@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}
}
@misc{HaegeleSchlagenhaufRappetal.2014,
  author    = {H{\"a}gele, Claudia and Schlagenhauf, Florian and Rapp, Michael Armin and Sterzer, Philipp and Beck, Anne and Bermpohl, Felix and Stoy, Meline and Str{\"o}hle, Andreas and Wittchen, Hans-Ulrich and Dolan, Raymond J. and Heinz, Andreas},
  title     = {Dimensional psychiatry},
  series = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {653},
  issn      = {1866-8364},
  doi       = {10.25932/publishup-43106},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-431064},
  pages     = {331 -- 341},
  year      = {2014},
  abstract  = {A dimensional approach in psychiatry aims to identify core mechanisms of mental disorders across nosological boundaries. We compared anticipation of reward between major psychiatric disorders, and investigated whether reward anticipation is impaired in several mental disorders and whether there is a common psychopathological correlate (negative mood) of such an impairment. We used functional magnetic resonance imaging (fMRI) and a monetary incentive delay (MID) task to study the functional correlates of reward anticipation across major psychiatric disorders in 184 subjects, with the diagnoses of alcohol dependence (n = 26), schizophrenia (n = 44), major depressive disorder (MDD, n = 24), bipolar disorder (acute manic episode, n = 13), attention deficit/hyperactivity disorder (ADHD, n = 23), and healthy controls (n = 54). Subjects' individual Beck Depression Inventory-and State-Trait Anxiety Inventory-scores were correlated with clusters showing significant activation during reward anticipation. During reward anticipation, we observed significant group differences in ventral striatal (VS) activation: patients with schizophrenia, alcohol dependence, and major depression showed significantly less ventral striatal activation compared to healthy controls. Depressive symptoms correlated with dysfunction in reward anticipation regardless of diagnostic entity. There was no significant correlation between anxiety symptoms and VS functional activation. Our findings demonstrate a neurobiological dysfunction related to reward prediction that transcended disorder categories and was related to measures of depressed mood. The findings underline the potential of a dimensional approach in psychiatry and strengthen the hypothesis that neurobiological research in psychiatric disorders can be targeted at core mechanisms that are likely to be implicated in a range of clinical entities.},
  language  = {en}
}