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21. Abstracts

Author

Arendt, T., Bigl, V., Beckmann, H., Senitz, D., Kalus, P., Lauer, M., Durany, N., Cruz-Sanchez, F. F., Thome, J., Rösler, M., Riederer, P., Heinsen, H., Rüb, U., Hökfelt, T., Jellinger, K. A., Leszek, J., Ransmayr, G., Berger, W., Federspiel, S., Butá, M., Nowakowski, C., Meisel, U., Reynolds, G. P., Sardar, A. M., Beasley, C. L., Aparicio-Legarza, M. I., Gsell, W., Frölich, L., Blum-Degen, D., Ozawa, H., Hashimoto, E., Danielczyk, W., Münch, G., Janetzky, B., Reichmann, H., Wodarz, N., Lesch, K. P., Kornhuber, J., Shoham, S., Youdim, M. B. H., Teherani, D. K., Simanyi, M., and Tipton, K. F.

Published
1997
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27. Abstracts Second Congress of the European Society for Clinical Neuropharmacology: Würzburg, November 9–11, 1995

Author

Agid, Y., Arendt, T., Gärtner, U., Holzer, M., Fruth, P., Brückner, M. K., Arzberger, T., Weindl, A., Baas, H., Demisch, L., Harder, S., Bürklin, F., Fischer, P. A., Bagli, M., Rao, M. L., Sobanski, T., Laux, G., Barbier, P., Fumagalli, F., Donati, E., Maggio, R., Racagni, G., Corsini, G. U., Riva, M., Berger, J., Löschl, B., Bernheimer, H., Lugowska, A., Tylki-Szymanska, A., Gieselmann, V., Molzer, B., Faé, I., Bernocchi, G., Scherini, E., Necchi, D., Bigl, M., Bleyl, D., Bigl, V., Eschrich, K., Block, F., Schwarz, M., Blum-Degen, D., Müller, Th., Kuhn, W., Gerlach, M., Przuntek, H., Riederer, R., Bonuccelli, U., Ceravolo, R., Nuti, A., D'Avino, C., Placidi, G., Perugi, G., Cassano, G. B., Del Dotto, P., Piccini, P., Colzi, A., Muratorio, A., Braak, H., Braak, E., Yilmazer, D. M., de Vos, R. A. I., Jansen, E. N. H., Bringmann, G., Clement, H. W., Grote, C., Rausch, F., Reichmann, H., Riederer, P., Sontag, K. -H., Wesemann, W., God, R., Feineis, D., Brückner, R., Protzen, J. -A., Fähr, S., Rausch, W. -D., Brunt, E. R. P., Pruim, J., Willemsen, A. J., van Weerden, T. W., Bryan-Lluka, L. J., Bönisch, H., Büttner, Th., Kühn, W., McMonagle, U., Calza, L., Pozza, M., Coraddu, F., Farci, G., Carlsson, A., Napolitano, A., Salvetti, S., Dell'Agnello, G., Renna, M., Conquet, F., Bashir, Z., Daniel, H., Ferraguti, F., Collingridge, G., Crépel, F., Coos Verhoef, J., Merkus, F. W. H. M., Junginger, H. E., Cruz-Sánchez, F. F., Kutschka, T., Beeg, M., Deuschle, M., Weber, B., Körner, A., Standhardt, H., Lammers, C. -H., Motzek-Noé, T., Heuser, I., Earl, C. D., Reum, T., Sautter, J., Xie, J. -X, Kupsch, A., Oertel, W. H., Morgenstern, R., Emilien, G. M., Maloteaux, J. M., Seghers, A., Charles, G., Erdmann, R., Högemann, D., Fichter, N., Lücking, C. H., Landwehrmeyer, G. B., Winter, T., Feuerstein, T. J., Fitzgeral, D., Anderson, M. C., Lawlor, B., Tipton, K. F., Frackowiak, R. S. J., Freo, U., Dam, M., Pizzolato, G., Merico, A., Ori, C., Sale, E., Battistin, L., Fritze, J., Froelich, L., Goetz, M., Gsell, W., Jellinger, K., Beckmann, H., Fünfgeld, E. W., Glinka, Y., Youdim, M. B. H., Götz, M. E., Breithaupt, W., Burger, R., Streifler, M., Simanyi, M., Müller, F., Danielczyk, W., Hirning, T., Sohlbach, M., Nafc, R., Sternadl, H., Winter, M., Nöth, U., Heim, C., Hartmann, J., Künig, G., Niedermeyer, B., Berger, W., Deckert, J., Abel, F., Heinsen, H., Senitz, D., Mayr, J., Ransmayr, G., Hartung, H. -P., Heils, A., Teufel, A., Petri, S., Seemann, M., Bengel, D., Degen, H. J., Lesch, K. P., Sontag, T., Heinen, F., Korinthenberg, R., Heiss, W. -D., Rüb, U., Gangus, B., Jungkunz, G., Bauer, M., Ulmar, G., Böcker, F., Schüler, M., Bethke, B., Lockemann, U., Hermans, E., Vanhoorde, P., Hesse, S., Hüll, M., Fiebich, B., Lieb, K., Strauss, S., Berger, M., Volk, B., Bauer, J., Iversen, L. L., Janetzky, B., Hauck, S., Jeanjean, A. P., Laterre, E. C., Bancher, C., Jost, W. H., Kalus, P., Kanner, B., Khrapova, E. V., Brusov, O. S., Knauber, J., Müller, W. E., Korczyn, A. D., Kornhuber, J., Parsons, C. G., Hartmann, S., Retz, W., Kamolz, S., Thome, J., Koutsilieri, E., Chen, T. -S., Kreutzberg, G. W., Krieglstein, J., Winkel, R., Danielcyk, S., Gerstner, A., Mattern, C., Häcker, R., Labunsky, D., Zhirnova, I., Komelkova, L., Popova, L., Avdiunina, I., Lakke, J. P. W. F., Lange, K. W., Steup, A., Tucha, O., Naumann, M., Lassmann, H., Leszek, J., Gasiorowski, K., Inglot, D., Lohse, M. J., Löschmann, P. -A., Eblen, F., Wüllner, U., Klockgether, T., Dichgans, J., Macrae, I. M., Mimmack, M. L., Emson, P., Norta, M., Borchert, H. -H., Medori, R., Chan, W. W., Heinemann, T., Melzacka, M., Kolasiewicz, W., Sieklucka, M., Jaros, T., Mesec, A., Šega, S., Kiauta, T., Moser, A., Vieregge, P., Siebecker, F., Münch, G., Schinzel, R., Michaelis, J., Cunningham, A., Da Prada, M., Borroni, E., Zürcher, G., Reiners, K., Neveu, P. J., Nitsch, R. M., Pavese, N., Lucetti, C., Rossi, G., Offen, D., Ziv, I., Stein, R., Barzilai, A., Hochman, A., Melamed, E., Ozawa, H., Hashimoto, E., Saito, T., Ymamoto, M., Takahata, N., Frölich, L., Paulus, W., Hermsteiner, E., Haug, B., Bandelow, B., Peckys, D., Gleichauf, O., Jackisch, R., Landwehrmeyer, B., Bloß, H. G., Plaschke, K., Müller, D., Hoyer, S., Avdyuna, L. A., Putzke, J., Spanagel, R., Tolle, T. R., Zieglgänsberger, W., Rabey, J. -M., Orlov, E., von Raison, F., Lehmann, K., Havemann-Reinecke, U., Butà, M., Federspiel, S., Maier, H., Abdel-mohsen, M., Abdel-moneim, M., Reynolds, G. P., Sardar, A. M., Eggett, C. J., Rosario, P., de la Morena, E., José Barro, M., Rossini, P. M., Roth, J., Růžička, E., Svobodová, I., Mečíř, P., Jech, R., Remeš, F., Kleinschroth, A., Schliebs, R., Roßner, S., Heider, M., Schubert, H., König, P., Schuttes, H., HaveIec, L., Schwartz, J. -C., Sendtner, M., Smith, A., Li, M., Griesbeck, O., Parsadanian, A., Holtmann, B., Carroll, P., Toyka, K. V., Thoenen, H., Sharkawy, A. A., Ibrahim, T. A., Pulkowski, U., Siesjö, B. K., Klessaschek, M., Sopper, S., Demuth, M., Dörries, R., Hemm, S., Stahl-Hennig, C., Brinkmann, R., ter Meulen, V., Sperk, G., Schwarzer, C., Stern, G., Storm, G., Strein, I., Struck, M., Stürenburg, H. J., Kunze, K., Svadovsky, A. I., Morgunov, K. V., Peresedov, V. V., Moshkin, A. V., Teherani, D. K., Baumer, A., Rösier, M., Rösler, M., Wiesbeck, G. A., Wodarz, N., Boning, J., Timerbaeva, S. L., Alekseeva, N. S., Toso, A., Barletta, D., Tuulik, V., Lossmann, E., Raja, A., Meister, A., Uitti, R. J., Rajput, A. H., Ahlskog, J. E., Offord, K. P., Schroeder, D. R., O'Brien, P. C., Vaglini, F., Fascetti, F., Pardini, C., Mancino, L., Velbinger, K., Hartmann, H., Eckert, A., Grüter, S., Behrens, S., Niemann, J., Guschelbauer, B., Lauk, M., Wissel, J., Poewe, W., Wurthman, C., Janzen, E. N. H., Goping, G., Adegemo, O. M., Gemma, A., Kuijpers, J., Pollard, H. B., Zielke, B., Ziemann, U., and Bruns, D.

