21 results on '"Renner, T. J."'
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2. No evidence for association between a functional promoter variant of the Norepinephrine Transporter gene SLC6A2 and ADHD in a family-based sample
- Author
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Renner, T. J., Nguyen, T. T., Romanos, M., Walitza, S., Röser, C., Reif, A., Schäfer, H., Warnke, A., Gerlach, M., and Lesch, K. P.
- Published
- 2011
- Full Text
- View/download PDF
3. Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree
- Author
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Lesch, K-P, Selch, S, Renner, T J, Jacob, C, Nguyen, T T, Hahn, T, Romanos, M, Walitza, S, Shoichet, S, Dempfle, A, Heine, M, Boreatti-Hümmer, A, Romanos, J, Gross-Lesch, S, Zerlaut, H, Wultsch, T, Heinzel, S, Fassnacht, M, Fallgatter, A, Allolio, B, Schäfer, H, Warnke, A, Reif, A, Ropers, H-H, and Ullmann, R
- Published
- 2011
- Full Text
- View/download PDF
4. Genome-wide linkage analysis of ADHD using high-density SNP arrays: novel loci at 5q13.1 and 14q12
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Romanos, M, Freitag, C, Jacob, C, Craig, D W, Dempfle, A, Nguyen, T T, Halperin, R, Walitza, S, Renner, T J, Seitz, C, Romanos, J, Palmason, H, Reif, A, Heine, M, Windemuth-Kieselbach, C, Vogler, C, Sigmund, J, Warnke, A, Schäfer, H, Meyer, J, Stephan, D A, and Lesch, K P
- Published
- 2008
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5. Allelic variants of SNAP25 in a family-based sample of ADHD
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Renner, T. J., Walitza, S., Dempfle, A., Eckert, L., Romanos, M., Gerlach, M., Schäfer, H., Warnke, A., Lesch, K. P., and Jacob, C.
- Published
- 2008
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- View/download PDF
6. No evidence for preferential transmission of common valine allele of the Val66Met polymorphism of the brain-derived neurotrophic factor gene (BDNF) in ADHD
- Author
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Schimmelmann, B. G., Friedel, S., Dempfle, A., Warnke, A., Lesch, K. P., Walitza, S., Renner, T. J., Romanos, M., Herpertz-Dahlmann, B., Linder, M., Schäfer, H., Seitz, C., Palmason, H., Freitag, C., Meyer, J., Konrad, K., Hinney, A., and Hebebrand, J.
- Published
- 2007
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7. Transmission disequilibrium of polymorphic variants in the tryptophan hydroxylase-2 gene in attention-deficit/hyperactivity disorder
- Author
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Walitza, S, Renner, T J, Dempfle, A, Konrad, K, Wewetzer, Ch, Halbach, A, Herpertz-Dahlmann, B, Remschmidt, H, Smidt, J, Linder, M, Flierl, L, Knölker, U, Friedel, S, Schäfer, H, Gross, C, Hebebrand, J, Warnke, A, and Lesch, K P
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- 2005
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8. Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
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Jarick, I, Volckmar, A-L, Pütter, C, Pechlivanis, S, Nguyen, T T, Dauvermann, M R, Beck, S, Albayrak, Ö, Scherag, S, Gilsbach, S, Cichon, S, Hoffmann, P, Degenhardt, F, Nöthen, M M, Schreiber, S, Wichmann, H-E, Jöckel, K-H, Heinrich, J, Tiesler, C MT, Faraone, S V, Walitza, S, Sinzig, J, Freitag, C, Meyer, J, Herpertz-Dahlmann, B, Lehmkuhl, G, Renner, T J, Warnke, A, Romanos, M, Lesch, K-P, Reif, A, Schimmelmann, B G, Hebebrand, J, Scherag, A, and Hinney, A
- Published
- 2014
- Full Text
- View/download PDF
9. OBESITY RISK ALLELE IS ASSOCIATED WITH CHILDHOOD ATTENTION-DEFICIT/HYPERACTIVITY DISORDER: A CROSSDISORDER ANALYSIS: 653 accepted poster
- Author
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Hinney, A., Albayrak, Pütter, C., Cichon, S., Hoffmann, P., Nöthen, M. M., Jöckel, K. H., Schreiber, S., Wichmann, H. E., Herpertz-Dahlmann, B., Lehmkuhl, G., Sinzig, J., Renner, T. J., Romanos, M., Warnke, A., Lesch, K. P., Reif, A., Schimmelmann, B. G., Scherag, A., and Hebebrand, J.
