Peter Schönknecht

University of Leipzig, Leipzig, Saxony, Germany

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Publications (179)541.7 Total impact

  • N Mauche · C Sander · P Jawinski · C Enzenbach · P Schönknecht · U Hegerl · T Hensch
    Pharmacopsychiatry 09/2015; 48(06). DOI:10.1055/s-0035-1558016 · 1.85 Impact Factor
  • F Schmidt · C Sander · M Dietz · C Nowak · T Schröder · H Himmerich · P Schönknecht · U Hegerl
    Pharmacopsychiatry 09/2015; 48(06). DOI:10.1055/s-0035-1558034 · 1.85 Impact Factor
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    ABSTRACT: Background The LIFE-Adult-Study is a population-based cohort study, which has recently completed the baseline examination of 10,000 randomly selected participants from Leipzig, a major city with 550,000 inhabitants in the east of Germany. It is the first study of this kind and size in an urban population in the eastern part of Germany. The study is conducted by the Leipzig Research Centre for Civilization Diseases (LIFE). Our objective is to investigate prevalences, early onset markers, genetic predispositions, and the role of lifestyle factors of major civilization diseases, with primary focus on metabolic and vascular diseases, heart function, cognitive impairment, brain function, depression, sleep disorders and vigilance dysregulation, retinal and optic nerve degeneration, and allergies. Methods/design The study covers a main age range from 40-79 years with particular deep phenotyping in elderly participants above the age of 60. The baseline examination was conducted from August 2011 to November 2014. All participants underwent an extensive core assessment programme (5-6 h) including structured interviews, questionnaires, physical examinations, and biospecimen collection. Participants over 60 underwent two additional assessment programmes (3-4 h each) on two separate visits including deeper cognitive testing, brain magnetic resonance imaging, diagnostic interviews for depression, and electroencephalography. Discussion The participation rate was 33 %. The assessment programme was accepted well and completely passed by almost all participants. Biomarker analyses have already been performed in all participants. Genotype, transcriptome and metabolome analyses have been conducted in subgroups. The first follow-up examination will commence in 2016.
    BMC Public Health 07/2015; 15(1). DOI:10.1186/s12889-015-1983-z · 2.26 Impact Factor
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    ABSTRACT: To date, limited data are available regarding the inter-site consistency of test-retest reproducibility of functional connectivity measurements, in particular with regard to integrity of the Default Mode Network (DMN) in elderly participants. We implemented a harmonized resting-state fMRI protocol on 13 clinical scanners at 3.0T using vendor-provided sequences. Each site scanned a group of 5 healthy elderly participants twice, at least a week apart. We evaluated inter-site differences and test-retest reproducibility of both temporal signal-to-noise ratio (tSNR) and functional connectivity measurements derived from: i) seed-based analysis (SBA) with seed in the posterior cingulate cortex (PCC), ii) group independent component analysis (ICA) separately for each site (site ICA), and iii) consortium ICA, with group ICA across the whole consortium. Despite protocol harmonization, significant and quantitatively important inter-site differences remained in the tSNR of resting-state fMRI data; these were plausibly driven by hardware and pulse sequence differences across scanners which could not be harmonized. Nevertheless, the tSNR test-retest reproducibility in the consortium was high (ICC=0.81). The DMN was consistently extracted across all sites and analysis methods. While significant inter-site differences in connectivity scores were found, there were no differences in the associated test-retest error. Overall, ICA measurements were more reliable than PCC-SBA, with site ICA showing higher reproducibility than consortium ICA. Across the DMN nodes, the PCC yielded the most reliable measurements (≈4% test-retest error, ICC=0.85), the medial frontal cortex the least reliable (≈12%, ICC=0.82) and the lateral parietal cortices were in between (site ICA). Altogether these findings support usage of harmonized multisite studies of resting-state functional connectivity to characterize longitudinal effects in studies that assess disease progression and treatment response.
