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Start Over Author "Byrne, E. M." Publisher nature publishing group
4 results on '"Byrne, E. M."'

1. Collaborative meta-analysis finds no evidence of a strong interaction between stress and 5-HTTLPR genotype contributing to the development of depression

Author

Culverhouse, R. C., Saccone, N. L., Horton, A. C., Ma, Y., Anstey, K. J., Banaschewski, T., Burmeister, M., Cohen-Woods, S., Etain, B., Fisher, H. L., Goldman, N., Guillaume, S., Horwood, J., Juhasz, G., Lester, K. J., Mandelli, L., Middeldorp, C. M., Olie, E., Villafuerte, S., Air, T. M., Araya, R., Bowes, L., Burns, R., Byrne, E. M., Coffey, C., Coventry, W. L., Gawronski, K. A. B., Glei, D., Hatzimanolis, A., Hottenga, J-J, Jaussent, I., Jawahar, C., Jennen-Steinmetz, C., Kramer, J. R., Lajnef, M., Little, K., zu Schwabedissen, H. M., Nauck, M., Nederhof, E., Petschner, P., Peyrot, W. J., Schwahn, C., Sinnamon, G., Stacey, D., Tian, Y., Toben, C., Van der Auwera, S., Wainwright, N., Wang, J-C, Willemsen, G., Anderson, I. M., Arolt, V., Aslund, C., Bagdy, G., Baune, B. T., Bellivier, F., Boomsma, D. I., Courtet, P., Dannlowski, U., de Geus, E. J. C., Deakin, J. F. W., Easteal, S., Eley, T., Fergusson, D. M., Goate, A. M., Gonda, X., Grabe, H. J., Holzman, C., Johnson, E. O., Kennedy, M., Laucht, M., Martin, N. G., Munafo, M. R., Nilsson, Kent W., Oldehinkel, A. J., Olsson, C. A., Ormel, J., Otte, C., Patton, G. C., Penninx, B. W. J. H., Ritchie, K., Sarchiapone, M., Scheid, J. M., Serretti, A., Smit, J. H., Stefanis, N. C., Surtees, P. G., Voelzke, H., Weinstein, M., Whooley, M., Nurnberger, J. I., Jr., Breslau, N., Bierut, L. J., Culverhouse, R. C., Saccone, N. L., Horton, A. C., Ma, Y., Anstey, K. J., Banaschewski, T., Burmeister, M., Cohen-Woods, S., Etain, B., Fisher, H. L., Goldman, N., Guillaume, S., Horwood, J., Juhasz, G., Lester, K. J., Mandelli, L., Middeldorp, C. M., Olie, E., Villafuerte, S., Air, T. M., Araya, R., Bowes, L., Burns, R., Byrne, E. M., Coffey, C., Coventry, W. L., Gawronski, K. A. B., Glei, D., Hatzimanolis, A., Hottenga, J-J, Jaussent, I., Jawahar, C., Jennen-Steinmetz, C., Kramer, J. R., Lajnef, M., Little, K., zu Schwabedissen, H. M., Nauck, M., Nederhof, E., Petschner, P., Peyrot, W. J., Schwahn, C., Sinnamon, G., Stacey, D., Tian, Y., Toben, C., Van der Auwera, S., Wainwright, N., Wang, J-C, Willemsen, G., Anderson, I. M., Arolt, V., Aslund, C., Bagdy, G., Baune, B. T., Bellivier, F., Boomsma, D. I., Courtet, P., Dannlowski, U., de Geus, E. J. C., Deakin, J. F. W., Easteal, S., Eley, T., Fergusson, D. M., Goate, A. M., Gonda, X., Grabe, H. J., Holzman, C., Johnson, E. O., Kennedy, M., Laucht, M., Martin, N. G., Munafo, M. R., Nilsson, Kent W., Oldehinkel, A. J., Olsson, C. A., Ormel, J., Otte, C., Patton, G. C., Penninx, B. W. J. H., Ritchie, K., Sarchiapone, M., Scheid, J. M., Serretti, A., Smit, J. H., Stefanis, N. C., Surtees, P. G., Voelzke, H., Weinstein, M., Whooley, M., Nurnberger, J. I., Jr., Breslau, N., and Bierut, L. J.