- Published
- 2012
10. Variation in the dopamine transporter gene impacts association between reward sensitivity and ventral striatal BOLD-response during reward anticipation
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Hahn, T., Plichta, M. M., Heinzel, S., Renner, T. J., Dresler, T., Markulin, F., Polak, T., Ehlis, A. C., Jakob, P. M., Lesch, K. P., and Fallgatter, A. J.
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- 2009
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11. Reduced NoGo-anteriorisation during continuous performance test in deletion syndrome 22q11.2
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Romanos, M, Ehlis, A C, Baehne, C G, Jacob, C, Renner, T J, Storch, A, Briegel, W, Walitza, S, Lesch, K P, Fallgatter, A J, University of Zurich, and Romanos, M
- Subjects
2738 Psychiatry and Mental Health ,610 Medicine & health ,10058 Department of Child and Adolescent Psychiatry ,2803 Biological Psychiatry - Published
- 2010
12. Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
- Author
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Jarick, I., Volckmar, A-L, Puetter, C., Pechlivanis, S., Nguyen, T. T., Dauvermann, M. R., Beck, S., Albayrak, Oe, Scherag, S., Gilsbach, S., Cichon, S., Hoffmann, P., Degenhardt, F., Noethen, M. M., Schreiber, S., Wichmann, H-E, Joeckel, K-H, Heinrich, J., Tiesler, C. M. T., Faraone, S. V., Walitza, S., Sinzig, J., Freitag, C., Meyer, J., Herpertz-Dahlmann, B., Lehmkuhl, G., Renner, T. J., Warnke, A., Romanos, M., Lesch, K-P, Reif, A., Schimmelmann, B. G., Hebebrand, J., Scherag, A., Hinney, A., Jarick, I., Volckmar, A-L, Puetter, C., Pechlivanis, S., Nguyen, T. T., Dauvermann, M. R., Beck, S., Albayrak, Oe, Scherag, S., Gilsbach, S., Cichon, S., Hoffmann, P., Degenhardt, F., Noethen, M. M., Schreiber, S., Wichmann, H-E, Joeckel, K-H, Heinrich, J., Tiesler, C. M. T., Faraone, S. V., Walitza, S., Sinzig, J., Freitag, C., Meyer, J., Herpertz-Dahlmann, B., Lehmkuhl, G., Renner, T. J., Warnke, A., Romanos, M., Lesch, K-P, Reif, A., Schimmelmann, B. G., Hebebrand, J., Scherag, A., and Hinney, A.
- Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency <= 1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (> 500kb) rare CNVs, we observed a nonsignificant (P = 0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P = 2.8 x 10(-4) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P = 1.2 x 10(-3) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P = 4.3 x 10(-2)). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.
- Published
- 2014
13. Partitioning the heritability of Tourette syndrome and obsessive compulsive disorder reveals differences in genetic architecture
- Author
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Davis, L. K., Yu, D., Keenan, C. L., Gamazon, E. R., Konkashbaev, A. I., Derks, E. M., Neale, B. M., Yang, J., Lee, S. H., Evans, P., Barr, C. L., Bellodi, L., Benarroch, F., Berrio, G. B., Bienvenu, O. J., Bloch, M. H., Blom, R. M., Bruun, R. D., Budman, C. L., Camarena, B., Campbell, D., Cappi, C., Cardona