    NeuroImage 07/2015; DOI:10.1016/j.neuroimage.2015.07.010 · 6.36 Impact Factor
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    ABSTRACT: In patients with affective disorders, the full-blown symptomatology of a depressive episode can develop very fast (eg, within 1 d) or slowly over weeks or months. These differences in the speed of onset of depression are likely to reflect stable intraindividual differences in neurobiological pathomechanisms. This article presents available data on this issue from published studies and from a recently unpublished study and discusses the relevance of these data for diagnostic, therapeutic, and research purposes. On the basis a database search, we reviewed the literature on speed of onset of depressive episodes. Results of a study for which only some of the data have previously been published involving 205 patients with unipolar or bipolar depression were also considered. Five older studies produced data concerning the speed of onset of depressive episodes. In addition, our research group has conducted 2 other more recent studies that used the Onset of Depression Inventory to assess the speed of onset of depressive episodes. The major findings of the studies we examined were that depression developed within 1 week in 50% to 58% of patients with a bipolar disorder, whereas only in 7.4% to 21.4% of those with unipolar depression. Different depressive episodes appeared to develop at a similar speed within individual subjects (correlation coefficients: 0.46 to 0.66). Consistent evidence from 2 studies that used the Onset of Depression Inventory revealed that rapid onset of a depressive episode is more common in patients with bipolar disorder than in those with unipolar major depressive disorder and may be an indication of a latent, not yet expressed, bipolar disorder. The neurobiology of the speed of onset of depressive episodes is a topic for future research.
    07/2015; 21(4):275-280. DOI:10.1097/PRA.0000000000000081
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    ABSTRACT: Recently, there has been an increased interest in the use of automatically segmented subfields of the human hippocampal formation derived from magnetic resonance imaging (MRI). However, little is known about the test-retest reproducibility of such measures, particularly in the context of multisite studies. Here, we report the reproducibility of automated Freesurfer hippocampal subfields segmentations in 65 healthy elderly enrolled in a consortium of 13 3T MRI sites (five subjects per site). Participants were scanned in two sessions (test and retest) at least one week apart. Each session included two anatomical 3D T1 MRI acquisitions harmonized in the consortium. We evaluated the test-retest reproducibility of subfields segmentation (i) to assess the effects of averaging two within-session T1 images and (ii) to compare subfields with whole hippocampus volume and spatial reliability. We found that within-session averaging of two T1 images significantly improved the reproducibility of all hippocampal subfields but not that of the whole hippocampus. Volumetric and spatial reproducibility across MRI sites were very good for the whole hippocampus, CA2-3, CA4-dentate gyrus (DG), subiculum (reproducibility error∼2% and DICE > 0.90), good for CA1 and presubiculum (reproducibility error ∼ 5% and DICE ∼ 0.90), and poorer for fimbria and hippocampal fissure (reproducibility error ∼ 15% and DICE < 0.80). Spearman's correlations confirmed that test-retest reproducibility improved with volume size. Despite considerable differences of MRI scanner configurations, we found consistent hippocampal subfields volumes estimation. CA2-3, CA4-DG, and sub-CA1 (subiculum, presubiculum, and CA1 pooled together) gave test-retest reproducibility similar to the whole hippocampus. Our findings suggest that the larger hippocampal subfields volume may be reliable longitudinal markers in multisite studies. Hum Brain Mapp, 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Human Brain Mapping 06/2015; 36(9). DOI:10.1002/hbm.22859 · 5.97 Impact Factor
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    ABSTRACT: α4β2* nicotinic receptors (α4β2* nAChRs) could provide a biomarker in neuropsychiatric disorders (e.g. Alzheimer´s and Parkinson’s disease, depressive disorders, and nicotine addiction). However, there is a lack of α4β2* nAChR specific PET radioligands with kinetics fast enough to enable quantification of nAChR within a reasonable time frame. Following on from promising preclinical results, the aim of the present study was to evaluate for the first time in humans the novel PET radioligand (-)-[18 F]Flubatine, formerly known as (-)-[18 F]NCFHEB, as a tool for α4β2* nAChR imaging and in vivo quantification.