Published
1995
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47. Bipolar disorder risk alleles in children with ADHD.

Author

Schimmelmann BG, Hinney A, Scherag A, Pütter C, Pechlivanis S, Cichon S, Jöckel KH, Schreiber S, Wichmann HE, Albayrak Ö, Dauvermann M, Konrad K, Wilhelm C, Herpertz-Dahlmann B, Lehmkuhl G, Sinzig J, Renner TJ, Romanos M, Warnke A, Lesch KP, Reif A, and Hebebrand J

Subjects
Adolescent, Attention Deficit Disorder with Hyperactivity complications, Bipolar Disorder complications, Child, Female, Genome-Wide Association Study, Haplotypes, Humans, Male, White People genetics, Alleles, Attention Deficit Disorder with Hyperactivity genetics, Bipolar Disorder genetics, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide
Abstract

Bipolar disorder (BD) and attention deficit/hyperactivity disorder (ADHD) may share common genetic risk factors as indicated by the high co-morbidity of BD and ADHD, their phenotypic overlap especially in pediatric populations, the high heritability of both disorders, and the co-occurrence in families. We therefore examined whether known polygenic BD risk alleles are associated with ADHD. We chose the eight best SNPs of the recent genome-wide association study (GWAS) of BD patients of German ancestry and the nine SNPs from international GWAS meeting a 'genome-wide significance' level of α = 5 × 10(-8). A GWAS was performed in 495 ADHD children and 1,300 population-based controls using HumanHap550v3 and Human660 W-Quadv1 BeadArrays. We found no significant association of childhood ADHD with single BD risk alleles surviving adjustment for multiple testing. Yet, risk alleles for BD and ADHD were directionally consistent at eight of nine loci with the strongest support for three SNPs in or near NCAN, BRE, and LMAN2L. The polygene analysis for the BP risk alleles at all 14 loci indicated a higher probability of being a BD risk allele carrier in the ADHD cases as compared to the controls. At a moderate power to detect association with ADHD, if true effects were close to estimates from GWAS for BD, our results suggest that the possible contribution of BD risk variants to childhood ADHD risk is considerably lower than for BD. Yet, our findings should encourage researchers to search for common genetic risk factors in BD and childhood ADHD in future studies.

