@article{Akdeniz2014, author = {Akdeniz, Ceren and Tost, Heike and Streit, Fabian and Haddad, Leila and Wüst, Stefan and Schäfer, Axel and Schneider, Michael and Rietschel, Marcella and Kirsch, Peter and Meyer-Lindenberg, Andreas}, doi = {10.1001/jamapsychiatry.2014.35}, journal = {JAMA Psychiatry}, month = {apr}, pages = {672}, title = {Neuroimaging Evidence for a Role of Neural Social Stress Processing in Ethnic Minority-Associated Environmental Risk}, url = {http://archpsyc.jamanetwork.com/data/journals/psych/930236/yoi140006.pdf}, volume = {71}, year = {2014} } @article{Binder2013, author = {Binder, Lutz and Schwörer, Harald and Hoppe, Sebastian and Streit, Frank and Neumann, Silke and Beckmann, Annett and Wachter, Rolf and Oellerich, Michael and Walson, Philip D.}, doi = {10.1097/ftd.0b013e31827d496c}, journal = {Therapeutic Drug Monitoring}, month = {feb}, pages = {63-70}, title = {Pharmacokinetics of Meropenem in Critically Ill Patients With Severe Infections}, url = {https://www.researchgate.net/profile/Phil_Walson/publication/234133296_Pharmacokinetics_of_Meropenem_in_Critically_Ill_Patients_With_Severe_Infections/links/53cfadc80cf2fd75bc59e38d.pdf}, volume = {35}, year = {2013} } @article{Chang2016, author = {Chang, Hong and Strohmaier, Jana and Ösby, Urban and Treutlein, Jens and Witt, Stephanie H. and Vedder, Helmut and Wright, Adam and Xiao, Xiao and Li, Lingyi and Peng, Tao and Landén, Mikael and Hultman, Christina M. and Hecker, Julian and Schulze, Thomas G. and Müller-Myhsok, Bertram and Reif, Andreas and Mitchell, Philip B. and Martin, Nicholas G. and Nöthen, Markus M. and Jamain, Stéphane and Leboyer, Marion and Kahn, Jean Pierre and Henry, Chantal and Rietschel, Marcella and Lavebratt, Catharina and Schalling, Martin and Mühleisen, Thomas W. and Leber, Markus and Mattheisen, Manuel and Hofmann, Andrea and Meier, Sandra and Herms, Stefan and Hoffmann, Per and Lacour, André and Lucae, Susanne and Maier, Wolfgang and Schwarz, Markus and Kammerer-Ciernioch, Jutta and Pfennig, Andrea and Hautzinger, Martin and Streit, Fabian and Schofield, Peter R. and Montgomery, Grant W. and Medland, Sarah E. and Schumacher, Johannes and Propping, Peter and Li, Ming and Bergen, Sarah E. and Forstner, Andreas J. and Cichon, Sven and Bellivier, Frank and Etain, Bruno and Backlund, Lena and Frisén, Louise and Grigoroiu-Serbanescu, Maria and Degenhardt, Franziska and Breuer, René and Bauer, Michael and Fullerton, Janice M. and Gordon, Scott D. and Becker, Tim}, doi = {10.1007/s12035-016-0041-x}, month = {aug}, title = {Identification of a Bipolar Disorder Vulnerable Gene CHDH at 3p21.1}, url = {https://oadoi.org/10.1007/s12035-016-0041-x}, year = {2016} } @article{Ferreira de Sá2014, abstract = {Stress glucocorticoids and insulin are important endocrine regulators of energy homeostasis, but little is known about their central interaction on the reward-related processing of food cues. According to a balanced group design, healthy food deprived men received either 40 IU intranasal insulin (n=13), 30 mg oral cortisol (n=12), both (n=15), or placebo (n=14). Acoustic startle responsiveness was assessed during presentation of food and non-food pictures. Cortisol enhanced startle responsiveness during visual presentation of "high glycemic" food, but not during presentation of neutral and pleasant non-food pictures. Insulin had no effect. Based on the "frustrative non-reward" model these results suggest that the reward value of high glycemic food items is specifically increased by cortisol.