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Dive into the research topics where Claudia Schilling is active.

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Featured researches published by Claudia Schilling.


International Psychogeriatrics | 2010

Matrix metalloproteinases in peripheral blood and cerebrospinal fluid in patients with Alzheimer's disease

Solveig Horstmann; Leila Budig; Humphrey Gardner; James A. Koziol; Michael Deuschle; Claudia Schilling; Simone Wagner

BACKGROUND Deposition of amyloid beta in senile plaques and in cerebral blood vessels is one hallmark of the pathogenesis of Alzheimers disease (AD). The ability of several matrix metalloproteinases (MMPs) to degrade amyloid precursor protein leading to aggregation of amyloid beta, as well as the increased expression of MMPs in post mortem brain tissue of Alzheimers patients, indicate that MMPs play an important role in the pathogenesis of AD. METHODS We investigated levels of MMP-2,-3,-9 and -10 in plasma and cerebrospinal fluid (CSF) of AD patients (n = 14) by gelatin and casein zymography. Comparisons between AD patients and controls relative to levels of MMP-2, MMP-3, MMP-9, and MMP-10 were made with Wilcoxon rank statistics. Pearson correlations were computed as measures of association. RESULTS MMP-3 in AD was significantly elevated in plasma (p = 0.006) and there was a trend towards increase in CSF (p = 0.05). MMP-2 in CSF of AD patients was significantly decreased (p = 0.02) while levels in plasma remained unchanged. MMP-9 and MMP-10 could not be detected in CSF; MMP-10 was unchanged in plasma, but MMP-9 was significantly decreased (p = 0.02). CONCLUSIONS These findings constitute further evidence for the important role of MMPs in the pathogenesis of AD.


Neuroendocrinology | 2009

Cortisol Metabolism in Depressed Patients and Healthy Controls

Benedikt Römer; Sabina Lewicka; Daniel Kopf; Florian Lederbogen; Bettina Hamann; Maria Gilles; Claudia Schilling; Vera Onken; Pascal Frankhauser; Michael Deuschle

Background: Chronic stress as well as major depressive disorders are associated with hypercortisolemia and impaired hypothalamic-pituitary-adrenocortical axis functioning. The aim of this study was to determine whether in major depression changes in the activity patterns of local modulators of glucocorticoid action might contribute to an increase in cortisol bioavailability and if they change during antidepressant treatment and clinical response. Methods: Concentrations of urinary total cortisol (UFF), urinary total cortisone (UFE), tetrahydrocortisone (THE), tetrahydrocortisol (THF) and allo-THF (5α-THF) were measured in 10-hour nocturnal urine samples of 19 depressed patients and 15 healthy controls. The activity of 11β-hydroxysteroid dehydrogenases (11β-HSD) as well as 5α- and 5β-reductases was assessed by calculating the ratios of glucocorticoid metabolites. Patients were treated for 28 days with either mirtazapine or venlafaxine. Enzyme activity was observed during the course of treatment and compared to healthy controls. Responders to treatment were selected for this analysis. Results: Depressed patients showed reduced 5α-reductase activity manifested as a significantly lower amount of 5α-THF (102.8 ± 167.2 vs. 194.6 ± 165.8 μg, p = 0.019). The increase in the UFF/UFE ratio (0.73 ± 0.32 vs. 0.29 ± 0.13, p < 0.0001) indicates reduced activity of renal 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). During pharmacological treatment, 5α-reductase activity in patients returned to the level of the control group, while the decrease in 11β-HSD2 activity persisted until day 28. Conclusions: Our results show changes in activity of intracellular modulators of steroid action in major depressive disorders, particularly a reduced activity of the intracellular cortisol-deactivating enzymes 5α-reductase and 11β-HSD2. These changes suggest an increase in cortisol bioavailability within tissues.


Schizophrenia Research | 2014

Reduced activation in ventral striatum and ventral tegmental area during probabilistic decision-making in schizophrenia

Franziska Rausch; Daniela Mier; Sarah Eifler; Christine Esslinger; Claudia Schilling; Frederike Schirmbeck; Susanne Englisch; Andreas Meyer-Lindenberg; Peter Kirsch; Mathias Zink

Patients with schizophrenia suffer from deficits in monitoring and controlling their own thoughts. Within these so-called metacognitive impairments, alterations in probabilistic reasoning might be one cognitive phenomenon disposing to delusions. However, so far little is known about alterations in associated brain functionality. A previously established task for functional magnetic resonance imaging (fMRI), which requires a probabilistic decision after a variable amount of stimuli, was applied to 23 schizophrenia patients and 28 healthy controls matched for age, gender and educational levels. We compared activation patterns during decision-making under conditions of certainty versus uncertainty and evaluated the process of final decision-making in ventral striatum (VS) and ventral tegmental area (VTA). We replicated a pre-described extended cortical activation pattern during probabilistic reasoning. During final decision-making, activations in several fronto- and parietocortical areas, as well as in VS and VTA became apparent. In both of these regions schizophrenia patients showed a significantly reduced activation. These results further define the network underlying probabilistic decision-making. The observed hypo-activation in regions commonly associated with dopaminergic neurotransmission fits into current concepts of disrupted prediction error signaling in schizophrenia and suggests functional links to reward anticipation. Forthcoming studies with patients at risk for psychosis and drug-naive first episode patients are necessary to elucidate the development of these findings over time and the interplay with associated clinical symptoms.


