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1. Genome-wide association study identifies 30 loci associated with bipolar disorder

Author

Stahl, EA, Breen, G, Forstner, AJ, McQuillin, A, Ripke, S, Trubetskoy, V, Mattheisen, M, Wang, Y, Coleman, JRI, Gaspar, HA, de Leeuw, CA, Steinberg, S, Pavlides, JMW, Trzaskowski, M, Byrne, EM, Pers, TH, Holmans, PA, Richards, AL, Abbott, L, Agerbo, E, Akil, H, Albani, D, Alliey-Rodriguez, N, Als, TD, Anjorin, A, Antilla, V, Awasthi, S, Badner, JA, Bækvad-Hansen, M, Barchas, JD, Bass, N, Bauer, M, Belliveau, R, Bergen, SE, Pedersen, CB, Bøen, E, Boks, MP, Boocock, J, Budde, M, Bunney, W, Burmeister, M, Bybjerg-Grauholm, J, Byerley, W, Casas, M, Cerrato, F, Cervantes, P, Chambert, K, Charney, AW, Chen, D, Churchhouse, C, Clarke, TK, Coryell, W, Craig, DW, Cruceanu, C, Curtis, D, Czerski, PM, Dale, AM, de Jong, S, Degenhardt, F, Del-Favero, J, DePaulo, JR, Djurovic, S, Dobbyn, AL, Dumont, A, Elvsåshagen, T, Escott-Price, V, Fan, CC, Fischer, SB, Flickinger, M, Foroud, TM, Forty, L, Frank, J, Fraser, C, Freimer, NB, Frisén, L, Gade, K, Gage, D, Garnham, J, Giambartolomei, C, Pedersen, MG, Goldstein, J, Gordon, SD, Gordon-Smith, K, Green, EK, Green, MJ ; https://orcid.org/0000-0002-9361-4874, Greenwood, TA, Grove, J, Guan, W, Guzman-Parra, J, Hamshere, ML, Hautzinger, M, Heilbronner, U, Herms, S, Hipolito, M, Hoffmann, P, Holland, D, Huckins, L, Jamain, S, Johnson, JS, Juréus, A, Fullerton, Janice ; https://orcid.org/0000-0003-4014-4490, Mitchell, Philip ; https://orcid.org/0000-0002-7954-5235, Shannon Weickert, Cynthia ; https://orcid.org/0000-0002-4560-0259, Stahl, EA, Breen, G, Forstner, AJ, McQuillin, A, Ripke, S, Trubetskoy, V, Mattheisen, M, Wang, Y, Coleman, JRI, Gaspar, HA, de Leeuw, CA, Steinberg, S, Pavlides, JMW, Trzaskowski, M, Byrne, EM, Pers, TH, Holmans, PA, Richards, AL, Abbott, L, Agerbo, E, Akil, H, Albani, D, Alliey-Rodriguez, N, Als, TD, Anjorin, A, Antilla, V, Awasthi, S, Badner, JA, Bækvad-Hansen, M, Barchas, JD, Bass, N, Bauer, M, Belliveau, R, Bergen, SE, Pedersen, CB, Bøen, E, Boks, MP, Boocock, J, Budde, M, Bunney, W, Burmeister, M, Bybjerg-Grauholm, J, Byerley, W, Casas, M, Cerrato, F, Cervantes, P, Chambert, K, Charney, AW, Chen, D, Churchhouse, C, Clarke, TK, Coryell, W, Craig, DW, Cruceanu, C, Curtis, D, Czerski, PM, Dale, AM, de Jong, S, Degenhardt, F, Del-Favero, J, DePaulo, JR, Djurovic, S, Dobbyn, AL, Dumont, A, Elvsåshagen, T, Escott-Price, V, Fan, CC, Fischer, SB, Flickinger, M, Foroud, TM, Forty, L, Frank, J, Fraser, C, Freimer, NB, Frisén, L, Gade, K, Gage, D, Garnham, J, Giambartolomei, C, Pedersen, MG, Goldstein, J, Gordon, SD, Gordon-Smith, K, Green, EK, Green, MJ ; https://orcid.org/0000-0002-9361-4874, Greenwood, TA, Grove, J, Guan, W, Guzman-Parra, J, Hamshere, ML, Hautzinger, M, Heilbronner, U, Herms, S, Hipolito, M, Hoffmann, P, Holland, D, Huckins, L, Jamain, S, Johnson, JS, Juréus, A, Fullerton, Janice ; https://orcid.org/0000-0003-4014-4490, Mitchell, Philip ; https://orcid.org/0000-0002-7954-5235, and Shannon Weickert, Cynthia ; https://orcid.org/0000-0002-4560-0259