}, author = {Ferreira de Sá, Diana S. and Schulz, André and Streit, Fabian E. and Oitzl, Melly S. and Turner, Jonathan D. and Blumenthal, Terry D. and Schächinger, Hartmut}, doi = {10.1016/j.psyneuen.2014.09.006}, journal = {Psychoneuroendocrinology}, month = {jan}, pages = {311-320}, title = {Cortisol, but not intranasal insulin, affects the central processing of visual food cues}, url = {https://oadoi.org/10.1016/j.psyneuen.2014.09.006}, volume = {50}, year = {2014} } @article{Haddad2014, abstract = {Urban upbringing has consistently been associated with schizophrenia, but which specific environmental exposures are reflected by this epidemiological observation and how they impact the developing brain to increase risk is largely unknown. On the basis of prior observations of abnormal functional brain processing of social stress in urban-born humans and preclinical evidence for enduring structural brain effects of early social stress, we investigated a possible morphological correlate of urban upbringing in human brain. In a sample of 110 healthy subjects studied with voxel-based morphometry, we detected a strong inverse correlation between early-life urbanicity and gray matter (GM) volume in the right dorsolateral prefrontal cortex (DLPFC, Brodmann area 9). Furthermore, we detected a negative correlation of early-life urbanicity and GM volumes in the perigenual anterior cingulate cortex (pACC) in men only. Previous work has linked volume reductions in the DLPFC to the exposure to psychosocial stress, including stressful experiences in early life. Besides, anatomical and functional alterations of this region have been identified in schizophrenic patients and high-risk populations. Previous data linking functional hyperactivation of pACC during social stress to urban upbringing suggest that the present interaction effect in brain structure might contribute to an increased risk for schizophrenia in males brought up in cities. Taken together, our results suggest a neural mechanism by which early-life urbanicity could impact brain architecture to increase the risk for schizophrenia.}, author = {Haddad, Leila and Schäfer, Axel and Streit, Fabian and Lederbogen, Florian and Grimm, Oliver and Wüst, Stefan and Deuschle, Michael and Kirsch, Peter and Tost, Heike and Meyer-Lindenberg, Andreas}, doi = {10.1093/schbul/sbu072}, journal = {Schizophrenia Bulletin: The Journal of Psychoses and Related Disorders}, month = {jun}, pages = {115-122}, title = {Brain Structure Correlates of Urban Upbringing, an Environmental Risk Factor for Schizophrenia}, url = {https://academic.oup.com/schizophreniabulletin/article-pdf/41/1/115/7708372/sbu072.pdf}, volume = {41}, year = {2014} } @article{Hou2016, abstract = {Bipolar disorder (BD) is a genetically complex mental illness characterized by severe oscillations of mood and behaviour. Genome-wide association studies (GWAS) have identified several risk loci that together account for a small portion of the heritability. To identify additional risk loci, we performed a two-stage meta-analysis of >9 million genetic variants in 9,784 bipolar disorder patients and 30,471 controls, the largest GWAS of BD to date. In this study, to increase power we used ∼2,000 lithium-treated cases with a long-term diagnosis of BD from the Consortium on Lithium Genetics, excess controls, and analytic methods optimized for markers on the X-chromosome. In addition to four known loci, results revealed genome-wide significant associations at two novel loci: an intergenic region on 9p21.3 (rs12553324, P = 5.87 × 10 (-) (9); odds ratio (OR) = 1.12) and markers within ERBB2 (rs2517959, P = 4.53 × 10 (-) (9); OR = 1.13). No significant X-chromosome associations were detected and X-linked markers explained very little BD heritability. The results add to a growing list of common autosomal variants involved in BD and illustrate the power of comparing well-characterized cases to an excess of controls in GWAS.