@article{WittBuchmannBlomeyeretal.2011,
  author    = {Witt, Stephanie H. and Buchmann, Arlette F. and Blomeyer, Dorothea and Nieratschker, Vanessa and Treutlein, Jens and Esser, G{\"u}nter and Schmidt, Martin H. and Bidlingmaier, Martin and Wiedemann, Klaus and Rietschel, Marcella and Laucht, Manfred and Wuest, Stefan and Zimmermann, Ulrich S.},
  title     = {An interaction between a neuropeptide Y gene polymorphism and early adversity modulates endocrine stress responses},
  series = {Psychoneuroendocrinology},
  volume    = {36},
  journal   = {Psychoneuroendocrinology},
  number    = {7},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0306-4530},
  doi       = {10.1016/j.psyneuen.2010.12.015},
  pages     = {1010 -- 1020},
  year      = {2011},
  abstract  = {Interindividual variability in the regulation of the human stress system accounts for a part of the individual's liability to stress-related diseases. These differences are influenced by environmental and genetic factors. Early childhood adversity is a well-studied environmental factor affecting an individual's stress response which has been shown to be modulated by gene environment interaction (GxE). Neuropeptide Y (NPY) plays a role in stress regulation and genetic variation in NPY may influence stress responses. In this study, we analyzed the association of a common variant in the NPY gene promoter, rs16147, with cortisol and ACTH responses to acute psychosocial stress in young adults from the Mannheim Study of Children at Risk (MARS), an ongoing epidemiological cohort study following the outcome of early adversity from birth into adulthood. We found evidence of a GxE interaction between rs16147 and early adversity significantly affecting HPA axis responses to acute psychosocial stress. These findings suggest that the neurobiological mechanisms linking early adverse experience and later neuroendocrine stress regulation are modulated by a gene variant whose functional relevance is documented by increasing convergent evidence from in vitro, animal and human studies.},
  language  = {en}
}
@article{BuchmannHolzBoeckerSchlieretal.2014,
  author    = {Buchmann, Arlette F. and Holz, Nathalie and Boecker-Schlier, Regina and Blomeyer, Dorothea and Rietschel, Marcella and Witt, Stephanie H. and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Brandeis, Daniel and Zimmermann, Ulrich S. and Laucht, Manfred},
  title     = {Moderating role of FKBP5 genotype in the impact of childhood adversity on cortisol stress response during adulthood},
  series = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  volume    = {24},
  journal   = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  number    = {6},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0924-977X},
  doi       = {10.1016/j.euroneuro.2013.12.001},
  pages     = {837 -- 845},
  year      = {2014},
  abstract  = {Recent research suggests an important role of FKBP5, a glucocorticoid receptor regulating co-chaperone, in the development of stress-related diseases such as depression and anxiety disorders. The present study aimed to replicate and extend previous evidence indicating that FKBP5 polymorphisms moderate hypothalamus-pituitary-adrenal (HPA) function by examining whether FKBP5 rs1360780 genotype and different measures of childhood adversity interact to predict stress-induced cortisol secretion. At age 19 years, 195 young adults (90 males, 105 females) participating in an epidemiological cohort study completed the Trier Social Stress Test (TSST) to assess cortisol stress responsiveness and were genotyped for the FKBP5 rs1360780. Childhood adversity was assessed using the Childhood Trauma Questionnaire (CTQ) and by a standardized parent interview yielding an index of family adversity. A significant interaction between genotype and childhood adversity on cortisol response to stress was demonstrated for exposure to childhood maltreatment as assessed by retrospective self-report (CTQ), but not for prospectively ascertained objective family adversity. Severity of childhood maltreatment was significantly associated with attenuated cortisol levels among carriers of the rs1360780 CC genotype, while no such effect emerged in carriers of the T allele. These findings point towards the functional involvement of FKBP5 in long-term alterations of neuroendocrine stress regulation related to childhood maltreatment, which have been suggested to represent a premorbid risk or resilience factor in the context of stress-related disorders. (C) 2013 Elsevier B.V. and ECNR This is an open access article under the CC BY-NC-ND license.},
  language  = {en}
}