Abstract

The hypothesis that the S allele of the 5-HTTLPR serotonin transporter promoter region is associated with increased risk of depression, but only in individuals exposed to stressful situations, has generated much interest, research and controversy since first proposed in 2003. Multiple meta-analyses combining results from heterogeneous analyses have not settled the issue. To determine the magnitude of the interaction and the conditions under which it might be observed, we performed new analyses on 31 data sets containing 38 802 European ancestry subjects genotyped for 5-HTTLPR and assessed for depression and childhood maltreatment or other stressful life events, and meta-analysed the results. Analyses targeted two stressors (narrow, broad) and two depression outcomes (current, lifetime). All groups that published on this topic prior to the initiation of our study and met the assessment and sample size criteria were invited to participate. Additional groups, identified by consortium members or self-identified in response to our protocol (published prior to the start of analysis) with qualifying unpublished data, were also invited to participate. A uniform data analysis script implementing the protocol was executed by each of the consortium members. Our findings do not support the interaction hypothesis. We found no subgroups or variable definitions for which an interaction between stress and 5-HTTLPR genotype was statistically significant. In contrast, our findings for the main effects of life stressors (strong risk factor) and 5-HTTLPR genotype (no impact on risk) are strikingly consistent across our contributing studies, the original study reporting the interaction and subsequent meta-analyses. Our conclusion is that if an interaction exists in which the S allele of 5-HTTLPR increases risk of depression only in stressed individuals, then it is not broadly generalisable, but must be of modest effect size and only observable in limited situations.

Published
2018
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2. Genome-wide association study of borderline personality disorder reveals genetic overlap with bipolar disorder, major depression and schizophrenia