Abstract

Bipolar disorder is a highly heritable psychiatric disorder. We performed a genome-wide association study (GWAS) including 20,352 cases and 31,358 controls of European descent, with follow-up analysis of 822 variants with P < 1 × 10 −4 in an additional 9,412 cases and 137,760 controls. Eight of the 19 variants that were genome-wide significant (P < 5 × 10 −8 ) in the discovery GWAS were not genome-wide significant in the combined analysis, consistent with small effect sizes and limited power but also with genetic heterogeneity. In the combined analysis, 30 loci were genome-wide significant, including 20 newly identified loci. The significant loci contain genes encoding ion channels, neurotransmitter transporters and synaptic components. Pathway analysis revealed nine significantly enriched gene sets, including regulation of insulin secretion and endocannabinoid signaling. Bipolar I disorder is strongly genetically correlated with schizophrenia, driven by psychosis, whereas bipolar II disorder is more strongly correlated with major depressive disorder. These findings address key clinical questions and provide potential biological mechanisms for bipolar disorder.

Published
2019

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

Author

Witt, SH, Streit, F, Jungkunz, M, Frank, J, Awasthi, S, Reinbold, CS, Treutlein, J, Degenhardt, F, Forstner, AJ, Heilmann-Heimbach, S, Dietl, L, Schwarze, CE, Schendel, D, Strohmaier, J, Abdellaoui, A, Adolfsson, R, Air, TM, Akil, H, Alda, M, Alliey-Rodriguez, N, Andreassen, OA, Babadjanova, G, Bass, NJ, Bauer, M, Baune, BT, Bellivier, F, Bergen, S, Bethell, A, Biernacka, JM, Blackwood, DHR, Boks, MP, Boomsma, DI, Børglum, AD, Borrmann-Hassenbach, M, Brennan, P, Budde, M, Buttenschøn, HN, Byrne, EM, Cervantes, P, Clarke, TK, Craddock, N, Cruceanu, C, Curtis, D, Czerski, PM, Dannlowski, U, Davis, T, de Geus, EJC, Di Florio, A, Djurovic, S, Domenici, E, Edenberg, HJ, Etain, B, Fischer, SB, Forty, L, Fraser, C, Frye, MA, Fullerton, JM ; https://orcid.org/0000-0003-4014-4490, Gade, K, Gershon, ES, Giegling, I, Gordon, SD, Gordon-Smith, K, Grabe, HJ, Green, EK, Greenwood, TA, Grigoroiu-Serbanescu, M, Guzman-Parra, J, Hall, LS, Hamshere, M, Hauser, J, Hautzinger, M, Heilbronner, U, Herms, S, Hitturlingappa, S, Hoffmann, P, Holmans, P, Hottenga, JJ, Jamain, S, Jones, I, Jones, LA, Juréus, A, Kahn, RS, Kammerer-Ciernioch, J, Kirov, G, Kittel-Schneider, S, Kloiber, S, Knott, SV, Kogevinas, M, Landén, M, Leber, M, Leboyer, M, Li, QS, Lissowska, J, Lucae, S, Martin, NG, Mayoral-Cleries, F, McElroy, SL, McIntosh, AM, McKay, JD, McQuillin, A, Mitchell, Philip ; https://orcid.org/0000-0002-7954-5235, Schofield, Peter ; https://orcid.org/0000-0003-2967-9662, Witt, SH, Streit, F, Jungkunz, M, Frank, J, Awasthi, S, Reinbold, CS, Treutlein, J, Degenhardt, F, Forstner, AJ, Heilmann-Heimbach, S, Dietl, L, Schwarze, CE, Schendel, D, Strohmaier, J, Abdellaoui, A, Adolfsson, R, Air, TM, Akil, H, Alda, M, Alliey-Rodriguez, N, Andreassen, OA, Babadjanova, G, Bass, NJ, Bauer, M, Baune, BT, Bellivier, F, Bergen, S, Bethell, A, Biernacka, JM, Blackwood, DHR, Boks, MP, Boomsma, DI, Børglum, AD, Borrmann-Hassenbach, M, Brennan, P, Budde, M, Buttenschøn, HN, Byrne, EM, Cervantes, P, Clarke, TK, Craddock, N, Cruceanu, C, Curtis, D, Czerski, PM, Dannlowski, U, Davis, T, de Geus, EJC, Di Florio, A, Djurovic, S, Domenici, E, Edenberg, HJ, Etain, B, Fischer, SB, Forty, L, Fraser, C, Frye, MA, Fullerton, JM ; https://orcid.org/0000-0003-4014-4490, Gade, K, Gershon, ES, Giegling, I, Gordon, SD, Gordon-Smith, K, Grabe, HJ, Green, EK, Greenwood, TA, Grigoroiu-Serbanescu, M, Guzman-Parra, J, Hall, LS, Hamshere, M, Hauser, J, Hautzinger, M, Heilbronner, U, Herms, S, Hitturlingappa, S, Hoffmann, P, Holmans, P, Hottenga, JJ, Jamain, S, Jones, I, Jones, LA, Juréus, A, Kahn, RS, Kammerer-Ciernioch, J, Kirov, G, Kittel-Schneider, S, Kloiber, S, Knott, SV, Kogevinas, M, Landén, M, Leber, M, Leboyer, M, Li, QS, Lissowska, J, Lucae, S, Martin, NG, Mayoral-Cleries, F, McElroy, SL, McIntosh, AM, McKay, JD, McQuillin, A, Mitchell, Philip ; https://orcid.org/0000-0002-7954-5235, and Schofield, Peter ; https://orcid.org/0000-0003-2967-9662