Published
2013
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48. A functional dopamine-beta-hydroxylase gene promoter polymorphism is associated with impulsive personality styles, but not with affective disorders.

Author

Hess C, Reif A, Strobel A, Boreatti-Hümmer A, Heine M, Lesch KP, and Jacob CP

Subjects
Attention Deficit Disorder with Hyperactivity genetics, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Polymerase Chain Reaction, Dopamine beta-Hydroxylase genetics, Mood Disorders genetics, Personality Disorders genetics, Polymorphism, Single Nucleotide, Promoter Regions, Genetic genetics
Abstract

Dopamine-beta-hydroxylase (DbetaH) catalyzes the conversion of dopamine to norepinephrine in central noradrenergic and adrenergic neurons and thus is critically involved in the biosynthesis of catecholamines. There are equivocal findings concerning the question whether or not DssH activity levels are altered in affective disorders or in subtypes of affective disorders. Moreover, information about the role of dopamine beta-hydroxylase (DBH) genotype, which explains a large part of the variance of enzymatic activity, in affective disorders and personality dimensions is limited. To resolve these inconsistencies, association tests were performed using four independent samples, healthy volunteers (N = 387), patients with affective disorders (N = 182), adult attention deficit hyperactivity disorder (ADHD) patients (N = 407), and patients with personality disorders (N = 637). In the latter two samples, the revised NEO personality inventory (NEO-PI-R) was administered. All participants were genotyped for a putatively functional single nucleotide polymorphism (C-1021T, rs1611115). No differences in DBH C-1021T genotype distribution were observed between patients with affective disorders and healthy control subjects. Also when the patient sample was divided into uni- and bipolar patients versus controls, no significant differences emerged. Furthermore, no clear-cut association was detected between the TT genotype and personality disorder clusters while there was a significant association with adult ADHD. However, personality disorder patients carrying the DBH TT genotype exhibited higher neuroticism and novelty seeking scores as compared to individuals with the CC or CT genotype. Analyses on the level of the neuroticism and novelty seeking subscales revealed that the DBH TT genotype was primarily associated with personality features related to impulsiveness and aggressive hostility. Also adult ADHD patients carrying the homozygous TT genotypes displayed by significantly increased neuroticism scores; when both personality disorder and adult ADHD patient were analyzed together, TT carriers also displayed by significantly lower conscientiousness levels. Our results thus do not implicate the DBH C-1021T polymorphism in the pathophysiology of depressive disorders or personality disorders, yet homozygosity at this locus appears to increase the risk towards personality traits related to impulsiveness, aggression and related disease states, namely adult ADHD. These data argue for a dimensional rather than categorical effect of genetic variance in DBH activity; accordingly, the inconsistency of previous findings concerning DbetaH levels in affective disorders might be caused by the underlying association of the TT genotype at DBH-1021 with impulsive personality traits.

Published
2009
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49. Behavioural and expressional phenotyping of nitric oxide synthase-I knockdown animals.

Author

Wultsch T, Chourbaji S, Fritzen S, Kittel S, Grünblatt E, Gerlach M, Gutknecht L, Chizat F, Golfier G, Schmitt A, Gass P, Lesch KP, and Reif A

Subjects
Animals, Arousal physiology, Basic Helix-Loop-Helix Transcription Factors genetics, CCAAT-Enhancer-Binding Protein-alpha genetics, Cerebellum metabolism, Corpus Striatum metabolism, Gene Expression Regulation physiology, Hippocampus metabolism, Humans, KATP Channels, Mice, Mice, Inbred C57BL, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Peroxiredoxin III, Peroxiredoxins genetics, Potassium Channels, Inwardly Rectifying genetics, Receptors, GABA-B genetics, Receptors, Glucocorticoid genetics, Up-Regulation genetics, Arousal genetics, Emotions physiology, Exploratory Behavior physiology, Maze Learning physiology, Mental Recall physiology, Nitric Oxide physiology, Nitric Oxide Synthase Type I genetics, Orientation physiology, Phenotype
Abstract