}, author = {Hou, Liping and Bergen, Sarah E. and Akula, Nirmala and Hultman, Christina M. and Song, Jie and Aubry, Jean-Michel and Badner, Judith A. and Barrett, Thomas B. and Landen, Mikael and Se, Bergen and Baune, Bernhard T. and Adli, Mazda and Berrettini, Wade H. and Bhattacharjee, Abesh Kumar and Alda, Martin and Biernacka, Joanna M. and Birner, Armin and Étain, Bruno and Bloss, Cinnamon S. and Ardau, Raffaella and Brichant-Petitjean, Clara and Bui, Elise T. and Arias, Barbara and Byerley, William and Cervantes, Pablo and Chillotti, Caterina and Cichon, Sven and Colom, Francesc and Backlund, Lena and Coryell, William and Craig, David W. and Cruceanu, Cristiana and Czerski, Piotr M. and Cm, Hultman and Davis, Tony and Dayer, Alexandre and Bauer, Michael and Degenhardt, Franziska and Del Zompo, Maria and DePaulo, J. Raymond and Edenberg, Howard J. and Etain, Bruno and Bellivier, Frank and Nothen, Markus M. and Falkai, Peter and Foroud, Tatiana and Forstner, Andreas J. and Benabarre, Antonio and Frisen, Louise and Frye, Mark A. and Bengesser, Susanne and Fullerton, Janice M. and Gard, Sebastien and Ösby, Urban and Garnham, Julie S. and Gershon, Elliot S. and Goes, Fernando S. and Greenwood, Tiffany A. and Grigoroiu-Serbanescu, Maria and Hauser, Joanna and Heilbronner, Urs and Heilmann-Heimbach, Stefanie and Osby, Urban and Herms, Stefan and Hipolito, Maria and Hitturlingappa, Shashi and Hoffmann, Per and Hofmann, Andrea and Jamain, Stephane and Jimenez, Esther and Kahn, Jean-Pierre and Kassem, Layla and Witt, Stephanie H. and Kelsoe, John R. and Wright, Adam and Kittel-Schneider, Sarah and Zandi, Peter P. and Kliwicki, Sebastian and Zhang, Peng and Zollner, Sebastian and Koller, Daniel L. and Konig, Barbara and Lackner, Nina and Laje, Gonzalo and Lang, Maren and Lavebratt, Catharina and Lawson, William B. and Leboyer, Marion and Leckband, Susan G. and Jm, Aubry and Liu, Chunyu and Maaser, Anna and Mahon, Pamela B. and Maier, Wolfgang and Maj, Mario and Manchia, Mirko and Mitchell, Philip B. and Martinsson, Lina and Mitjans, Marina and McCarthy, Michael J. and Mondimore, Francis M. and McElroy, Susan L. and Monteleone, Palmiero and McInnis, Melvin G. and Ja, Badner and McKinney, Rebecca and Muhleisen, Thomas W. and Nöthen, Markus M. and Nievergelt, Caroline M. and Novak, Tomas and Tb, Barrett and Nurnberger, John I. and Pfennig, Andrea and Nwulia, Evaristus A. and Potash, James B. and Propping, Peter and Reif, Andreas and Reininghaus, Eva and Rice, John and Rietschel, Marcella and Rouleau, Guy A. and Rybakowski, Janusz K. and Schalling, Martin and Scheftner, William A. and Schofield, Peter R. and Bt, Baune and Schork, Nicholas J. and Schulze, Thomas G. and Schumacher, Johannes and Schweizer, Barbara W. and Severino, Giovanni and Shekhtman, Tatyana and Shilling, Paul D. and Simhandl, Christian and Slaney, Claire M. and Smith, Erin N. and Squassina, Alessio and Stamm, Thomas and Strohmaier, Jana and Stopkova, Pavla and Szelinger, Szabolcs and Streit, Fabian and Tighe, Sarah K. and Tortorella, Alfonso and Turecki, Gustavo and Vieta, Eduard and Volkert, Julia and McMahon, Francis J. and Wh, Berrettini}, doi = {10.1093/hmg/ddw181}, month = {mar}, title = {Genome-wide association study of 40,000 individuals identifies two novel loci associated with bipolar disorder}, url = {https://academic.oup.com/hmg/article-pdf/25/15/3383/8624729/ddw181.pdf}, year = {2016} } @article{Kranz2012, author = {Kranz, Thorsten M. and Ekawardhani, Savira and Lin, Michelle K. and Witzmann, Simone R. and Streit, Fabian and Schuelter, Ulrike and Bauer, Hans and Henseler, Darja and Turner, Jonathan D. and Muller, Claude P. and Reif, Andreas and Schote, Andrea B. and Meyer, Jobst}, doi = {10.1016/j.jpsychires.2012.08.008}, journal = {Journal of Psychiatric Research}, month = {jan}, pages = {1414-1420}, title = {The chromosome 15q14 locus for bipolar disorder and schizophrenia: Is C15orf53 a major candidate gene?