@article{BrevikvanDonkelaarWeberetal.2016,
  author    = {Brevik, Erlend J and van Donkelaar, Marjolein M. J. and Weber, Heike and S{\´a}nchez-Mora, Cristina and Jacob, Christian and Rivero, Olga and Kittel-Schneider, Sarah and Garcia-martinez, Iris and Aebi, Marcel and van Hulzen, Kimm and Cormand, Bru and Ramos-Quiroga, Josep A and Lesch, Klaus-Peter and Reif, Andreas and Ribases, Marta and Franke, Barbara and Posserud, Maj-Britt and Johansson, Stefan and Lundervold, Astri J. and Haavik, Jan and Zayats, Tetyana},
  title     = {Genome-wide analyses of aggressiveness in attention-deficit hyperactivity disorder},
  series = {American Journal of Medical Genetics Part B-Neuropsychiatric Genetics},
  volume    = {171B},
  journal   = {American Journal of Medical Genetics Part B-Neuropsychiatric Genetics},
  number    = {5},
  organization    = {IMAGE Consortium},
  doi       = {10.1002/ajmg.b.32434},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-188116},
  pages     = {733-747},
  year      = {2016},
  abstract  = {Aggressiveness is a behavioral trait that has the potential to be harmful to individuals and society. With an estimated heritability of about 40\%, genetics is important in its development. We performed an exploratory genome-wide association (GWA) analysis of childhood aggressiveness in attention deficit hyperactivity disorder (ADHD) to gain insight into the underlying biological processes associated with this trait. Our primary sample consisted of 1,060 adult ADHD patients (aADHD). To further explore the genetic architecture of childhood aggressiveness, we performed enrichment analyses of suggestive genome-wide associations observed in aADHD among GWA signals of dimensions of oppositionality (defiant/vindictive and irritable dimensions) in childhood ADHD (cADHD). No single polymorphism reached genome-wide significance (P<5.00E-08). The strongest signal in aADHD was observed at rs10826548, within a long noncoding RNA gene (beta = -1.66, standard error (SE) = 0.34, P = 1.07E-06), closely followed by rs35974940 in the neurotrimin gene (beta = 3.23, SE = 0.67, P = 1.26E-06). The top GWA SNPs observed in aADHD showed significant enrichment of signals from both the defiant/vindictive dimension (Fisher's P-value = 2.28E-06) and the irritable dimension in cADHD (Fisher's P-value = 0.0061). In sum, our results identify a number of biologically interesting markers possibly underlying childhood aggressiveness and provide targets for further genetic exploration of aggressiveness across psychiatric disorders.},
  language  = {en}
}
@article{ZieglerRichterMahretal.2016,
  author    = {Ziegler, C. and Richter, J. and Mahr, M. and Gajewska, A. and Schiele, M.A. and Gehrmann, A. and Schmidt, B. and Lesch, K.-P. and Lang, T. and Helbig-Lang, S. and Pauli, P. and Kircher, T. and Reif, A. and Rief, W. and Vossbeck-Elsebusch, A.N. and Arolt, V. and Wittchen, H.-U. and Hamm, A.O. and Deckert, J. and Domschke, K.},
  title     = {MAOA gene hypomethylation in panic disorder-reversibility of an epigenetic risk pattern by psychotherapy},
  series = {Translational Psychiatry},
  journal   = {Translational Psychiatry},
  number    = {6},
  doi       = {10.1038/tp.2016.41},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164422},
  pages     = {e773},
  year      = {2016},
  abstract  = {Epigenetic signatures such as methylation of the monoamine oxidase A (MAOA) gene have been found to be altered in panic disorder (PD). Hypothesizing temporal plasticity of epigenetic processes as a mechanism of successful fear extinction, the present psychotherapy-epigenetic study for we believe the first time investigated MAOA methylation changes during the course of exposure-based cognitive behavioral therapy (CBT) in PD. MAOA methylation was compared between N=28 female Caucasian PD patients (discovery sample) and N=28 age- and sex-matched healthy controls via direct sequencing of sodium bisulfite-treated DNA extracted from blood cells. MAOA methylation was furthermore analyzed at baseline (T0) and after a 6-week CBT (T1) in the discovery sample parallelized by a waiting time in healthy controls, as well as in an independent sample of female PD patients (N=20). Patients exhibited lower MAOA methylation than healthy controls (P<0.001), and baseline PD severity correlated negatively with MAOA methylation (P=0.01). In the discovery sample, MAOA methylation increased up to the level of healthy controls along with CBT response (number of panic attacks; T0-T1: +3.37±2.17\%), while non-responders further decreased in methylation (-2.00±1.28\%; P=0.001). In the replication sample, increases in MAOA methylation correlated with agoraphobic symptom reduction after CBT (P=0.02-0.03). The present results support previous evidence for MAOA hypomethylation as a PD risk marker and suggest reversibility of MAOA hypomethylation as a potential epigenetic correlate of response to CBT. The emerging notion of epigenetic signatures as a mechanism of action of psychotherapeutic interventions may promote epigenetic patterns as biomarkers of lasting extinction effects.},
  language  = {en}
}