as disconnection syndromes. Here, connectivity changes in neural networks (the connectome) are suggested to be the most relevant and characteristic features for such processes or diseases. To further elucidate the impact of aging on neural networks, we investigated the interaction between plasticity processes, brain connectivity, and healthy aging by measuring levels of serum BDNF and resting-state fMRI data in 25 young (mean age 24.8 +/- 2.7 (SD) years) and 23 old healthy participants (mean age, 68.6 +/- 4.1 years). To identify neural hubs most essentially related to serum BDNF, we applied graph theory approaches, namely the new data-driven and parameter-free approach eigenvector centrality (EC) mapping. The analysis revealed a positive correlation between serum BDNF and EC in the premotor and motor cortex in older participants in contrast to young volunteers, where we did not detect any association. This positive relationship between serum BDNF and EC appears to be specific for older adults. Our results might indicate that the amount of physical activity and learning capacities, leading to higher BDNF levels, increases brain connectivity in (pre)motor areas in healthy aging in agreement with rodent animal studies. Pilot results have to be replicated in a larger sample including behavioral data to disentangle the cause for the relationship between BDNF levels and connectivity.

Authors: K. Mueller, K. Arelin, H. E. Moller, J. Sacher, J. Kratzsch, T. Luck, S. Riedel-Heller, A. Villringer, M. L. Schroeter

Date Published: 2nd Feb 2016

Publication Type: Not specified

Incident Subjective Cognitive Decline Does Not Predict Mortality in the Elderly--Results from the Longitudinal German Study on Ageing, Cognition, and Dementia (AgeCoDe).
LIFE Adult

Abstract (Expand)

OBJECTIVE: Subjective cognitive decline (SCD) might represent the first symptomatic representation of Alzheimer's disease (AD), which is associated with increased mortality. Only few studies, … however, have analyzed the association of SCD and mortality, and if so, based on prevalent cases. Thus, we investigated incident SCD in memory and mortality. METHODS: Data were derived from the German AgeCoDe study, a prospective longitudinal study on the epidemiology of mild cognitive impairment (MCI) and dementia in primary care patients over 75 years covering an observation period of 7.5 years. We used univariate and multivariate Cox regression analyses to examine the relationship of SCD and mortality. Further, we estimated survival times by the Kaplan Meier method and case-fatality rates with regard to SCD. RESULTS: Among 971 individuals without objective cognitive impairment, 233 (24.0%) incidentally expressed SCD at follow-up I. Incident SCD was not significantly associated with increased mortality in the univariate (HR = 1.0, 95% confidence interval = 0.8-1.3, p = .90) as well as in the multivariate analysis (HR = 0.9, 95% confidence interval = 0.7-1.2, p = .40). The same applied for SCD in relation to concerns. Mean survival time with SCD was 8.0 years (SD = 0.1) after onset. CONCLUSION: Incident SCD in memory in individuals with unimpaired cognitive performance does not predict mortality. The main reason might be that SCD does not ultimately lead into future cognitive decline in any case. However, as prevalence studies suggest, subjectively perceived decline in non-memory cognitive domains might be associated with increased mortality. Future studies may address mortality in such other cognitive domains of SCD in incident cases.

Authors: S. Roehr, T. Luck, K. Heser, A. Fuchs, A. Ernst, B. Wiese, J. Werle, H. Bickel, C. Brettschneider, A. Koppara, M. Pentzek, C. Lange, J. Prokein, S. Weyerer, E. Mosch, H. H. Konig, W. Maier, M. Scherer, F. Jessen, S. G. Riedel-Heller

Date Published: 15th Jan 2016

Publication Type: Not specified

Human Diseases: dementia

First evidence for glial pathology in late life minor depression: S100B is increased in males with minor depression.
LIFE Adult

Abstract (Expand)

Minor depression is diagnosed when a patient suffers from 2 to 4 depressive symptoms for at least 2 weeks. Though minor depression is a widespread phenomenon, its pathophysiology has hardly been studied. … To get a first insight into the pathophysiological mechanisms underlying this disorder we assessed serum levels of biomarkers for plasticity, glial and neuronal function: brain-derived neurotrophic factor (BDNF), S100B and neuron specific enolase (NSE). 27 subjects with minor depressive episode and 82 healthy subjects over 60 years of age were selected from the database of the Leipzig population-based study of civilization diseases (LIFE). Serum levels of BDNF, S100B and NSE were compared between groups, and correlated with age, body-mass index (BMI), and degree of white matter hyperintensities (score on Fazekas scale). S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66). NSE correlated with Fazekas score in patients with minor depression (rs = 0.436, p = 0.048) and in the whole sample (rs = 0.252, p = 0.019). S100B correlated with BMI (rs = 0.246, p = 0.031) and with age in healthy subjects (rs = 0.345, p = 0.002). Increased S100B in males with minor depression, without alterations in BDNF and NSE, supports the glial hypothesis of depression. Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

Authors: M. Polyakova, C. Sander, K. Arelin, L. Lampe, T. Luck, M. Luppa, J. Kratzsch, K. T. Hoffmann, S. Riedel-Heller, A. Villringer, P. Schoenknecht, M. L. Schroeter

Date Published: 27th Oct 2015

Publication Type: Not specified

Human Diseases: mental depression

Mortality in Individuals with Subjective Cognitive Decline: Results of the Leipzig Longitudinal Study of the Aged (LEILA75+).
LIFE Adult

Abstract (Expand)

BACKGROUND: Studies have shown that dementia and cognitive impairment can increase mortality, but less is known about the association between subjectively perceived cognitive deficits (subjective … cognitive decline, SCD) and mortality risk. OBJECTIVE: In this study, we analyzed mortality in non-demented individuals with SCD in a general population sample aged 75+ years. METHOD: Data were derived from the Leipzig Longitudinal Study of the Aged (LEILA75+). We used the Kaplan-Meier survival method to estimate survival times of individuals with and without SCD and multivariable Cox proportional hazards regression to assess the association between SCD and mortality risk, controlled for covariates. RESULTS: Out of 953 non-demented individuals at baseline, 117 (12.3% ) expressed SCD. Participants with SCD showed a significantly higher case-fatality rate per 1,000 person-years (114.8, 95% CI = 90.5-145.7 versus 71.7, 95% CI = 64.6-79.5) and a significantly shorter mean survival time than those without (5.4 versus 6.9 years, p < 0.001). The association between SCD and mortality remained significant in the Cox analysis; SCD increased mortality risk by about 50% (adjusted Hazard Ratio = 1.51) during the study period. Besides SCD, older age, male gender, diabetes mellitus, stroke, and lower global cognitive functioning were also significantly associated with increased mortality. CONCLUSION: Our findings suggest an increased mortality risk in non-demented older individuals with SCD. Even though further studies are required to analyze potential underlying mechanisms, subjective reports on cognitive deficits may be taken seriously in clinical practice not only for an increased risk of developing dementia and AD but also for a broader range of possible adverse health outcomes.

Authors: T. Luck, S. Roehr, F. Jessen, A. Villringer, M. C. Angermeyer, S. G. Riedel-Heller

Date Published: 24th Sep 2015

Publication Type: Not specified

Human Diseases: dementia

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