@article{ErhardtAkulaSchumacheretal.2012,
  author    = {Erhardt, A. and Akula, N. and Schumacher, J. and Czamara, D. and Karbalai, N. and M{\"u}ller-Myhsok, B. and Mors, O. and Borglum, A. and Kristensen, A. S. and Woldbye, D. P. D. and Koefoed, P. and Eriksson, E. and Maron, E. and Metspalu, A. and Nurnberger, J. and Philibert, R. A. and Kennedy, J. and Domschke, K. and Reif, A. and Deckert, J. and Otowa, T. and Kawamura, Y. and Kaiya, H. and Okazaki, Y. and Tanii, H. and Tokunaga, K. and Sasaki, T. and Ioannidis, J. P. A. and McMahon, F. J. and Binder, E. B.},
  title     = {Replication and meta-analysis of TMEM132D gene variants in panic disorder},
  series = {Translational Psychiatry},
  volume    = {2},
  journal   = {Translational Psychiatry},
  number    = {e156},
  doi       = {10.1038/tp.2012.85},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133324},
  year      = {2012},
  abstract  = {A recent genome-wide association study in patients with panic disorder (PD) identified a risk haplotype consisting of two single-nucleotide polymorphisms (SNPs) (rs7309727 and rs11060369) located in intron 3 of TMEM132D to be associated with PD in three independent samples. Now we report a subsequent confirmation study using five additional PD case-control samples (n = 1670 cases and n 2266 controls) assembled as part of the Panic Disorder International Consortium (PanIC) study for a total of 2678 cases and 3262 controls in the analysis. In the new independent samples of European ancestry (EA), the association of rs7309727 and the risk haplotype rs7309727-rs11060369 was, indeed, replicated, with the strongest signal coming from patients with primary PD, that is, patients without major psychiatric comorbidities (n 1038 cases and n 2411 controls). This finding was paralleled by the results of the meta-analysis across all samples, in which the risk haplotype and rs7309727 reached P-levels of P = 1.4e-8 and P = 1.1e-8, respectively, when restricting the samples to individuals of EA with primary PD. In the Japanese sample no associations with PD could be found. The present results support the initial finding that TMEM132D gene contributes to genetic susceptibility for PD in individuals of EA. Our results also indicate that patient ascertainment and genetic background could be important sources of heterogeneity modifying this association signal in different populations.},
  language  = {en}
}
@article{LudwigSaemannAlexanderetal.2013,
  author    = {Ludwig, K. U. and S{\"a}mann, P. and Alexander, M. and Becker, J. and Bruder, J. and Moll, K. and Spieler, D. and Czisch, M. and Warnke, A. and Docherty, S. J. and Davis, O. S. P. and Plomin, R. and N{\"o}then, M. M. and Landerl, K. and M{\"u}ller-Myhsok, B. and Hoffmann, P. and Schumacher, J. and Schulte-K{\"o}rne, G. and Czamara, D.},
  title     = {A common variant in Myosin-18B contributes to mathematical abilities in children with dyslexia and intraparietal sulcus variability in adults},
  series = {Translational Psychiatry},
  volume    = {3},
  journal   = {Translational Psychiatry},
  number    = {e229},
  doi       = {10.1038/tp.2012.148},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-131513},
  year      = {2013},
  abstract  = {The ability to perform mathematical tasks is required in everyday life. Although heritability estimates suggest a genetic contribution, no previous study has conclusively identified a genetic risk variant for mathematical performance. Research has shown that the prevalence of mathematical disabilities is increased in children with dyslexia. We therefore correlated genome-wide data of 200 German children with spelling disability, with available quantitative data on mathematic ability. Replication of the top findings in additional dyslexia samples revealed that rs133885 was a genome-wide significant marker for mathematical abilities\((P_{comb}=7.71 x 10^{-10}, n=699)\), with an effect size of 4.87\%. This association was also found in a sample from the general population (P=0.048, n=1080), albeit with a lower effect size. The identified variant encodes an amino-acid substitution in MYO18B, a protein with as yet unknown functions in the brain. As areas of the parietal cortex, in particular the intraparietal sulcus (IPS), are involved in numerical processing in humans, we investigated whether rs133885 was associated with IPS morphology using structural magnetic resonance imaging data from 79 neuropsychiatrically healthy adults. Carriers of the MYO18B risk-genotype displayed a significantly lower depth of the right IPS. This validates the identified association between rs133885 and mathematical disability at the level of a specific intermediate phenotype.},
  language  = {en}
}