Movement Disorders | 2010

Restless legs syndrome: evidence for nocturnal hypothalamic-pituitary-adrenal system activation.

Claudia Schilling; Michael Schredl; Philipp Strobl; Michael Deuschle

Epidemiological studies consistently point to a relationship between restless legs syndrome (RLS) and cardiovascular disease. The mechanism underlying this association is unclear. Activation of the hypothalamic‐pituitary‐adrenal (HPA) system has been shown to contribute to the metabolic syndrome and an enhanced cardiovascular risk. We investigated cortisol levels as an indicator of HPA system activity in RLS during the nighttime, when RLS symptoms are at their maximum. We assessed nocturnal urinary cortisol excretion in 73 patients with RLS and 34 healthy controls, controlling for age and gender. Urine sampling was paralleled by polysomnographic recordings. We found significantly enhanced nocturnal cortisol excretion in RLS, demonstrating nocturnal HPA system overactivity in RLS. HPA system overactivity is a possible mechanism contributing to the enhanced load of cardiovascular disease in RLS patients. Nocturnal cortisol release showed weak correlations with some polysomnographic parameters of disturbed sleep, making a potential contribution of RLS‐induced sleep disruption to HPA system activation conceivable.


Journal of Sleep Research | 2014

Pineal gland volume in primary insomnia and healthy controls: a magnetic resonance imaging study.

Jan Malte Bumb; Claudia Schilling; Frank Enning; Leila Haddad; Franc Paul; Florian Lederbogen; Michael Deuschle; Michael Schredl; Ingo Nölte

Little is known about the relation between pineal volume and insomnia. Melatonin promotes sleep processes and, administered as a drug, it is suitable to improve primary and secondary sleep disorders in humans. Recent magnetic resonance imaging studies suggest that human plasma and saliva melatonin levels are partially determined by the pineal gland volume. This study compares the pineal volume in a group of patients with primary insomnia to a group of healthy people without sleep disturbance. Pineal gland volume (PGV) was measured on the basis of high‐resolution 3 Tesla MRI (T1‐magnetization prepared rapid gradient echo) in 23 patients and 27 controls, matched for age, gender and educational status. Volume measurements were performed conventionally by manual delineation of the pineal borders in multi‐planar reconstructed images. Pineal gland volume was significantly smaller (P < 0.001) in patients (48.9 ± 26.6 mm3) than in controls (79 ± 30.2 mm3). In patients PGV correlated negatively with age (r = −0.532; P = 0.026). Adjusting for the effect of age, PGV and rapid eye movement (REM) latency showed a significant positive correlation (rS = 0.711, P < 0.001) in patients. Pineal volume appears to be reduced in patients with primary insomnia compared to healthy controls. Further studies are needed to clarify whether low pineal volume is the basis or the consequence of functional sleep changes to elucidate the molecular pathology for the pineal volume loss in primary insomnia.


Neuroscience Letters | 2014

Hypocretin in cerebrospinal fluid is positively correlated with Tau and pTau

Michael Deuschle; Claudia Schilling; F. Markus Leweke; Frank Enning; Thomas Pollmächer; Hermann Esselmann; Jens Wiltfang; Lutz Frölich; Isabella Heuser

It has been suggested that sleep-wake regulation as well as hypocretins play a role in the pathophysiology of Alzheimers disease. We analyzed Aβ40, Aβ42, Tau protein, phosphorylated Tau (pTau) protein as well as hypocretin-1 concentrations in the CSF of a detection sample of 10 patients with Alzheimers disease (AD) as well as 10 age- and gender-matched patients with major depression as a comparison group of different pathology. In order to replicate the findings, we used a confirmation sample of 17 AD patients and 8 patients with major depression. We found hypocretin-1 concentrations in CSF not to differ between patients with depression and AD. However, hypocretin-1 was significantly related to Tau (r=0.463, p<0.001) and pTau (r=0.630, p<0.0001). These effects were more pronounced in depressed patients when compared to AD patients. We conclude that hypocretin-1 may play a role in the metabolism of Tau proteins across different diagnostic entities including AD. It has to be determined whether there is a causal relationship between hypocretin-1 and Tau as well as pTau.


Journal of Clinical Psychopharmacology | 2013

Leptin plasma concentrations increase during antidepressant treatment with amitriptyline and mirtazapine, but not paroxetine and venlafaxine: leptin resistance mediated by antihistaminergic activity?