    NeuroImage 05/2015; 118. DOI:10.1016/j.neuroimage.2015.05.065 · 6.36 Impact Factor
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    ABSTRACT: In preclinical studies, the hypothalamic polypeptide melanin-concentrating hormone (MCH) has been shown to be involved in depression-like behavior and modulations of MCH and MCH-receptors were proposed as potential new antidepressant drug targets. For the first time, MCH serum levels were explored in 30 patients with major depressive disorder (MDD) prior to (T1) and after 2 (T2) and 4 weeks (T3) of antidepressant treatment and in 30 age- and sex-matched healthy controls by applying a fluorescence immunoassay. Levels of MCH did not differ significantly between un-medicated patients (444.11±174.63pg/mL SD) and controls (450.68±210.03pg/mL SD). In MDD patients, MCH levels significantly decreased from T1 to T3 (F=4.663; p=0.013). Post-hoc analyses showed that these changes were limited to patients treated with mirtazapine but not escitalopram and female but not male patients. MCH-levels showed high correlations from T1 to T3 (r≥0.964, p<0.001) and were found to correlate significantly with parameters of sleep within the controls. Small sample size. No follow-up measures were performed within the control group. Our findings suggest peripheral MCH-levels not to be altered in depression but possibly reflecting depression-related state properties that can be modulated by sleep, medication and sex. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Affective Disorders 04/2015; 180:207-213. DOI:10.1016/j.jad.2015.03.039 · 3.38 Impact Factor
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    ABSTRACT: The "Onset of Depression Inventory" (ODI) represents a patient interview which aims to register the speed of onset of depression systematically. The purpose of this study was to evaluate the patient-relative agreement regarding the speed of onset of depression in the patients. The ODI was investigated in 31 patients with a depressive episode. Moreover, 31 patients' relatives participated in an interview for which a modified version of the ODI (for relatives of depressed patients; ODI-A) was applied. There was a significant association between patients' estimation of the speed of onset of the depressive episode and relatives' estimation of this parameter in the case of patients and relatives living in a common household (rho = 0.68; p = 0.006). There was an agreement between patients and their relatives regarding the speed of onset of the current depressive episodes, however only if they lived in a common household.
    International Journal of Psychiatry in Clinical Practice 03/2015; 19(3):1-11. DOI:10.3109/13651501.2015.1028413 · 1.39 Impact Factor
  • P. Toro · J.I. Reculé · P. Diaz · J.M. Allendes · P. Schönknecht · J. Schröder
    European Psychiatry 03/2015; 30:204. DOI:10.1016/S0924-9338(15)30164-4 · 3.44 Impact Factor
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    Frank Martin Schmidt · Roland Mergl · Barbara Stach · Ina Jahn · Peter Schönknecht
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    ABSTRACT: Objectives. Alterations in neuronal and glial integrity are considered to be of pathogenic impact on major depressive disorder (MDD). For MDD, data on cerebrospinal fluid (CSF) levels of neuron-specific enolase (NSE) are lacking and scarce for glial protein S100B. Methods. We measured CSF levels of NSE and S100B in 31 patients with MDD and 32 mentally healthy controls using electrochemiluminescence immunoassays (ECLIA). Results. Adjusted means of NSE were significantly elevated in the MDD patients (11.73 ng/ml (9.95-13.52 95% CI) compared to the controls (6.17 ng/ml (4.55-7.78), F = 9.037, P = 0.004. Effect size for adjusted mean group difference of 5.57 ng/ml was found invariably high (Cohen's d = 1.23). Differentiating MDD from controls, a NSE cut-off of 7.94 ng/ml showed sensitivity of 81% (95% CI 63.7-90.8) and specificity of 75% (95% CI 57.9-86.7). Adjusted levels of S100B did not differ significantly between the two groups (1.12 ng/ml (0.77-1.48) in MDD, 0.97 ng/ml (0.64-1.30) in controls). Conclusions. Our results of elevated CSF-NSE levels support neuronal pathology in MDD and the potential use of CSF-NSE as marker in clinical diagnostics. Missing group differences in S100B do not promote a specific glial pathology in depressive disorders.