Silgado, J. C., Cath, D. C., Cavallini, M. C., Chavira, D. A., Chouinard, S., Conti, D. V., Cook, E. H., Coric, V., Cullen, B. A., Deforce, D., Delorme, R., Dion, Y., Edlund, C. K., Egberts, K., Falkai, P., Fernandez, T. V., Gallagher, P. J., Garrido, H., Geller, D., Girard, Simon, Grabe, H. J., Grados, M. A., Greenberg, B. D., Gross-Tsur, V., Haddad, S., Heiman, G. A., Hemmings, S. M.J., Hounie, A. G., Illmann, C., Jankovic, J., Jenike, M. A., Kennedy, J. L., King, R. A., Kremeyer, B., Kurlan, R., Lanzagorta, N., Leboyer, M., Leckman, J. F., Lennertz, L., Liu, C., Lochner, C., Lowe, T. L., Macciardi, F., McCracken, J. T., McGrath, L. M., Mesa Restrepo, S. C., Moessner, R., Morgan, J., Muller, H., Murphy, D. L., Naarden, A. L., Ochoa, W. C., Ophoff, R. A., Osiecki, L., Pakstis, A. J., Pato, M. T., Pato, C. N., Piacentini, J., Pittenger, C., Pollak, Y., Rauch, S. L., Renner, T. J., Reus, V. I., Richter, M. A., Riddle, M. A., Robertson, M. M., Romero, R., Rosario, M. C., Rosenberg, D., Rouleau, G. A., Ruhrmann, S., Ruiz-Linares, A., Sampaio, A. S., Samuels, J., Sandor, P., Sheppard, B., Singer, H. S., Smit, J. H., Stein, D. J., Strengman, E., Tischfield, J. A., Valencia Duarte, A. V., Vallada, H., Van Nieuwerburgh, F., Veenstra-Vanderweele, J., Walitza, S., Wang, Y., Wendland, J. R., Westenberg, H. G.M., Shugart, Y. Y., Miguel, E. C., McMahon, W., Wagner, M., Nicolini, H., Posthuma, D., Hanna, G. L., Heutink, P., Denys, D., Arnold, P. D., Oostra, B. A., Nestadt, G., Freimer, N. B., Pauls, D. L., Wray, N. R., Stewart, S. E., Mathews, C. A., Knowles, J. A., Cox, N. J., Scharf, J. M., Davis, L. K., Yu, D., Keenan, C. L., Gamazon, E. R., Konkashbaev, A. I., Derks, E. M., Neale, B. M., Yang, J., Lee, S. H., Evans, P., Barr, C. L., Bellodi, L., Benarroch, F., Berrio, G. B., Bienvenu, O. J., Bloch, M. H., Blom, R. M., Bruun, R. D., Budman, C. L., Camarena, B., Campbell, D., Cappi, C., Cardona Silgado, J. C., Cath, D. C., Cavallini, M. C., Chavira, D. A., Chouinard, S., Conti, D. V., Cook, E. H., Coric, V., Cullen, B. A., Deforce, D., Delorme, R., Dion, Y., Edlund, C. K., Egberts, K., Falkai, P., Fernandez, T. V., Gallagher, P. J., Garrido, H., Geller, D., Girard, Simon, Grabe, H. J., Grados, M. A., Greenberg, B. D., Gross-Tsur, V., Haddad, S., Heiman, G. A., Hemmings, S. M.J., Hounie, A. G., Illmann, C., Jankovic, J., Jenike, M. A., Kennedy, J. L., King, R. A., Kremeyer, B., Kurlan, R., Lanzagorta, N., Leboyer, M., Leckman, J. F., Lennertz, L., Liu, C., Lochner, C., Lowe, T. L., Macciardi, F., McCracken, J. T., McGrath, L. M., Mesa Restrepo, S. C., Moessner, R., Morgan, J., Muller, H., Murphy, D. L., Naarden, A. L., Ochoa, W. C., Ophoff, R. A., Osiecki, L., Pakstis, A. J., Pato, M. T., Pato, C. N., Piacentini, J., Pittenger, C., Pollak, Y., Rauch, S. L., Renner, T. J., Reus, V. I., Richter, M. A., Riddle, M. A., Robertson, M. M., Romero, R., Rosario, M. C., Rosenberg, D., Rouleau, G. A., Ruhrmann, S., Ruiz-Linares, A., Sampaio, A. S., Samuels, J., Sandor, P., Sheppard, B., Singer, H. S., Smit, J. H., Stein, D. J., Strengman, E., Tischfield, J. A., Valencia Duarte, A. V., Vallada, H., Van Nieuwerburgh, F., Veenstra-Vanderweele, J., Walitza, S., Wang, Y., Wendland, J. R., Westenberg, H. G.M., Shugart, Y. Y., Miguel, E. C., McMahon, W., Wagner, M., Nicolini, H., Posthuma, D., Hanna, G. L., Heutink, P., Denys, D., Arnold, P. D., Oostra, B. A., Nestadt, G., Freimer, N. B., Pauls, D. L., Wray, N. R., Stewart, S. E., Mathews, C. A., Knowles, J. A., Cox, N. J., and Scharf, J. M.
