@misc{TschornKuhlmannRieckmannetal.2020,
  author    = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas},
  title     = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {1},
  issn      = {1866-8364},
  doi       = {10.25932/publishup-55731},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-557315},
  pages     = {11},
  year      = {2020},
  abstract  = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.},
  language  = {en}
}
@article{TschornKuhlmannRieckmannetal.2020,
  author    = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas},
  title     = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease},
  series = {Acta Neuropsychiatrica},
  volume    = {33},
  journal   = {Acta Neuropsychiatrica},
  number    = {1},
  publisher = {Cambridge Univ. Press},
  address   = {Cambridge},
  issn      = {1601-5215},
  doi       = {10.1017/neu.2020.31},
  pages     = {22 -- 30},
  year      = {2020},
  abstract  = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.},
  language  = {en}
}
@article{StroehleSchmidtSchultzetal.2015,
  author    = {Stroehle, Andreas and Schmidt, Dietlinde K. and Schultz, Florian and Fricke, Nina and Staden, Theresa and Hellweg, Rainer and Priller, Josef and Rapp, Michael Armin and Rieckmann, Nina},
  title     = {Drug and Exercise Treatment of Alzheimer Disease and Mild Cognitive Impairment: A Systematic Review and Meta-Analysis of Effects on Cognition in Randomized Controlled Trials},
  series = {The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry},
  volume    = {23},
  journal   = {The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry},
  number    = {12},
  publisher = {Elsevier},
  address   = {New York},
  issn      = {1064-7481},
  doi       = {10.1016/j.jagp.2015.07.007},
  pages     = {1234 -- 1249},
  year      = {2015},
  abstract  = {Objective: Demographic changes are increasing the pressure to improve therapeutic strategies against cognitive decline in Alzheimer disease (AD) and mild cognitive impairment (MCI). Besides drug treatment, physical activity seems to be a promising intervention target as epidemiological and clinical studies suggest beneficial effects of exercise training on cognition. Using comparable inclusion and exclusion criteria, we analyzed the efficacy of drug therapy (cholinesterase inhibitors, memantine, and Ginkgo biloba) and exercise interventions for improving cognition in AD and MCI populations. Methods: We searched The Cochrane Library, EBSCO, OVID, Web of Science, and U.S Food and Drug Administration data from inception through October 30, 2013. Randomized controlled trials in which at least one treatment arm consisted of an exercise or a pharmacological intervention for AD or MCI patients, and which had either a non-exposed control condition or a control condition that received another intervention. Treatment discontinuation rates and Standardized Mean Change score using Raw score standardization (SMCR) of cognitive performance were calculated. Results: Discontinuation rates varied substantially and ranged between 0\% and 49\% with a median of 18\%. Significantly increased discontinuation rates were found for galantamine and rivastigmine as compared to placebo in AD studies. Drug treatments resulted in a small pooled effect on cognition (SMCR: 0.23, 95\% CI: 0.20 to 0.25) in AD studies (N = 45, 18,434 patients) and no effect in any of the MCI studies (N = 5, 3,693 patients; SMCR: 0.03, 95\% CI: 0.00 to 0.005). Exercise interventions had a moderate to strong pooled effect size (SMCR: 0.83, 95\% CI: 0.59 to 1.07) in AD studies (N = 4, 119 patients), and a small effect size (SMCR: 0.20, 95\% CI: 0.11 to 0.28) in MCI (N = 6, 443 patients). Conclusions: Drug treatments have a small but significant impact on cognitive functioning in AD and exercise has the potential to improve cognition in AD and MCI. Head-to-head trials with sufficient statistical power are necessary to directly compare efficacy, safety, and acceptability. Combining these two approaches might further increase the efficacy of each individual intervention. Identifier: PROSPERO (2013:CRD42013003910).},
  language  = {en}
}
@article{TschornRieckmannAroltetal.2019,
  author    = {Tschorn, Mira and Rieckmann, Nina and Arolt, Volker and Beer, Katja and Haverkamp, Wilhelm and Martus, Peter and Waltenberger, Johannes and M{\"u}ller-Nordhorn, Jacqueline and Str{\"o}hle, Andreas},