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 × 10-7) and PKP4 (P=8.67 × 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 (rg=0.28 [P=2.99 × 10-3]), SCZ (rg=0.34 [P=4.37 × 10-5]) and MDD (rg=0.57 [P=1.04 × 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. Bioavailability of Cinnarizine in Dogs: Effect of SNEDDS Loading Level and Correlation with Cinnarizine Solubilization During In Vitro Lipolysis.

Author

Larsen, Anne T., Åkesson, Pernilla, Juréus, Anna, Saaby, Lasse, Abu-Rmaileh, Ragheb, Abrahamsson, Bertil, Østergaard, Jesper, and Müllertz, Anette

Subjects
DRUG bioavailability, CINNARIZINE, DRUG solubility, IN vitro studies, LIPOLYSIS, EXCIPIENTS, DRUG delivery systems, DRUG administration
Abstract

Purpose: To investigate the effect of increasing the loading level of the poorly soluble drug cinnarizine in a self-nanoemulsifying drug delivery system (SNEDDS) both in vitro and in vivo. Methods: A fixed dose of cinnarizine was administered orally to dogs in solution in different amounts of SNEDDS vehicle. Furthermore, the SNEDDSs were characterised using the dynamic in vitro lipolysis model. Results: Statistical differences in bioavailability were not obtained between the different amounts of SNEDDS vehicle, in spite of differences in the tendency of cinnarizine to precipitate during in vitro lipolysis of the treatments. Use of the SNEDDS concept decreased the variation in cinnarizine exposure observed between dogs as compared to administering cinnarizine in an aqueous suspension. Conclusions: Optimization of SNEDDSs towards keeping the drug compound in solution upon in vitro lipolysis of the SNEDDSs may not be as important as previously suggested. [ABSTRACT FROM AUTHOR]

Published
2013
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4. Low background and high contrast PET imaging of amyloid-β with [C]AZD2995 and [C]AZD2184 in Alzheimer's disease patients.

Author

Forsberg, Anton, Juréus, Anders, Cselényi, Zsolt, Eriksdotter, Maria, Freund-Levi, Yvonne, Jeppsson, Fredrik, Swahn, Britt-Marie, Sandell, Johan, Julin, Per, Schou, Magnus, Andersson, Jan, Johnström, Peter, Varnäs, Katarina, Halldin, Christer, Farde, Lars, and Svensson, Samuel

Subjects
*ALZHEIMER'S disease diagnosis, *AMYLOID beta-protein, *POSITRON emission tomography, *RADIOLIGAND assay, *TRITIUM
Abstract

Purpose: The aim of this study was to evaluate AZD2995 side by side with AZD2184 as novel PET radioligands for imaging of amyloid-β in Alzheimer's disease (AD). Methods: In vitro binding of tritium-labelled AZD2995 and AZD2184 was studied and compared with that of the established amyloid-β PET radioligand PIB. Subsequently, a first-in-human in vivo PET study was performed using [C]AZD2995 and [C]AZD2184 in three healthy control subjects and seven AD patients. Results: AZD2995, AZD2184 and PIB were found to share the same binding site to amyloid-β. [H]AZD2995 had the highest signal-to-background ratio in brain tissue from patients with AD as well as in transgenic mice. However, [C]AZD2184 had superior imaging properties in PET, as shown by larger effect sizes comparing binding potential values in cortical regions of AD patients and healthy controls. Nevertheless, probably due to a lower amount of nonspecific binding, the group separation of the distribution volume ratio values of [C]AZD2995 was greater in areas with lower amyloid-β load, e.g. the hippocampus. Conclusion: Both AZD2995 and AZD2184 detect amyloid-β with high affinity and specificity and also display a lower degree of nonspecific binding than that reported for PIB. Overall [C]AZD2184 seems to be an amyloid-β radioligand with higher uptake and better group separation when compared to [C]AZD2995. However, the very low nonspecific binding of [C]AZD2995 makes this radioligand potentially interesting as a tool to study minute levels of amyloid-β. This sensitivity may be important in investigating, for example, early prodromal stages of AD or in the longitudinal study of a disease modifying therapy. [ABSTRACT FROM AUTHOR]

Published
2013
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