}, url = {https://www.researchgate.net/profile/Thorsten_Kranz/publication/230785840_The_chromosome_15q14_locus_for_bipolar_disorder_and_schizophrenia_Is_C15orf53_a_major_candidate_gene/links/54296b680cf238c6ea7ecb4f.pdf}, volume = {46}, year = {2012} } @article{Kumsta2009, abstract = {Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis has been associated with the etiology of major depression. One of the factors underlying altered glucocorticoid signaling might be variability of the glucocorticoid receptor gene (GR, NR3C1). GR polymorphisms have been associated with variability in glucocorticoid sensitivity and endocrine responses to psychosocial stress. Furthermore, a common GR SNP (rs10482605), located in the promoter region, has been associated with major depression. We performed functional characterization of this SNP in vitro using a reporter gene assay under different stimulation conditions. Furthermore, we genotyped 219 subjects previously genotyped for four common GR SNPs to further characterize GR haplotype structure. The minor C allele of the rs10482605 SNP showed reduced transcriptional activity under unstimulated conditions and under different stimulation conditions in two brain derived cell lines. Linkage analyses revealed that the rs10482605 SNP is in high linkage disequilibrium with a A/G SNP in exon 9beta (rs6198), associated with relative glucocorticoid resistance and increased GRbeta mRNA stability. We provide evidence that two functional GR SNPs in linkage disequilibrium are responsible for both regulation of GR expression and mRNA stability. This newly characterized haplotype could increase the risk for the development of stress related disorders, including major depression.}, author = {Kumsta, Robert and Moser, Dirk and Streit, Fabian and Koper, Jan Willem and Meyer, Jobst and Wüst, Stefan}, doi = {10.1002/ajmg.b.30837}, journal = {American Journal of Medical Genetics Part B: Neuropsychiatric Genetics}, month = {jun}, pages = {476-482}, title = {Characterization of a glucocorticoid receptor gene (GR,NR3C1) promoter polymorphism reveals functionality and extends a haplotype with putative clinical relevance}, url = {https://oadoi.org/10.1002/ajmg.b.30837}, volume = {150B}, year = {2009} } @article{Lang2016, abstract = {AbstractBackgroundPathological gambling is a behavioural addiction with negative economic, social, and psychological consequences. Identification of contributing genes and pathways may improve understanding of aetiology and facilitate therapy and prevention. Here, we report the first genome-wide association study of pathological gambling. Our aims were to identify pathways involved in pathological gambling, and examine whether there is a genetic overlap between pathological gambling and alcohol dependence.MethodsFour hundred and forty-five individuals with a diagnosis of pathological gambling according to the Diagnostic and Statistical Manual of Mental Disorders were recruited in Germany, and 986 controls were drawn from a German general population sample. A genome-wide association study of pathological gambling comprising single marker, gene-based, and pathway analyses, was performed. Polygenic risk scores were generated using data from a German genome-wide association study of alcohol dependence.ResultsNo genome-wide significant association with pathological gambling was found for single markers or genes. Pathways for Huntington's disease (P-value = 6.63 × 10−3); 5′-adenosine monophosphate-activated protein kinase signalling (P-value = 9.57 × 10−3); and apoptosis (P-value = 1.75 × 10−2) were significant. Polygenic risk score analysis of the alcohol dependence dataset yielded a one-sided nominal significant P-value in subjects with pathological gambling, irrespective of comorbid alcohol dependence status.ConclusionsThe present results accord with previous quantitative formal genetic studies which showed genetic overlap between non-substance- and substance-related addictions. Furthermore, pathway analysis suggests shared pathology between Huntington's disease and pathological gambling. This finding is consistent with previous imaging studies.}, author = {Lang, M. and Leménager, T. and Streit, F. and Fauth-Bühler, M. and Frank, J. and Juraeva, D. and Witt, S. H. and Degenhardt, F. and Hofmann, A. and Heilmann-Heimbach, S. and Kiefer, F. and Brors, B. and Grabe, H.