@article{HolzBoeckerSchlierHohmetal.2015,
  author    = {Holz, Nathalie E. and Boecker-Schlier, Regina and Hohm, Erika and Zohsel, Katrin and Buchmann, Arlette F. and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Baumeister, Sarah and Hohmann, Sarah and Wolf, Isabella and Plichta, Michael M. and Esser, G{\"u}nter and Schmidt, Martin and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {The Long-Term Impact of Early Life Poverty on Orbitofrontal Cortex Volume in Adulthood: Results from a Prospective Study Over 25 Years},
  series = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
  volume    = {40},
  journal   = {Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology},
  number    = {4},
  publisher = {Nature Publ. Group},
  address   = {London},
  issn      = {0893-133X},
  doi       = {10.1038/npp.2014.277},
  pages     = {996 -- 1004},
  year      = {2015},
  abstract  = {Converging evidence has highlighted the association between poverty and conduct disorder (CD) without specifying neurobiological pathways. Neuroimaging research has emphasized structural and functional alterations in the orbitofrontal cortex (OFC) as one key mechanism underlying this disorder. The present study aimed to clarify the long-term influence of early poverty on OFC volume and its association with CD symptoms in healthy participants of an epidemiological cohort study followed since birth. At age 25 years, voxel-based morphometry was applied to study brain volume differences. Poverty (0 = non-exposed (N = 134), I = exposed (N = 33)) and smoking during pregnancy were determined using a standardized parent interview, and information on maternal responsiveness was derived from videotaped mother infant interactions at the age of 3 months. CD symptoms were assessed by diagnostic interview from 8 to 19 years of age. Information on life stress was acquired at each assessment and childhood maltreatment was measured using retrospective self-report at the age of 23 years. Analyses were adjusted for sex, parental psychopathology and delinquency, obstetric adversity, parental education, and current poverty. Individuals exposed to early life poverty exhibited a lower OFC volume. Moreover, we replicated previous findings of increased CD symptoms as a consequence of childhood poverty. This effect proved statistically mediated by OFC volume and exposure to life stress and smoking during pregnancy, but not by childhood maltreatment and maternal responsiveness. These findings underline the importance of studying the impact of early life adversity on brain alterations and highlight the need for programs to decrease income-related disparities.},
  language  = {en}
}
@article{HolzBuchmannBoeckerSchlieretal.2015,
  author    = {Holz, Nathalie E. and Buchmann, Arlette F. and Boecker-Schlier, Regina and Blomeyer, Dorothea and Baumeister, Sarah and Wolf, Isabella and Rietschel, Marcella and Witt, Stephanie H. and Plichta, Michael M. and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume},
  series = {Brain structure \& function},
  volume    = {220},
  journal   = {Brain structure \& function},
  number    = {3},
  publisher = {Springer},
  address   = {Heidelberg},
  issn      = {1863-2653},
  doi       = {10.1007/s00429-014-0729-5},
  pages     = {1355 -- 1368},
  year      = {2015},
  abstract  = {Accumulating evidence suggests a role of FKBP5, a co-chaperone regulating the glucocorticoid receptor sensitivity, in the etiology of depression and anxiety disorders. Based on recent findings of altered amygdala activity following childhood adversity, the present study aimed at clarifying the impact of genetic variation in FKBP5 on threat-related neural activity and coupling as well as morphometric alterations in stress-sensitive brain systems. Functional magnetic resonance imaging during an emotional face-matching task was performed in 153 healthy young adults (66 males) from a high-risk community sample followed since birth. Voxel-based morphometry was applied to study structural alterations and DNA was genotyped for FKBP5 rs1360780. Childhood adversity was measured using retrospective self-report (Childhood Trauma Questionnaire) and by a standardized parent interview assessing childhood family adversity. Depression was assessed by the Beck Depression Inventory. There was a main effect of FKBP5 on the left amygdala, with T homozygotes showing the highest activity, largest volume and increased coupling with the left hippocampus and the orbitofrontal cortex (OFC). Moreover, amygdala-OFC coupling proved to be associated with depression in this genotype. In addition, our results support previous evidence of a gene-environment interaction on right amygdala activity with respect to retrospective assessment of childhood adversity, but clarify that this does not generalize to the prospective assessment. These findings indicated that activity in T homozygotes increased with the level of adversity, whereas the opposite pattern emerged in C homozygotes, with CT individuals being intermediate. The present results point to a functional involvement of FKBP5 in intermediate phenotypes associated with emotional processing, suggesting a possible mechanism for this gene in conferring susceptibility to stress-related disorders.},
  language  = {en}
}
@book{ThiekenBesselCallsenetal.2015,
  author    = {Thieken, Annegret and Bessel, Tina and Callsen, Ines and Falter, Daniela and Hasan, Issa and Kienzler, Sarah and Kox, Thomas and Kreibich, Heidi and Kuhlicke, Christian and Kunz, Michael and Matthias, Max and Meyer, Volker and M{\"u}hr, Bernhard and M{\"u}ller, Meike and Otto, Antje and Pech, Ina and Petrow, Theresia and Pisi, Sebastian and Rother, Karl-Heinz and Schr{\"o}ter, Kai},
  title     = {Das Hochwasser im Juni 2013},
  series = {Schriftenreihe des DKKV ; 53},
  journal   = {Schriftenreihe des DKKV ; 53},
  publisher = {Deutsches Komitee Katastrophenvorsorge},
  address   = {Bonn},
  isbn      = {978-3-933181-62-6},
  publisher      = {Universit{\"a}t Potsdam},
  pages     = {207},
  year      = {2015},
  language  = {de}
}