Claudia Schilling; Maria Gilles; Werner F. Blum; Emmerich Daseking; Michael Colla; Bettina Weber-Hamann; Florian Lederbogen; Bertram Krumm; Isabella Heuser; Stefan A. Wudy; Daniel Kopf; Michael Deuschle

Abstract Treatment with several psychopharmacological agents has been associated with increased leptin plasma concentrations. We measured leptin plasma concentrations in 76 adult depressed patients after a 6-day washout phase and again after 35 days of treatment with amitriptyline or paroxetine, as well as in 73 depressed patients after 28 days of treatment with either mirtazapine or venlafaxine. Leptin plasma concentrations increased during treatment with amitriptyline and mirtazapine, even after controlling for increased body mass index and irrespective of response to treatment [14.5 (13.8) vs 20.3 (18.7) ng/mL, and 12.2 (15.8) vs 14.4 (16.5) ng/mL in the 2 cohorts, respectively]. In contrast, paroxetine and venlafaxine treatment was not associated with changes in leptin plasma concentrations [14.8 (12.0) vs 13.6 (10.6); 15.9 (17.3) vs 13.5 (14.6) ng/mL] nor with weight gain. We conclude that treatment with amitriptyline or mirtazapine is associated with an increase in leptin secretion beyond change in weight. Thus, high leptin levels apparently are ineffective in the control of weight gain, indicating leptin resistance. Leptin resistance may be mediated by an antihistaminergic effect on hypothalamic nuclei integrating signals relevant for energy balance.


Psychiatry Research-neuroimaging | 2010

Antidepressant treatment with mirtazapine, but not venlafaxine, lowers cortisol concentrations in saliva: A randomised open trial

Barbara Scharnholz; Bettina Weber-Hamann; Florian Lederbogen; Claudia Schilling; Maria Gilles; Vera Onken; Pascal Frankhauser; Daniel Kopf; Michael Deuschle

Lowering the concentrations of free cortisol in depressed patients may be an important prerequisite to prevent glucocorticoid-related sequelae of depression. We tested the hypothesis that the hypothalamus-pituitary-adrenal (HPA) system-dampening effects of venlafaxine and mirtazapine differ. We compared the course of morning (08.00h) and afternoon saliva cortisol (16.00h) in 42 mirtazapine- and 45 venlafaxine-treated depressed patients during a 1-week wash-out and a 4-week treatment period in a randomised open trial. Mirtazapine lowered afternoon cortisol from week 1 to 4. In contrast, during the course of the entire treatment period, venlafaxine did not attenuate saliva cortisol concentrations. Treatment effects of mirtazapine on cortisol concentrations did not differ in remitters and non-remitters to treatment. High baseline cortisol concentrations, on the other hand, were related to an unfavourable course during venlafaxine treatment and patients remitting during venlafaxine treatment had significantly lower afternoon cortisol concentrations in saliva, when compared to non-remitting patients. Thus, mirtazapine and venlafaxine show different effects on HPA system activity as measured by saliva cortisol. This may be of relevance with regard to physical sequelae of depression.


Clinical Neuropharmacology | 2013

Heart Rate Variability During Antidepressant Treatment With Venlafaxine and Mirtazapine

Johannes Terhardt; Florian Lederbogen; Anne Feuerhack; Bettina Hamann-Weber; Maria Gilles; Claudia Schilling; Olivera Lecei; Michael Deuschle

AbstractHeart rate variability (HRV) reflects the cardiac autonomic regulation, and reduced HRV is considered a pathophysiological link between depression and cardiovascular mortality. So far, there is only limited information on the effects of venlafaxine and mirtazapine on HRV.We studied 28 nondepressed controls and 41 moderately depressed patients being treated with venlafaxine (n = 20) and mirtazapine (n = 21). Heart rate, blood pressure, and HRV were measured after a 6-day washout as well as after 14 and 28 days of treatment in supine and upright position.We found increased heart rate and reduced HRV in the depressed patients compared with the nondepressed controls. Moreover, HRV total power declined during the treatment period. Medication and remission status after 4 weeks were not related to the change in HRV.We conclude that depression is related to reduced HRV, which might reflect sympathovagal dysbalance. The widely used antidepressants venlafaxine and mirtazapine led to further decline in HRV. Clinicians should consider HRV effects in the selection of antidepressants.


Pharmacopsychiatry | 2010

Does night-time cortisol excretion normalize in the long-term course of depression?

Barbara Scharnholz; Florian Lederbogen; A. Feuerhack; A. Bach; Daniel Kopf; P. Frankhauser; V. Onken; Claudia Schilling; Maria Gilles; Bettina Hamann; Michael Deuschle

INTRODUCTION While there is extensive literature on HPA system activity in acutely depressed patients, there is only limited information about the presence of hypercortisolemia during the interepisode interval of affective disorders. We hypothesized an increase in HPA system activity in depressed patients compared to controls, and proposed that night-time cortisol excretion during follow-up will depend on clinical outcome. METHODS We measured night-time cortisol excretion in 27 patients during an acute episode of major depression as well as a 20-week follow-up. 40 healthy subjects served as control group. RESULTS During the acute episode depressed patients showed increased levels of night-time cortisol excretion compared to healthy controls. Both, patients with full and sustained remission (n=8) as well as patients with incomplete remission or relapse (n=19) showed declining cortisol excretion in night-time urine during follow-up. At the end of follow-up cortisol excretion did not differ between patients with affective disorder and healthy controls. DISCUSSION Irrespective of residual depressive symptoms, HPA system activity declines after the generally investigated acute depressive episode.

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