-J. and John, U. and Bischof, A. and Bischof, G. and Völker, U. and Homuth, G. and Beutel, M. and Lind, P. A. and Medland, S. E. and Slutske, W. S. and Martin, N. G. and Völzke, H. and Nöthen, M. M. and Meyer, C. and Rumpf, H.-J. and Wurst, F. M. and Rietschel, M. and Mann, K. F.}, doi = {10.1016/j.eurpsy.2016.04.001}, journal = {European Psychiatry}, month = {aug}, pages = {38-46}, title = {Genome-wide association study of pathological gambling}, url = {https://doi.org/10.1016/j.eurpsy.2016.04.001}, volume = {36}, year = {2016} } @article{Lederbogen2011, abstract = {More than half of the world's population now lives in cities, making the creation of a healthy urban environment a major policy priority. Cities have both health risks and benefits, but mental health is negatively affected: mood and anxiety disorders are more prevalent in city dwellers and the incidence of schizophrenia is strongly increased in people born and raised in cities. Although these findings have been widely attributed to the urban social environment, the neural processes that could mediate such associations are unknown. Here we show, using functional magnetic resonance imaging in three independent experiments, that urban upbringing and city living have dissociable impacts on social evaluative stress processing in humans. Current city living was associated with increased amygdala activity, whereas urban upbringing affected the perigenual anterior cingulate cortex, a key region for regulation of amygdala activity, negative affect and stress. These findings were regionally and behaviourally specific, as no other brain structures were affected and no urbanicity effect was seen during control experiments invoking cognitive processing without stress. Our results identify distinct neural mechanisms for an established environmental risk factor, link the urban environment for the first time to social stress processing, suggest that brain regions differ in vulnerability to this risk factor across the lifespan, and indicate that experimental interrogation of epidemiological associations is a promising strategy in social neuroscience.}, author = {Lederbogen, Florian and Kirsch, Peter and Haddad, Leila and Streit, Fabian and Tost, Heike and Schuch, Philipp and Wüst, Stefan and Pruessner, Jens C. and Rietschel, Marcella and Deuschle, Michael and Meyer-Lindenberg, Andreas}, doi = {10.1038/nature10190}, journal = {Nature}, month = {jun}, pages = {498-501}, title = {City living and urban upbringing affect neural social stress processing in humans}, url = {https://www.researchgate.net/profile/Andreas_Meyer-Lindenberg/publication/51242929_City_living_and_urban_upbringing_affect_neural_social_stress_processing_in_humans_Nature/links/0fcfd50ae0f4d3b8c1000000.pdf}, volume = {474}, year = {2011} } @article{Mattheisen2013, author = {Mattheisen, Manuel and Streit, Fabian}, month = {nov}, title = {Duplications in RB1CC1 are associated with schizophrenia; identification in largeEuropean sample sets.}, year = {2013} } @article{Müller2013, author = {Müller, Matthias J. and Preuss, Christoph and Paul, Thomas and Streit, Frank and Brandhorst, Gunnar and Seeliger, Stephan}, doi = {10.1089/bfm.2012.0084}, journal = {Breastfeeding Medicine}, month = {jun}, pages = {327-329}, title = {Serotonergic Overstimulation in a Preterm Infant After Sertraline Intake via Breastmilk}, url = {https://oadoi.org/10.1089/bfm.2012.0084}, volume = {8}, year = {2013} } @article{Oellerich2014, author = {Oellerich, Michael and Schütz, Ekkehard and Kanzow, Philipp and Schmitz, Jessica and Beck, Julia and Kollmar, Otto and Streit, Frank and Walson, Philip D.