The gaseous messenger nitric oxide (NO) has been implicated in a wide range of behaviors, including aggression, anxiety, depression, and cognitive functioning. To further elucidate the physiological role of NO and its down-stream mechanisms, we conducted behavioral and expressional phenotyping of mice lacking the neuronal isoform of nitric oxide synthase (NOS-I), the major source of NO in the central nervous system. No differences were observed in activity-related parameters; in contrast to the a priori hypothesis, derived from pharmacological treatments, depression-related tests (Forced Swim Test, Learned Helplessness) also yielded no significantly different results. A subtle anxiolytic phenotype however was present, with knockdown mice displaying a higher open arm time as compared to their respective wildtypes, yet all other investigated anxiety-related parameters were unchanged. The most prominent feature however was gender-independent cognitive impairment in spatial learning and memory, as assessed by the Water Maze test and an automatized holeboard paradigm. No significant dysregulation of monoamine transporters was evidenced by qRT PCR. To further examine the underlying molecular mechanisms, the transcriptome of knockdown animals was thus examined in the hippocampus, striatum and cerebellum by microarray analysis. A set of >120 differentially expressed genes was identified, whereat the hippocampus and the striatum showed similar expressional profiles as compared to the cerebellum in hierarchical clustering. Among the most significantly up-regulated genes were Peroxiredoxon 3, Atonal homologue 1, Kcnj1, Kcnj8, CCAAT/enhancer binding protein (C/EBP), alpha, 3 genes involved in GABA(B) signalling and, intriguingly, the glucocorticoid receptor GR. While GABAergic genes might underlie reduced anxiety, dysregulation of the glucocorticoid receptor can well contribute to a blunted stress response as found in NOS1 knockdown mice. Furthermore, by CREB inhibition, glucocorticoid receptor upregulation could at least partially explain cognitive deficits in these animals. Taken together, NOS1 knockdown mice display a characteristic behavioural profile consisting of reduced anxiety and impaired learning and memory, paralleled by differential expression of the glucocorticoid receptor and GABAergic genes. Further research has to assess the value of these mice as animal models e.g. for Alzheimer's disease or attention deficit disorder, in order to clarify a possible pathophysiological role of NO therein.

Published
2007
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50. FZD3 is not a risk gene for schizophrenia: a case-control study in a Caucasian sample.

Author

Reif A, Melchers M, Strobel A, Jacob CP, Herterich S, Lesch KP, and Zimmer M

Subjects
Adolescent, Adult, Bipolar Disorder diagnosis, Case-Control Studies, Chronic Disease, Female, Gene Frequency genetics, Genetic Markers genetics, Germany, Haplotypes genetics, Humans, Male, Polymorphism, Single Nucleotide genetics, Psychotic Disorders diagnosis, Schizophrenia diagnosis, Bipolar Disorder genetics, Frizzled Receptors genetics, Genetic Predisposition to Disease genetics, Psychotic Disorders genetics, Receptors, G-Protein-Coupled genetics, Schizophrenia genetics
Abstract

Background: Polymorphisms in the human frizzeled-3 (FZD3) gene have been associated with schizophrenia in an Asian population sample. However, this finding could not be confirmed in subsequent studies investigating other populations. Here we attempted to replicate this finding in a sample of 192 German chronically ill schizophrenic subjects., Methods: Three single nucleotide polymorphisms in the FZD3 gene have been genotyped by primer extension and MALDI-TOF measurement. Subsequently, associations for single markers as well as haplotypes were tested., Results: In German patients, neither single markers nor haplotypes in FZD3 were associated with schizophrenia. Further exploratory analyses using a different diagnostic approach did also not yield significant results., Conclusions: FZD3 is unlikely to play a role in the genetic predisposition towards schizophrenia in the Caucasian population.

Published
2007
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