Author

Witt, S. H., Streit, F., Jungkunz, M., Frank, J., Awasthi, S., Reinbold, C. S., Treutlein, J., Degenhardt, F., Forstner, A. J., Heilmann-Heimbach, S., Dietl, L., Schwarze, C. E., Schendel, D., Strohmaier, J., Abdellaoui, A., Adolfsson, R., Air, T. M., Akil, H., Alda, M., Alliey-Rodriguez, N., Andreassen, O. A., Babadjanova, G., Bass, N. J., Bauer, M., Baune, B. T., Bellivier, F., Bergen, S., Bethell, A., Biernacka, J. M., Blackwood, D. H. R., Boks, M. P., Boomsma, D. I., Borglum, A. D., Borrmann-Hassenbach, M., Brennan, P., Budde, M., Buttenschon, H. N., Byrne, E. M., Cervantes, P., Clarke, T-K, Craddock, N., Cruceanu, C., Curtis, D., Czerski, P. M., Dannlowski, U., Davis, T., de Geus, E. J. C., Di Florio, A., Djurovic, S., Domenici, E., Edenberg, H. J., Etain, B., Fischer, S. B., Forty, L., Fraser, C., Frye, M. A., Fullerton, J. M., Gade, K., Gershon, E. S., Giegling, I., Gordon, S. D., Gordon-Smith, K., Grabe, H. J., Green, E. K., Greenwood, T. A., Grigoroiu-Serbanescu, M., Guzman-Parra, J., Hall, L. S., Hamshere, M., Hauser, J., Hautzinger, M., Heilbronner, U., Herms, S., Hitturlingappa, S., Hoffmann, P., Holmans, P., Hottenga, J-J, Jamain, S., Jones, I., Jones, L. A., Jureus, A., Kahn, R. S., Kammerer-Ciernioch, J., Kirov, G., Kittel-Schneider, S., Kloiber, S., Knott, S. V., Kogevinas, M., Landen, M., Leber, M., Leboyer, M., Li, Q. S., Lissowska, J., Lucae, S., Martin, N. G., Mayoral-Cleries, F., McElroy, S. L., McIntosh, A. M., McKay, J. D., McQuillin, A., Medland, S. E., Middeldorp, C. M., Milaneschi, Y., Mitchell, P. B., Montgomery, G. W., Morken, G., Mors, O., Muehleisen, T. W., Mueller-Myhsok, B., Myers, R. M., Nievergelt, C. M., Nurnberger, J. I., O'Donovan, M. C., Loohuis, L. M. O., Ophoff, R., Oruc, L., Owen, M. J., Paciga, S. A., Penninx, B. W. J. H., Perry, A., Pfennig, A., Potash, J. B., Preisig, M., Reif, A., Rivas, F., Rouleau, G. A., Schofield, P. R., Schulze, T. G., Schwarz, M., Scott, L., Sinnamon, G. C. B., Stahl, E. A., Strauss, J., Turecki, G., Van der Auwera, S., Vedder, H., Vincent, J. B., Willemsen, G., Witt, C. C., Wray, N. R., Xi, H. S., Tadic, A., Dahmen, N., Schott, B. H., Cichon, S., Noethen, M. M., Ripke, S., Mobascher, A., Rujescu, D., Lieb, K., Roepke, S., Schmahl, C., Bohus, M., Rietschel, M., Witt, S. H., Streit, F., Jungkunz, M., Frank, J., Awasthi, S., Reinbold, C. S., Treutlein, J., Degenhardt, F., Forstner, A. J., Heilmann-Heimbach, S., Dietl, L., Schwarze, C. E., Schendel, D., Strohmaier, J., Abdellaoui, A., Adolfsson, R., Air, T. M., Akil, H., Alda, M., Alliey-Rodriguez, N., Andreassen, O. A., Babadjanova, G., Bass, N. J., Bauer, M., Baune, B. T., Bellivier, F., Bergen, S., Bethell, A., Biernacka, J. M., Blackwood, D. H. R., Boks, M. P., Boomsma, D. I., Borglum, A. D., Borrmann-Hassenbach, M., Brennan, P., Budde, M., Buttenschon, H. N., Byrne, E. M., Cervantes, P., Clarke, T-K, Craddock, N., Cruceanu, C., Curtis, D., Czerski, P. M., Dannlowski, U., Davis, T., de Geus, E. J. C., Di Florio, A., Djurovic, S., Domenici, E., Edenberg, H. J., Etain, B., Fischer, S. B., Forty, L., Fraser, C., Frye, M. A., Fullerton, J. M., Gade, K., Gershon, E. S., Giegling, I., Gordon, S. D., Gordon-Smith, K., Grabe, H. J., Green, E. K., Greenwood, T. A., Grigoroiu-Serbanescu, M., Guzman-Parra, J., Hall, L. S., Hamshere, M., Hauser, J., Hautzinger, M., Heilbronner, U., Herms, S., Hitturlingappa, S., Hoffmann, P., Holmans, P., Hottenga, J-J, Jamain, S., Jones, I., Jones, L. A., Jureus, A., Kahn, R. S., Kammerer-Ciernioch, J., Kirov, G., Kittel-Schneider, S., Kloiber, S., Knott, S. V., Kogevinas, M., Landen, M., Leber, M., Leboyer, M., Li, Q. S., Lissowska, J., Lucae, S., Martin, N. G., Mayoral-Cleries, F., McElroy, S. L., McIntosh, A. M., McKay, J. D., McQuillin, A., Medland, S. E., Middeldorp, C. M., Milaneschi, Y., Mitchell, P. B., Montgomery, G. W., Morken, G., Mors, O., Muehleisen, T. W., Mueller-Myhsok, B., Myers, R. M., Nievergelt, C. M., Nurnberger, J. I., O'Donovan, M. C., Loohuis, L. M. O., Ophoff, R., Oruc, L., Owen, M. J., Paciga, S. A., Penninx, B. W. J. H., Perry, A., Pfennig, A., Potash, J. B., Preisig, M., Reif, A., Rivas, F., Rouleau, G. A., Schofield, P. R., Schulze, T. G., Schwarz, M., Scott, L., Sinnamon, G. C. B., Stahl, E. A., Strauss, J., Turecki, G., Van der Auwera, S., Vedder, H., Vincent, J. B., Willemsen, G., Witt, C. C., Wray, N. R., Xi, H. S., Tadic, A., Dahmen, N., Schott, B. H., Cichon, S., Noethen, M. M., Ripke, S., Mobascher, A., Rujescu, D., Lieb, K., Roepke, S., Schmahl, C., Bohus, M., and Rietschel, M.

