@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}
}
@article{KalliesRappFydrichetal.2018,
  author    = {Kallies, Gunnar and Rapp, Michael Armin and Fydrich, Thomas and Fehm, Lydia and Tschorn, Mira and Teran, Christina and Schwefel, Melanie and Pietrek, Anou F. and Henze, Romy and Hellweg, Rainer and Str{\"o}hle, Andreas and Heinzel, Stephan and Heissel, Andreas},
  title     = {Serum brain-derived neurotrophic factor (BDNF) at rest and after acute aerobic exercise in major depressive disorder},
  series = {Psychoneuroendocrinology},
  volume    = {102},
  journal   = {Psychoneuroendocrinology},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2018.12.015},
  pages     = {212 -- 215},
  year      = {2018},
  abstract  = {Physiological mechanisms of an anti-depressive effect of physical exercise in major depressive disorder (MDD) seem to involve alterations in brain-derived neurotrophic factor (BDNF) level. However, previous studies which investigated this effect in a single bout of exercise, did not control for confounding peripheral factors that contribute to BDNF-alterations. Therefore, the underlying cause of exercise-induced BDNF-changes remains unclear. The current study aims to investigate serum BDNF (sBDNF)-changes due to a single-bout of graded aerobic exercise in a group of 30 outpatients with MDD, suggesting a more precise analysis method by taking plasma volume shift and number of platelets into account. Results show that exercise-induced increases in sBDNF remain significant (p<.001) when adjusting for plasma volume shift and controlling for number of platelets. The interaction of sBDNF change and number of platelets was also significant (p=.001) indicating larger sBDNF-increase in participants with smaller number of platelets. Thus, findings of this study suggest an involvement of peripheral as well as additional possibly brain-derived mechanisms explaining exercise-related BDNF release in MDD. For future studies in the field of exercise-related BDNF research, the importance of controlling for peripheral parameters is emphasized.},
  language  = {en}
}