- Abstract
The direct estimation of heritability from genome-wide common variant data as implemented in the program Genome-wide Complex Trait Analysis (GCTA) has provided a means to quantify heritability attributable to all interrogated variants. We have quantified the variance in liability to disease explained by all SNPs for two phenotypically-related neurobehavioral disorders, obsessive-compulsive disorder (OCD) and Tourette Syndrome (TS), using GCTA. Our analysis yielded a heritability point estimate of 0.58 (se = 0.09, p = 5.64e-12) for TS, and 0.37 (se = 0.07, p = 1.5e-07) for OCD. In addition, we conducted multiple genomic partitioning analyses to identify genomic elements that concentrate this heritability. We examined genomic architectures of TS and OCD by chromosome, MAF bin, and functional annotations. In addition, we assessed heritability for early onset and adult onset OCD. Among other notable results, we found that SNPs with a minor allele frequency of less than 5% accounted for 21% of the TS heritability and 0% of the OCD heritability. Additionally, we identified a significant contribution to TS and OCD heritability by variants significantly associated with gene expression in two regions of the brain (parietal cortex and cerebellum) for which we had available expression quantitative trait loci (eQTLs). Finally we analyzed the genetic correlation between TS and OCD, revealing a genetic correlation of 0.41 (se = 0.15, p = 0.002). These results are very close to previous heritability estimates for TS and OCD based on twin and family studies, suggesting that very little, if any, heritability is truly missing (i.e., unassayed) from TS and OCD GWAS studies of common variation. The results also indicate that there is some genetic overlap between these two phenotypically-related neuropsychiatric disorders, but suggest that the two disorders have distinct genetic architectures.
- Published
- 2013
14. Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
- Author
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Jarick, I, primary, Volckmar, A-L, additional, Pütter, C, additional, Pechlivanis, S, additional, Nguyen, T T, additional, Dauvermann, M R, additional, Beck, S, additional, Albayrak, Ö, additional, Scherag, S, additional, Gilsbach, S, additional, Cichon, S, additional, Hoffmann, P, additional, Degenhardt, F, additional, Nöthen, M M, additional, Schreiber, S, additional, Wichmann, H-E, additional, Jöckel, K-H, additional, Heinrich, J, additional, Tiesler, C M T, additional, Faraone, S V, additional, Walitza, S, additional, Sinzig, J, additional, Freitag, C, additional, Meyer, J, additional, Herpertz-Dahlmann, B, additional, Lehmkuhl, G, additional, Renner, T J, additional, Warnke, A, additional, Romanos, M, additional, Lesch, K-P, additional, Reif, A, additional, Schimmelmann, B G, additional, Hebebrand, J, additional, Scherag, A, additional, and Hinney, A, additional
- Published
- 2012
- Full Text
- View/download PDF
15. Addendum: Genome-wide association study in German patients with attention deficit/hyperactivity disorder
- Author
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Hinney, Anke, Scherag, Andre, Jarick, I., Albayrak, Özgür, Putter, C., Pechlivanis, Sonali, Dauvermann, M. R., Beck, S., Weber, H., Scherag, S., Nguyen, T. T., Volckmar, A. L., Knoll, N., Faraone, S. V., Neale, B. M., Franke, B., Cichon, S., Hoffmann, P., Nothen, M. M., Schreiber, S., Jöckel, Karl-Heinz, Wichmann, H. E., Freitag, C., Lempp, T., Meyer, J., Gilsbach, S., Herpertz-Dahlmann, B., Sinzig, J., Lehmkuhl, G., Renner, T. J., Warnke, A., Romanos, M., Lesch, K. P., Reif, A., von Schimmelmann, Benno, Hebebrand, Johannes, and Psychiat GWAS Consortium, xxx
- Subjects
Cellular and Molecular Neuroscience ,Psychiatry and Mental health ,Medizin ,Genetics (clinical) - Published
- 2012
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- View/download PDF
16. Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree
- Author
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Lesch, K-P, primary, Selch, S, additional, Renner, T J, additional, Jacob, C, additional, Nguyen, T T, additional, Hahn, T, additional, Romanos, M, additional, Walitza, S, additional, Shoichet, S, additional, Dempfle, A, additional, Heine, M, additional, Boreatti-Hümmer, A, additional, Romanos, J, additional, Gross-Lesch, S, additional, Zerlaut, H, additional, Wultsch, T, additional, Heinzel, S, additional, Fassnacht, M, additional, Fallgatter, A, additional, Allolio, B, additional, Schäfer, H, additional, Warnke, A, additional, Reif, A, additional, Ropers, H-H, additional, and Ullmann, R, additional
- Published
- 2010
- Full Text
- View/download PDF
17. Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder
- Author
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Volckmar, A-L, Dauvermann, M R, Schimmelmann, B G, Schreiber, S, Walitza, S, Tiesler, C M T, Cichon, S, Scherag, A, Freitag, C, Jarick, I, Herpertz-Dahlmann, B, Reif, A, Heinrich, J, Beck, S, Hinney, A, Albayrak, O, Degenhardt, F, Lesch, K-P, Sinzig, J, Wichmann, H-E, Nguyen, T T, Lehmkuhl, G, Pechlivanis, S, Gilsbach, S, Scherag, S, Warnke, A, Meyer, J, Hebebrand, J, Pütter, C, Nöthen, M M, Renner, T J, Faraone, S V, Romanos, M, Hoffmann, P, and Jöckel, K-H
- Subjects
mental disorders ,3. Good health - Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency 1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10(-4) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10(-3) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10(-2)). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.Molecular Psychiatry advance online publication, 20 November 2012; doi:10.1038/mp.2012.161.