    The World Journal of Biological Psychiatry 02/2015; 16(2):106-113. DOI:10.3109/15622975.2014.952776 · 4.18 Impact Factor
  • U. Hegerl · P. Schönknecht · T. Hensch · S. Olbrich · M. Kluge · H. Himmerich · C. Sander
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    ABSTRACT: Peripheral brain-derived neurotrophic factor (BDNF) is decreased in acute major depressive disorder (MDD) and bipolar disorder (BD) and recovered after treatment. Here we validated on a meta-analytical level whether BDNF restores differentially according to treatment response and whose measurements could be used as a biomarker, plasma or serum. Using strict inclusion criteria, we compared BDNF in healthy controls and patients with MDD (38 studies, n=6619), and BD (17 studies, n=1447). Pre- and post-treatment BDNF levels were meta-analyzed according to treatment response in patients from 21 MDD studies (n=735) and 7 BD studies (n=88). Serum and plasma subgroups were analyzed, publication bias was assessed and heterogeneity was investigated. Serum and plasma BDNF were decreased in acute MDD and BD, and did not differ in euthymia in comparison with control subjects. Antidepressive treatment increased serum BDNF levels in MDD in responders (Cohen׳s d (d)=1.27, p=4.4E-07) and remitters (d=0.89, p=0.01), significantly more than in non-responders (d=0.11, p=0.69). For plasma BDNF in MDD and for BD, the evidence was insufficient for a meta-analysis. Although no significant difference was found between serum and plasma ES, variance of plasma ES was higher. Between-study heterogeneity was explained only partially; signs of publication bias in serum studies. Serum BDNF might be regarded as a biomarker for the successful treatment of MDD. Serum measurements seem more reliable than plasma ones. Further research should focus on defining optimal time points for BDNF measurements and increase evidence for the usage of BDNF as a predictive biomarker in BD. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Affective Disorders 11/2014; 174C:432-440. DOI:10.1016/j.jad.2014.11.044 · 3.38 Impact Factor
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    Maria Strauss · Roland Mergl · Christian Sander · Peter Schönknecht · Ulrich Hegerl
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    ABSTRACT: Background: Depressive episodes show large interindividual differences concerning their speed of onset and speed of recovery, which might suggest differences in underlying pathophysiological processes. The aim of the present study was to assess whether there is a relationship between the speed of onset and the speed of recovery from depressive episodes. Methods: The speed of onset and the speed of recovery from depression were assessed using a structured patient interview, the Onset of Depression Inventory (ODI). In total, 28 patients with bipolar depression and 91 patients with unipolar depression were included. Results: The mean speed of onset of depression was significantly faster than the mean speed of recovery from depression (35.25, range 0-360 days vs. 59.60, range 0.13-720 days; Z = -3.40; p = 0.001). The correlation between these variables was positive, but numerically low (ρ = 0.22; p = 0.016). The speed of onset of the previous episode and that of the present episode were significantly correlated (ρ = 0.45; p < 0.001). Limitations: Data are based on retrospective patient reports within a naturalistic study. Conclusions: While the speed of onset of depressive episodes has been found to show large interindividual variability and some intraindividual stability, the data of this study do not indicate that the neurobiological processes involved in the onset of and in the recovery from depressive episodes are closely linked. © 2014 S. Karger AG, Basel.
    Psychopathology 10/2014; 48(1). DOI:10.1159/000367601 · 2.08 Impact Factor
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    ABSTRACT: Unlabelled: (-)-(18)F-flubatine is a promising tracer for neuroimaging of nicotinic acetylcholine receptors (nAChRs), subtype α4β2, using PET. Radiation doses after intravenous administration of the tracer in mice and piglets were assessed to determine the organ doses (ODs) and the effective dose (ED) to humans. The results were compared with subsequent clinical investigations in human volunteers. Methods: Twenty-seven female CD1 mice (weight ± SD, 28.2 ± 2.1 g) received intravenous injection of 0.75 ± 0.33 MBq of (-)-(18)F-flubatine. Up to 240 min after injection, 3 animals per time point were sacrificed and the organs harvested, weighed, and counted in a γ counter to determine mass and activity, respectively. Furthermore, whole-body PET scans of 5 female piglets (age ± SD, 44 ± 3 d; weight ± SD, 13.7 ± 1.7 kg) and 3 humans (2 men and 1 woman; age ± SD, 59.6 ± 3.9 y; weight ± SD, 74.3 ± 3.1 kg) were obtained up to 236 min (piglets) and 355 min (humans) after injection of 186.6 ± 7.4 and 353.7 ± 10.2 MBq of (-)-(18)F-flubatine, respectively, using a PET/CT scanner. The CT was used for delineation of the organs. Exponential curves were fitted to the time-activity-data, and time and mass scales were adapted to the human anatomy. The ODs were calculated using OLINDA/EXM (version 1.0); EDs were calculated with the tissue-weighting factors of ICRP103. Results: After the injection of (-)-(18)F-flubatine, there were no adverse or clinically detectable pharmacologic effects in any of the subjects. The highest activities after injection were found in the kidneys, urinary bladder, and liver. The urinary bladder receives the highest OD in all investigated species, followed by the kidneys and the liver for animals and humans, respectively. On the basis of mouse, piglet, and human kinetic data, the projected human ED of (-)-(18)F-flubatine was estimated to be 12.5 μSv/MBq in mice, 14.7 ± 0.7 μSv/MBq in piglets, and 23.4 ± 0.4 μSv/MBq in humans. Conclusion: As has been demonstrated for other PET radiotracers, preclinical (i.e., animal-derived) dosimetry underestimates the ED to humans, in the current case of (-)-(18)F-flubatine by 34%-44%.