}, doi = {10.1097/ftd.0000000000000044}, journal = {Therapeutic Drug Monitoring}, month = {apr}, pages = {136-140}, title = {Use of Graft-Derived Cell-Free DNA as an Organ Integrity Biomarker to Reexamine Effective Tacrolimus Trough Concentrations After Liver Transplantation: }, url = {https://oadoi.org/10.1097/ftd.0000000000000044}, volume = {36}, year = {2014} } @article{Rietschel2016, abstract = {Measuring cortisol in hair is a promising method to assess long-term alterations of the biological stress response system, and hair cortisol concentrations (HCC) may be altered in psychiatric disorders and in subjects suffering from chronic stress. However, the pattern of associations between HCC, chronic stress and mental health require clarification. Our exploratory study: (1) assessed the association between HCC and perceived stress, symptoms of depression and neuroticism, and the trait extraversion (as a control variable); and (2) made use of the twin design to estimate the genetic and environmental covariance between the variables of interest. Hair samples from 109 (74 female) subjects (age range 12–21 years, mean 15.1) including 8 monozygotic (MZ) and 21 dizygotic (DZ) twin pairs were analyzed. Perceived stress was measured with the Perceived Stress Scale and/or the Daily Life and Stressors Scale, neuroticism, and extraversion with the NEO-Five Factor Inventory or the Junior Eysenck Personality Questionnaire, and depressive symptoms with the Somatic and Psychological Health Report. We found a modest positive association between HCC and the three risk factors — perceived stress, symptoms of depression, and neuroticism (r = 0.22–0.33) — but no correlation with extraversion (-0.06). A median split revealed that the associations between HCC and risk factors were stronger (0.47–0.60) in those subjects with HCC >11.36 pg/mg. Furthermore, our results suggest that the genetic effects underlying HCC are largely shared with those that influence perceived stress, depressive symptoms, and neuroticism. These results of our proof of principle study warrant replication in a bigger sample but raise the interesting question of the direction of causation between these variables.}, author = {Rietschel, Liz and Streit, Fabian and Zhu, Gu and McAloney, Kerrie and Kirschbaum, Clemens and Frank, Josef and Wright, Margaret J. and Hansell, Narelle K. and McGrath, John J. and Witt, Stephanie H. and Rietschel, Marcella and Martin, Nicholas G.}, doi = {10.1017/thg.2016.50}, journal = {Twin Research and Human Genetics}, month = {jul}, pages = {438-446}, title = {Hair cortisol and its association with psychological risk factors for psychiatric disorders: a pilot study in adolescent twins}, url = {https://boris.unibe.ch/85826/8/Hair%20Cortisol%20and%20Its%20Association%20With%20Psychological%20Risk%20Factors%20for%20Psychiatric%20Disorders%20A%20Pilot%20Study%20in%20Adolescent%20Twins.pdf}, volume = {19}, year = {2016} } @article{Streit2014, abstract = {Abstract We have previously shown that urban upbringing and city living were associated with stress-induced activity in the amygdala and the perigenual anterior cingulate cortex (pACC). This finding might link the epidemiological risk factor "urbanicity" to neurobiological mechanisms of psychiatric disorders. However, given the heritability of stress related phenotypes, it appears likely that genetic factors can modulate the effect of urbanicity on social stress processing. In the present exploratory study, we investigated if a functional sequence variation in the neuropeptide S receptor gene (NPSR1 rs324981) is associated with brain activation patterns under acute psychosocial stress and if it modulates the link between urbanicity and central stress processing. In animals, neuropeptide S has strong anxiolytic effects and it induces hypothalamus-pituitary-adrenal (HPA) axis activation. In humans, rs324981 was found to be associated with anxiety and stress related phenotypes. Forty-two subjects were exposed to a psychosocial stress task for scanner environments (ScanSTRESS). While no main effect of rs324981 on amygdala and pACC activity was detected, we found a distinct interaction between rs324981 and urban upbringing modulating right amygdala responses. Moreover, right amygdala responses were significantly higher in subjects who also showed a salivary cortisol response to the stress exposure. The present finding of a gene x environment interaction further supports the view that the brain NPS system is involved in central stress regulation. This study provides first evidence for the assumption that a NPSR1 variant modulates brain activation under stress, interacting with the environmental risk factor urban upbringing.