18. Genetic variants of KCNJ6 influence activation of the anterior cingulate cortex in ADHD but not in healthy probands.
- Author
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Renner, T. J., Ehlis, A. C., Röser, C., Jacob, C., Gerlach, M., Warnke, A., Lesch, K. P., and Fallgatter, A. J.
- Abstract
Introduction and objective: In imploring mutual genetics of substance use disorders and ADHD, KCNJ6, encoding the potassium channel subunit 2, associated with nicotine abuse [1], is an interesting candidate. We investigated the influence of two promoter polymorphisms on Anterior Cingulate Cortex (ACC) activation in an adult German ADHD sample. Methods: EEGs of 218 German adults affected by ADHD and 118 healthy probands were recorded during a cued Continuous Performance Test. Centroid locations and NoGo-Anteriorization (NGA), as well as genotypes of rs6517442 and rs7275707 were determined. Statistical analysis comprised ANOVAs and post hoc t tests. Results: Influence of rs6517442 and rs7275707 on both, Go and Nogo centroids was found specifically in the ADHD-group. Discussion: Influence of both investigated KCNJ6 promoter SNPs on Go and Nogo centroids was found in adult ADHD patients, but not in healthy probands. This result implies interplay of KCNJ6 and ADHDrelevant factors, altering brain activation in ADHD. Conclusion: The results implicate a role of KCNJ6, involved in pathophysiologically relevant neurosystems [2], in ADHD. Our findings may support efforts of identifying ADHD endophenotypes modulated by KCNJ6 with respect to ACC activation [3]. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
19. Allelic variants of SNAP25 in a family-based sample of ADHD
- Author
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Manfred Gerlach, Helmut Schäfer, K.P. Lesch, Astrid Dempfle, L. Eckert, Marcel Romanos, Tobias J. Renner, Christian Jacob, Susanne Walitza, Andreas Warnke, University of Zurich, and Renner, T J
- Subjects
Male ,Candidate gene ,Synaptic cleft ,Adolescent ,Genotype ,Synaptosomal-Associated Protein 25 ,610 Medicine & health ,Biology ,Neurotransmission ,Polymorphism, Single Nucleotide ,2738 Psychiatry and Mental Health ,Gene Frequency ,Germany ,SNP ,Humans ,Genetic Predisposition to Disease ,Allele ,Child ,Gene ,Biological Psychiatry ,Genetics ,Family Health ,Intron ,SNAP25 ,10058 Department of Child and Adolescent Psychiatry ,Introns ,Psychiatry and Mental health ,2728 Neurology (clinical) ,Neurology ,Attention Deficit Disorder with Hyperactivity ,2808 Neurology ,Female ,Neurology (clinical) ,2803 Biological Psychiatry - Abstract
Altered neurotransmission has been suggested to be a crucial factor in the pathophysiology of attention-deficit/hyperactivity disorder ADHD. Subsequently genes encoding for synaptic proteins have been investigated in candidate gene studies. These proteins mediate the release of neurotransmitters into the synaptic cleft in the process of signal transduction by forming a transient complex, enabling the junction of vesicle and synaptic membrane. One of the core proteins of this complex is the synaptosomal-associated protein 25 (SNAP25). It is one of the most validated candidate genes in ADHD according to meta-analyses. However, differing results were observed in previous studies, some of which were not able to observe association with ADHD. In this study we aimed to investigate association of genetic variants of SNAP25 located in the putative promoter region of SNAP25 and a SNP in intron 8, previously reported to associated with ADHD. A family based design was applied to detect preferential transmission of genetic variants. In our German ADHD sample no preferential transmission of either variant could be observed. Further investigation considering sub-sample analysis regarding response to D-amphetamine could enlight the role of SNAP25 in ADHD.