    Journal of Nuclear Medicine 10/2014; 55(11). DOI:10.2967/jnumed.114.137059 · 6.16 Impact Factor
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    ABSTRACT: Background The relationship between leptin and affective disorders is still unknown. Methods We measured free and bound leptin in 13 drug naïve subjects. Results Leptin did not significantly differ between patients and controls. Conclusions As part of future studies, it also appears useful to distinguish between free and bound leptin.
    Psychiatry Research 10/2014; 219(2). DOI:10.1016/j.psychres.2014.05.030 · 2.47 Impact Factor
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    ABSTRACT: Introduction (-)-[18 F]Flubatine is a PET tracer with high affinity and selectivity for the nicotinic acetylcholine α4β2 receptor subtype. A clinical trial assessing the availability of this subtype of nAChRs was performed. From a total participant number of 21 Alzheimer’s disease (AD) patients and 20 healthy controls (HCs), the following parameters were determined: plasma protein binding, metabolism and activity distribution between plasma and whole blood. Methods Plasma protein binding and fraction of unchanged parent compound were assessed by ultracentrifugation and HPLC, respectively. The distribution of radioactivity (parent compound + metabolites) between plasma and whole blood was determined ex vivo at different time-points after injection by gamma counting after separation of whole blood by centrifugation into the cellular and non-cellular components. In additional experiments in vitro, tracer distribution between these blood components was assessed for up to 90 min. Results A fraction of 15 ± 2 % of (-)-[18 F]Flubatine was found to be bound to plasma proteins. Metabolic degradation of (-)-[18 F]Flubatine was very low, resulting in almost 90 % unchanged parent compound at 90 min p.i. with no significant difference between AD and HC. The radioactivity distribution between plasma and whole blood changed in vivo only slightly over time from 0.82 ± 0.03 at 3 min p.i. to 0.87 ± 0.03 at 270 min p.i. indicating the contribution of only a small amount of metabolites. In vitro studies revealed that (-)-[18 F]Flubatine was instantaneously distributed between cellular and non-cellular blood parts. Discussion (-)-[18 F]Flubatine exhibits very favourable characteristics for a PET radiotracer such as slow metabolic degradation and moderate plasma protein binding. Equilibrium of radioactivity distribution between plasma and whole blood is reached instantaneously and remains almost constant over time allowing both convenient sample handling and facilitated fractional blood volume contribution assessment.
    Nuclear Medicine and Biology 07/2014; 41(6). DOI:10.1016/j.nucmedbio.2014.03.018 · 2.41 Impact Factor
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    ABSTRACT: Early-onset (EOD) and late-onset depression (LOD) are associated with different neuropsychological syndromes and structural brain changes. In this article, neuroimaging studies examining structural brain changes in elderly depressed patients are reviewed. The presented findings support current assumptions that depression in the elderly generally is associated with volume reductions in brain structures, notably in the hippocampus and the orbitofrontal cortex (OFC). Concerning structural cerebral differences between EOD and LOD, the review yielded conflicting results—only for OFC, but not for amygdala or hippocampus, pronounced effects in LOD than in EOD can be assumed. © 2014 Wiley Periodicals, Inc. Int J Imaging Syst Technol, 24, 149–160, 2014
    International Journal of Imaging Systems and Technology 06/2014; 24(2). DOI:10.1002/ima.22089 · 1.30 Impact Factor
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    Journal of Psychiatric Research 06/2014; 53(1). DOI:10.1016/j.jpsychires.2014.02.021 · 3.96 Impact Factor

Publication Stats

2k Citations
541.70 Total Impact Points


  • 2008–2015
    • University of Leipzig
      • Klinik und Poliklinik für Psychiatrie und Psychotherapie
      Leipzig, Saxony, Germany
    • University Hospital Frankfurt
      Frankfurt, Hesse, Germany
  • 2013
    • Otto-von-Guericke-Universität Magdeburg
      Magdeburg, Saxony-Anhalt, Germany
  • 1999–2012
    • Universität Heidelberg
      • • Department of Geriatric Psychiatry
      • • Section Gerontopsychiatrische Research
      Heidelburg, Baden-Württemberg, Germany
  • 2003
    • German Cancer Research Center
      • Division of Radiology
      Heidelberg, Baden-Wuerttemberg, Germany