Abstract

Borderline personality disorder (BOR) is determined by environmental and genetic factors, and characterized by affective instability and impulsivity, diagnostic symptoms also observed in manic phases of bipolar disorder (BIP). Up to 20% of BIP patients show comorbidity with BOR. This report describes the first case-control genome-wide association study (GWAS) of BOR, performed in one of the largest BOR patient samples worldwide. The focus of our analysis was (i) to detect genes and gene sets involved in BOR and (ii) to investigate the genetic overlap with BIP. As there is considerable genetic overlap between BIP, major depression (MDD) and schizophrenia (SCZ) and a high comorbidity of BOR and MDD, we also analyzed the genetic overlap of BOR with SCZ and MDD. GWAS, gene-based tests and gene-set analyses were performed in 998 BOR patients and 1545 controls. Linkage disequilibrium score regression was used to detect the genetic overlap between BOR and these disorders. Single marker analysis revealed no significant association after correction for multiple testing. Gene-based analysis yielded two significant genes: DPYD (P = 4.42 x 10(-7)) and PKP4 (P = 8.67 x 10(-7)); and gene-set analysis yielded a significant finding for exocytosis (GO: 0006887, PFDR = 0.019; FDR, false discovery rate). Prior studies have implicated DPYD, PKP4 and exocytosis in BIP and SCZ. The most notable finding of the present study was the genetic overlap of BOR with BIP (r(g) = 0.28 [P = 2.99 x 10(-3)]), SCZ (r(g) = 0.34 [P = 4.37 x 10(-5)]) and MDD (r(g) = 0.57 [P = 1.04 x 10(-3)]). We believe our study is the first to demonstrate that BOR overlaps with BIP, MDD and SCZ on the genetic level. Whether this is confined to transdiagnostic clinical symptoms should be examined in future studies.

Published
2017

3. Genetic effects influencing risk for major depressive disorder in China and Europe

Author

Bigdeli, T B, Ripke, S, Peterson, R E, Trzaskowski, M, Bacanu, S-A, Abdellaoui, A, Andlauer, T F M, Beekman, A T F, Berger, K, Blackwood, D H R, Boomsma, D I, Breen, G, Buttenschøn, H N, Byrne, E M, Cichon, S, Clarke, T-K, Couvy-Duchesne, B, Craddock, N, de Geus, E J C, Degenhardt, F, Dunn, E C, Edwards, A C, Fanous, A H, Forstner, A J, Frank, J, Gill, M, Gordon, S D, Grabe, H J, Hamilton, S P, Hardiman, O, Hayward, C, Heath, A C, Henders, A K, Herms, S, Hickie, I B, Hoffmann, P, Homuth, G, Hottenga, J-J, Ising, M, Jansen, R, Kloiber, S, Knowles, J A, Lang, M, Li, Q S, Lucae, S, MacIntyre, D J, Madden, P A F, Martin, N G, McGrath, P J, McGuffin, P, McIntosh, A M, Medland, S E, Mehta, D, Middeldorp, C M, Milaneschi, Y, Montgomery, G W, Mors, O, Müller-Myhsok, B, Nauck, M, Nyholt, D R, Nöthen, M M, Owen, M J, Penninx, B W J H, Pergadia, M L, Perlis, R H, Peyrot, W J, Porteous, D J, Potash, J B, Rice, J P, Rietschel, M, Riley, B P, Rivera, M, Schoevers, R, Schulze, T G, Shi, J, Shyn, S I, Smit, J H, Smoller, J W, Streit, F, Strohmaier, J, Teumer, A, Treutlein, J, Van der Auwera, S, van Grootheest, G, van Hemert, A M, Völzke, H, Webb, B T, Weissman, M M, Wellmann, J, Willemsen, G, Witt, S H, Levinson, D F, Lewis, C M, Wray, N R, Flint, J, Sullivan, P F, and Kendler, K S

