TY - JOUR A1 - Tschorn, Mira A1 - Kuhlmann, Stella Linnea A1 - Rieckmann, Nina A1 - Beer, Katja A1 - Grosse, Laura A1 - Arolt, Volker A1 - Waltenberger, Johannes A1 - Haverkamp, Wilhelm A1 - Müller-Nordhorn, Jacqueline A1 - Hellweg, Rainer A1 - Ströhle, Andreas T1 - Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease JF - Acta Neuropsychiatrica N2 - 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. KW - depression KW - BDNF KW - coronary heart disease KW - heart failure KW - somatic comorbidity KW - acute coronary syndrome Y1 - 2020 U6 - https://doi.org/10.1017/neu.2020.31 SN - 1601-5215 VL - 33 IS - 1 SP - 22 EP - 30 PB - Cambridge Univ. Press CY - Cambridge ER - TY - JOUR A1 - Buchmann, Arlette F. A1 - Hellweg, Rainer A1 - Rietschel, Marcella A1 - Treutlein, Jens A1 - Witt, Stephanie H. A1 - Zimmermann, Ulrich S. A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Banaschewski, Tobias A1 - Laucht, Manfred A1 - Deuschle, Michael T1 - BDNF Val 66 Met and 5-HTTLPR genotype moderate the impact of early psychosocial adversity on plasma brain-derived neurotrophic factor and depressive symptoms - a prospective study JF - European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology N2 - Recent studies have emphasized an important role for neurotrophins, such as brain-derived neurotrophic factor (BDNF), in regulating the plasticity of neural circuits involved in the pathophysiology of stress-related diseases. The aim of the present study was to examine the interplay of the BDNF Val(66)Met and the serotonin transporter promoter (5-HTTLPR) polymorphisms in moderating the impact of early-life adversity on BDNF plasma concentration and depressive symptoms. Participants were taken from an epidemiological cohort study following the long-term outcome of early risk factors from birth into young adulthood. In 259 individuals (119 males, 140 females), genotyped for the BDNF Val(66)Met and the 5-HTTLPR polymorphisms, plasma BDNF was assessed at the age of 19 years. In addition, participants completed the Beck Depression Inventory (BDI). Early adversity was determined according to a family adversity index assessed at 3 months of age. Results indicated that individuals homozygous for both the BDNF Val and the 5-HTTLPR L allele showed significantly reduced BDNF levels following exposure to high adversity. In contrast, BDNF levels appeared to be unaffected by early psychosocial adversity in carriers of the BDNF Met or the 5-HTTLPR S allele. While the former group appeared to be most susceptible to depressive symptoms, the impact of early adversity was less pronounced in the latter group. This is the first preliminary evidence indicating that early-life adverse experiences may have lasting sequelae for plasma BDNF levels in humans, highlighting that the susceptibility to this effect is moderated by BDNF Val(66)Met and 5-HTTLPR genotype. KW - BDNF KW - 5-HTTLPR KW - Human KW - Early psychosocial adversity KW - Longitudinal study KW - Depression Y1 - 2013 U6 - https://doi.org/10.1016/j.euroneuro.2012.09.003 SN - 0924-977X VL - 23 IS - 8 SP - 902 EP - 909 PB - Elsevier CY - Amsterdam ER -