- Published
- 2007
20. Exploring the genetic link between RLS and ADHD.
- Author
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Schimmelmann BG, Friedel S, Nguyen TT, Sauer S, Ganz Vogel CI, Konrad K, Wilhelm C, Sinzig J, Renner TJ, Romanos M, Palmason H, Dempfle A, Walitza S, Freitag C, Meyer J, Linder M, Schäfer H, Warnke A, Lesch KP, Herpertz-Dahlman B, Hinney A, and Hebebrand J
- Subjects
- Adolescent, Child, Family Health, Female, Genome-Wide Association Study, Genotype, Homeodomain Proteins genetics, Humans, MAP Kinase Kinase 5 genetics, Male, Myeloid Ecotropic Viral Integration Site 1 Protein, Neoplasm Proteins genetics, Nerve Tissue Proteins, Transcription Factors genetics, Attention Deficit Disorder with Hyperactivity complications, Attention Deficit Disorder with Hyperactivity genetics, Polymorphism, Single Nucleotide genetics, Restless Legs Syndrome complications, Restless Legs Syndrome genetics
- Abstract
Attention deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder of childhood onset. Clinical and biological evidence points to shared common central nervous system (CNS) pathology of ADHD and restless legs syndrome (RLS). It was hypothesized that variants previously found to be associated with RLS in two large genome-wide association studies (GWA), will also be associated with ADHD. SNPs located in MEIS1 (rs2300478), BTBD9 (rs9296249, rs3923809, rs6923737), and MAP2K5 (rs12593813, rs4489954) as well as three SNPs tagging the identified haplotype in MEIS1 (rs6710341, rs12469063, rs4544423) were genotyped in a well characterized German sample of 224 families comprising one or more affected sibs (386 children) and both parents. We found no evidence for preferential transmission of the hypothesized variants to ADHD. Subsequent analyses elicited nominal significant association with haplotypes consisting of the three SNPs in BTBD9 (chi2 = 14.8, df = 7, nominal p = 0.039). According to exploratory post hoc analyses, the major contribution to this finding came from the A-A-A-haplotype with a haplotype-wise nominal p-value of 0.009. However, this result did not withstand correction for multiple testing. In view of our results, RLS risk alleles may have a lower effect on ADHD than on RLS or may not be involved in ADHD. The negative findings may additionally result from genetic heterogeneity of ADHD, i.e. risk alleles for RLS may only be relevant for certain subtypes of ADHD. Genes relevant to RLS remain interesting candidates for ADHD; particularly BTBD9 needs further study, as it has been related to iron storage, a potential pathophysiological link between RLS and certain subtypes of ADHD.
- Published
- 2009
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- View/download PDF
21. [Neurobiology of attention-deficit hyperactivity disorder].
- Author
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Renner TJ, Gerlach M, Romanos M, Herrmann M, Reif A, Fallgatter AJ, and Lesch KP
- Subjects
- Attention Deficit Disorder with Hyperactivity diagnosis, Attention Deficit Disorder with Hyperactivity genetics, Attention Deficit Disorder with Hyperactivity psychology, Comorbidity, Genetic Predisposition to Disease genetics, Humans, Neurotransmitter Agents genetics, Phenotype, Risk Factors, Attention Deficit Disorder with Hyperactivity physiopathology, Brain physiopathology, Neurotransmitter Agents physiology
- Abstract
Attention-deficit hyperactivity disorder (ADHD) is defined as a clinically heterogeneous neurodevelopmental syndrome with the contribution of numerous genetic and environmental risk factors. The goal of interdisciplinary and translational neurobiological research is to clarify the interdependent relationship between molecular mechanisms and structural-functional substrates in the pathogenesis of ADHD and its significance to the disorder's long-term course. Work on ADHD-specific molecular genetic and developmental biological essentials of brain function and on the structural-functional basis of behavior holds the promise of developing predictors and differential strategies for effective therapy of severe and chronic courses of ADHD. To define evolutionary conserved ADHD-relevant principles of structure and function of the brain and behavior typical to the syndrome, an integrated approach in the elucidation of specific neuro- and psychobiological mechanisms and thus systemic pathophysiology of ADHD is crucial. Regarding compromised neurodevelopment, pathophysiological models of ADHD, particularly its syndromal and comorbid dimensions, therefore require the combination of molecular genetic, neuroimaging, neuropsychology, behavioral, and psychosocial strategies to explain complete causal chains.
- Published
- 2008
- Full Text
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