}, author = {Streit, Fabian and Haddad, Leila and Paul, Torsten and Frank, Josef and Schäfer, Axel and Nikitopoulos, Jörg and Akdeniz, Ceren and Lederbogen, Florian and Treutlein, Jens and Witt, Stephanie and Meyer-Lindenberg, Andreas and Rietschel, Marcella and Kirsch, Peter and Wüst, Stefan}, doi = {10.3109/10253890.2014.921903}, journal = {Stress: The International Journal on the Biology of Stress}, month = {may}, pages = {352-361}, title = {A functional variant in the neuropeptide S receptor 1 gene moderates the influence of urban upbringing on stress processing in the amygdala}, url = {https://www.researchgate.net/profile/Andreas_Meyer-Lindenberg/publication/262109205_A_functional_variant_in_the_neuropeptide_S_receptor_1_gene_moderates_the_influence_of_urban_upbringing_on_stress_processing_in_the_amygdala/links/550a75390cf20ed529e33132.pdf}, volume = {17}, year = {2014} } @article{Streit2016, author = {Streit, Fabian and Memic, Amra and Hasandedić, Lejla and Rietschel, Liz and Frank, Josef and Lang, Maren and Witt, Stephanie H. and Forstner, Andreas J. and Degenhardt, Franziska and Wüst, Stefan and Nöthen, Markus M. and Kirschbaum, Clemens and Strohmaier, Jana and Oruc, Lilijana and Rietschel, Marcella}, doi = {10.1016/j.psyneuen.2016.03.010}, journal = {Psychoneuroendocrinology}, month = {jul}, pages = {26-34}, title = {Perceived stress and hair cortisol: Differences in bipolar disorder and schizophrenia}, url = {https://oadoi.org/10.1016/j.psyneuen.2016.03.010}, volume = {69}, year = {2016} } @article{Strohmaier2011, abstract = {Objectives. Sexual dysfunction (SD) is a frequently reported side-effect of antidepressant treatment, particularly of selective serotonin reuptake inhibitors (SSRIs). In the multicentre clinical and pharmacogenetic GENDEP study (Genome-based Therapeutic Drugs for Depression), the effect of the serotonin transporter gene promoter polymorphism 5-HTTLPR on sexual function was investigated during treatment with escitalopram (SSRI) and nortriptyline (tricyclic antidepressant). Methods. A total of 494 subjects with an episode of DSM-IV major depression were randomly assigned to treatment with escitalopram or nortriptyline. Over 12 weeks, depressive symptoms and SD were measured weekly with the Montgomery-Asberg Depression Rating Scale, the Antidepressant Side-Effect Checklist, the UKU Side Effect Rating Scale, and the Sexual Functioning Questionnaire. Results. The incidence of reported SD after 12 weeks of treatment was relatively low, and did not differ significantly between antidepressants (14.9% escitalopram, 19.7% nortriptyline). There was no significant interaction between the 5-HTTLPR and antidepressant on SD. Improvement in depressive symptoms and younger age were both associated with lower SD. The effect of age on SD may have been moderated by the 5-HTTLPR. Conclusions. In GENDEP, rates of reported SD during treatment were lower than those described in previous reports. There was no apparent effect of the 5-HTTLPR on the observed decline in SD. © 2011 Informa Healthcare. ; SCOPUS: ar.j ; info:eu-repo/semantics/published}, author = {Strohmaier, Jana and Wüst, Stefan and Uher, Rudolf and Henigsberg, Neven and Mors, Ole and Hauser, Joanna and Souery, Daniel and Zobel, Astrid and Dernovsek, Mojca Z. and Streit, Fabian and Schmäl, Christine and Kozel, Dejan and Placentino, Anna and Farmer, Anne and McGuffin, Peter and Aitchison, Katherine J. and