Abstract

Major depressive disorder (MDD) is a common, complex psychiatric disorder and a leading cause of disability worldwide. Despite twin studies indicating its modest heritability (~30–40%), extensive heterogeneity and a complex genetic architecture have complicated efforts to detect associated genetic risk variants. We combined single-nucleotide polymorphism (SNP) summary statistics from the CONVERGE and PGC studies of MDD, representing 10 502 Chinese (5282 cases and 5220 controls) and 18 663 European (9447 cases and 9215 controls) subjects. We determined the fraction of SNPs displaying consistent directions of effect, assessed the significance of polygenic risk scores and estimated the genetic correlation of MDD across ancestries. Subsequent trans-ancestry meta-analyses combined SNP-level evidence of association. Sign tests and polygenic score profiling weakly support an overlap of SNP effects between East Asian and European populations. We estimated the trans-ancestry genetic correlation of lifetime MDD as 0.33; female-only and recurrent MDD yielded estimates of 0.40 and 0.41, respectively. Common variants downstream of GPHN achieved genome-wide significance by Bayesian trans-ancestry meta-analysis (rs9323497; log10 Bayes Factor=8.08) but failed to replicate in an independent European sample (P=0.911). Gene-set enrichment analyses indicate enrichment of genes involved in neuronal development and axonal trafficking. We successfully demonstrate a partially shared polygenic basis of MDD in East Asian and European populations. Taken together, these findings support a complex etiology for MDD and possible population differences in predisposing genetic factors, with important implications for future genetic studies.

Published
2017
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4. Genome-Wide Association Study of Major Depressive Disorder: New Results, Meta-Analysis, and Lessons Learned

Author

Wray, N R, Pergadia, M L, Blackwood, D H R, Penninx, B W J H, Nyholt, D R, MacIntyre, D J, McGhee, K A, Maclean, A W, Smit, J H, Hottenga, J J, Willemsen, G, Middeldorp, C M, de Geus, E J C, McGuffin, P, Hickie, I B, van den Oord, E J C G, Macgregor, S, McEvoy, B P, Medland, S E, Statham, D J, Henders, A K, Montgomery, G W, Boomsma, D I, Madden, P A F, Gordon, S. D., Lewis, C. M., Liu, J. Z., Byrne, E. M., Heath, A. C., Martin, N. G., Sullivan, P. F., and Ripke, Stephan

Subjects
major depressive disorder, depression, genome-wide association study, CACNA1C, ADCY3, GAL
Abstract

Major depressive disorder (MDD) is a common complex disorder with a partly genetic etiology. We conducted a genome-wide association study of the MDD2000+ sample (2431 cases, 3673 screened controls and >1 M imputed single-nucleotide polymorphisms (SNPs)). No SNPs achieved genome-wide significance either in the MDD2000+ study, or in meta-analysis with two other studies totaling 5763 cases and 6901 controls. These results imply that common variants of intermediate or large effect do not have main effects in the genetic architecture of MDD. Suggestive but notable results were (a) gene-based tests suggesting roles for adenylate cyclase 3 (ADCY3, 2p23.3) and galanin (GAL, 11q13.3); published functional evidence relates both of these to MDD and serotonergic signaling; (b) support for the bipolar disorder risk variant SNP rs1006737 in CACNA1C (P=0.020, odds ratio=1.10); and (c) lack of support for rs2251219, a SNP identified in a meta-analysis of affective disorder studies (P=0.51). We estimate that sample sizes 1.8- to 2.4-fold greater are needed for association studies of MDD compared with those for schizophrenia to detect variants that explain the same proportion of total variance in liability. Larger study cohorts characterized for genetic and environmental risk factors accumulated prospectively are likely to be needed to dissect more fully the etiology of MDD.

Published
2012
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