  title     = {Erkennungsg{\"u}te dreier deutschsprachiger Screeninginstrumente f{\"u}r Depression bei hospitalisierten Patienten mit koronarer Herzerkrankung},
  series = {Psychiatrische Praxis},
  volume    = {46},
  journal   = {Psychiatrische Praxis},
  number    = {1},
  publisher = {Thieme},
  address   = {Stuttgart},
  issn      = {0303-4259},
  doi       = {10.1055/s-0042-123434},
  pages     = {41 -- 48},
  year      = {2019},
  abstract  = {Ziel Vergleich der Erkennungsg{\"u}te von drei Depressions-Screeninginstrumenten bei Patienten mit koronarer Herzerkrankung (KHK). Methodik 1019 KHK-Patienten erhielten den Patient Health Questionnaire (PHQ-9 und PHQ-2) und die Hospital Anxiety and Depression Scale (HADS-D) sowie ein klinisches Interview (Composite International Diagnostic Interview) als Referenzstandard. Ergebnisse Bez{\"u}glich der Erkennungsg{\"u}te waren PHQ-9 und HADS-D dem PHQ-2 {\"u}berlegen. Optimale Cut-off-Werte waren 7 (PHQ-9 und HADS-D) und 2 (PHQ-2). Schlussfolgerung PHQ-9 und HADS-D haben eine vergleichbare Diskriminationsf{\"a}higkeit f{\"u}r depressive St{\"o}rungen bei KHK-Patienten.},
  language  = {de}
}
@article{MuckelbauerEnglertRieckmannetal.2015,
  author    = {Muckelbauer, Rebecca and Englert, Heike and Rieckmann, Nina and Chen, Chih-Mei and Wegscheider, Karl and V{\"o}ller, Heinz and Katus, Hugo A. and Willich, Stefan N. and M{\"u}ller-Nordhorn, Jacqueline},
  title     = {Long-term effect of a low-intensity smoking intervention embedded in an adherence program for patients with hypercholesterolemia: Randomized controlled trial},
  series = {Preventive medicine : an international journal devoted to practice and theory},
  volume    = {77},
  journal   = {Preventive medicine : an international journal devoted to practice and theory},
  publisher = {Elsevier},
  address   = {San Diego},
  issn      = {0091-7435},
  doi       = {10.1016/j.ypmed.2015.05.026},
  pages     = {155 -- 161},
  year      = {2015},
  abstract  = {Objective. We evaluated the long-term effect of a smoking intervention embedded in an adherence program in patients with an increased risk for cardiovascular disease. Method. Secondary analysis of a randomized controlled trial: In 2002-2004,8108 patients with hypercholesterolemia were enrolled from general practices in Germany. Patients received a 12-month adherence program and statin medication (intervention) or statin medication only (control). The program aimed to improve adherence to medication and lifestyle by educational material, mailings, and phone calls. Smoking was self-reported at baseline and every 6 months during the 3-year follow-up. Results. In total, 7640 patients were analyzed. At baseline, smoking prevalence was 21.7\% in the intervention and 21.5\% in the control group. Prevalence decreased in both groups to 16.6\% vs. 19.5\%, 153\% vs. 16.8\%, and 14.2\% vs. 15.6\% at the 12-, 24-, and 36-month follow-up. The intervention had a beneficial effect on smoking differing over time (group x time: P = 0.005). The effect was largest after 6 and 12 months [odds ratios (95\% confidence intervals): 0.67 (0.54-0.82) and 0.63 (0.51-0.78)]. The effect decreased until the 18-month follow-up [0.72 (0.58-0.90)] and was not significant after 24 months. Conclusion. A low-intensity smoking intervention embedded in an adherence program can contribute to smoking cessation although the intervention effect diminished over time. (C) 2015 Elsevier Inc. All rights reserved.},
  language  = {en}
}
@article{DeekenHaeuslerNordheimetal.2017,
  author    = {Deeken, Friederike and H{\"a}usler, Andreas and Nordheim, Johanna and Rapp, Michael Armin and Knoll, Nina and Rieckmann, Nina},
  title     = {Psychometric properties of the Perceived Stress Scale in a sample of German dementia patients and their caregivers},
  series = {International psychogeriatrics},
  volume    = {30},
  journal   = {International psychogeriatrics},
  number    = {1},
  publisher = {Cambridge Univ. Press},
  address   = {New York},
  issn      = {1041-6102},
  doi       = {10.1017/S1041610217001387},
  pages     = {39 -- 47},
  year      = {2017},