Rietschel, Marcella}, doi = {10.3109/15622975.2011.559270}, journal = {The World Journal of Biological Psychiatry}, month = {mar}, pages = {528-538}, title = {Sexual dysfunction during treatment with serotonergic and noradrenergic antidepressants: Clinical description and the role of the5-HTTLPR}, url = {http://www.ncbi.nlm.nih.gov/pubmed/21388237}, volume = {12}, year = {2011} } @article{Strohmaier2015, abstract = {Shorter telomere length (TL) has found to be associated with lower birth weight and with lower cognitive ability and psychiatric disorders. However, the direction of causation of these associations and the extent to which they are genetically or environmentally mediated are unclear. Within-pair comparisons of monozygotic (MZ) and dizygotic (DZ) twins can throw light on these questions. We investigated correlations of within pair differences in telomere length, IQ, and anxiety/depression in an initial sample from Brisbane (242 MZ pairs, 245 DZ same sex (DZSS) pairs) and in replication samples from Amsterdam (514 MZ pairs, 233 DZSS pairs) and Melbourne (19 pairs selected for extreme high or low birth weight difference). Intra-pair differences of birth weight and telomere length were significantly correlated in MZ twins, but not in DZSS twins. Greater intra-pair differences of telomere length were observed in the 10% of MZ twins with the greatest difference in birth weight compared to the bottom 90% in both samples and also in the Melbourne sample. Intra-pair differences of telomere length and IQ, but not of TL and anxiety/depression, were correlated in MZ twins, and to a smaller extent in DZSS twins. Our findings suggest that the same prenatal effects that reduce birth weight also influence telomere length in MZ twins. The association between telomere length and IQ is partly driven by the same prenatal effects that decrease birth weight.}, author = {Strohmaier, Jana and van Dongen, Jenny and Willemsen, Gonneke and Nyholt, Dale R. and Zhu, Gu and Codd, Veryan and Novakovic, Boris and Hansell, Narelle and Wright, Margaret J. and Rietschel, Liz and Streit, Fabian and Henders, Anjali K. and Montgomery, Grant W. and Samani, Nilesh J. and Gillespie, Nathan A. and Hickie, Ian B. and Craig, Jeffrey M. and Saffery, Richard and Boomsma, Dorret I. and Rietschel, Marcella and Martin, Nicholas G.}, doi = {10.1017/thg.2015.3}, journal = {Twin Research and Human Genetics}, month = {mar}, pages = {198-209}, title = {Low Birth Weight in MZ Twins Discordant for Birth Weight is Associated with Shorter Telomere Length and lower IQ, but not Anxiety/Depression in Later Life}, url = {https://genepi.qimr.edu.au/contents/p/staff/Strohmaier_TRHG_BirthWeightEPUB.pdf}, volume = {18}, year = {2015} } @article{Treutlein2016, author = {Treutlein, Jens and Strohmaier, Jana and Frank, Josef and Witt, Stephanie H. and Rietschel, Liz and Forstner, Andreas J. and Lang, Maren and Degenhardt, Franziska and Dukal, Helene and Herms, Stefan and Hoffmann, Per and Streit, Fabian and Cichon, Sven and Nöthen, Markus M. and Rietschel, Marcella}, doi = {10.1097/ypg.0000000000000149}, journal = {Psychiatric Genetics}, month = {aug}, pages = {34-37}, title = {Association between neuropeptide Y receptor Y2 promoter variant rs6857715 and major depressive disorder.}, url = {https://oadoi.org/10.1097/ypg.0000000000000149}, volume = {27}, year = {2016} } @article{Zänkert2015, author = {Zänkert, Sandra and Streit, Fabian and Haddad, Leila and Akdeniz, Ceren and Trost, Heike and Kumsta, Robert and Entringer, Sonja and Yim, Ilona S. and Witt, Stephanie and Kirsch, Peter and Rietschel, Marcella and Wüst, Stefan}, doi = {10.1016/j.psyneuen.2015.07.550}, journal = {Psychoneuroendocrinology}, month = {nov}, pages = {59}, title = {Sex modulates the interaction between neuropeptide S gene variants and endocrine and central stress responses}, url = {https://oadoi.org/10.1016/j.psyneuen.2015.07.550}, volume = {61}, year = {2015} }