  abstract  = {Background: The aim of the present study was to investigate the psychometric characteristics of the Perceived Stress Scale (PSS) in a sample of dementia patients and their spousal caregivers. Methods: We investigated the reliability and validity of the 14-item PSS in a sample of 80 couples, each including one spouse who had been diagnosed with mild to moderate dementia (mean age 75.55, SD = 5.85, 38.7\% female) and one spousal caregiver (mean age 73.06, SD = 6.75, 61.3\% female). We also examined the factor structure and sensitivity of the scale with regard to gender differences. Results: Exploratory factor analysis of the PSS revealed a two-factor solution for the scale; the first factor reflected general stress while the second factor consisted of items reflecting the perceived ability to cope with stressors. A confirmatory factor analysis verified that the data were a better fit for the two-factor model than a one-factor model. The two factors of the PSS showed good reliability for patients as well as for caregivers ranging between alpha = 0.73 and alpha = 0.82. Perceived stress was significantly positively correlated with depressive symptomatology in both caregivers and patients. Mean PSS scores did not significantly differ between male and female patients nor did they differ between male and female caregivers. Conclusion: The present data indicate that the PSS provides a reliable and valid measure of perceived stress in dementia patients and their caregivers.},
  language  = {en}
}
@misc{KuhlmannTschornAroltetal.2017,
  author    = {Kuhlmann, Stella L. and Tschorn, Mira and Arolt, Volker and Beer, Katja and Brandt, Julia and Grosse, Laura and Haverkamp, Wilhelm and Mueller-Nordhorn, Jacqueline and Rieckmann, Nina and Waltenberger, Johannes and Warnke, Katharina and Hellweg, Rainer and Stroehle, Andreas},
  title     = {Serum brain-derived neurotrophic factor and depressive symptoms in coronary heart disease patients: Role of cognitive functions Reply},
  series = {Psychoneuroendocrinology},
  volume    = {79},
  journal   = {Psychoneuroendocrinology},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2017.02.010},
  pages     = {175 -- 176},
  year      = {2017},
  language  = {en}
}
@article{KuhlmannTschornAroltetal.2017,
  author    = {Kuhlmann, Stella and Tschorn, Mira and Arolt, Volker and Beer, Katja and Brandt, Julia and Grosse, Laura and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Rieckmann, Nina and Waltenberger, Johannes and Warnke, Katharina and Hellweg, Rainer and Str{\"o}hle, Andreas},
  title     = {Serum brain-derived neurotrophic factor and stability of depressive symptoms in coronary heart disease patients},
  series = {Psychoneuroendocrinology : an international journal ; the official journal of the International Society of Psychoneuroendocrinology},
  volume    = {77},
  journal   = {Psychoneuroendocrinology : an international journal ; the official journal of the International Society of Psychoneuroendocrinology},
  publisher = {Elsevier Science},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2016.12.015},
  pages     = {196 -- 202},
  year      = {2017},
  abstract  = {Objective: Brain-derived neurotrophic factor (BDNF) supports neurogenesis, angiogenesis, and promotes the survival of various cell types in the brain and the coronary system. Moreover, BDNF is associated with both coronary heart disease (CHD) and depression. The current study aims to investigate whether serum BDNF levels are associated with the course of depressive symptoms in CHD patients. Methods: At baseline, N = 225 CHD patients were enrolled while hospitalized. Of these, N = 190 (84\%) could be followed up 6 months later. Depressive symptoms were assessed both at baseline and at the 6-months follow-up using the Patient Health Questionnaire (PHQ-9). Serum BDNF concentrations were measured using fluorometric Enzyme-linked immunosorbent assays (ELISA). Results: Logistic regression models showed that lower BDNF levels were associated with persistent depressive symptoms, even after adjustment for age, sex, smoking and potential medical confounders. The incidence of depressive symptoms was not related to lower BDNF levels. However, somatic comorbidity (as measured by the Charlson Comorbidity Index) was significantly associated with the incidence of depressive symptoms. Conclusions: Our findings suggest a role of BDNF in the link between CHD and depressive symptoms. Particularly, low serum BDNF levels could be considered as a valuable biomarker for the persistence of depressive symptoms among depressed CHD patients.},
  language  = {en}
}