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1. Self-reported suicidal ideation among individuals with first episode psychosis and healthy controls:Findings from the international multicentre EU-GEI study

Author

Heuschen, C. B.B.C.M., Bolhuis, K., Zantvoord, J. B., Bockting, C. L., Denys, D. A.J.P., Lok, A., Arango, C., Arrojo, M., Bernardo, M., Bobes, J., Del-Ben, C. M., Di Forti, M., Gayer-Anderson, C., Jones, P. B., Jongsma, H. E., Kirkbride, J. B., La Cascia, C., Lasalvia, A., Tosato, S., Llorca, P. M., Menezes, P. R., Murray, R. M., Quattrone, D., Rutten, B. P., Sanjuán, J., Selten, J. P., Szöke, A., Tarricone, I., Tortelli, A., Velthorst, E., de Haan, L., Schirmbeck, F., Heuschen, C. B.B.C.M., Bolhuis, K., Zantvoord, J. B., Bockting, C. L., Denys, D. A.J.P., Lok, A., Arango, C., Arrojo, M., Bernardo, M., Bobes, J., Del-Ben, C. M., Di Forti, M., Gayer-Anderson, C., Jones, P. B., Jongsma, H. E., Kirkbride, J. B., La Cascia, C., Lasalvia, A., Tosato, S., Llorca, P. M., Menezes, P. R., Murray, R. M., Quattrone, D., Rutten, B. P., Sanjuán, J., Selten, J. P., Szöke, A., Tarricone, I., Tortelli, A., Velthorst, E., de Haan, L., and Schirmbeck, F.

Abstract

Introduction: Suicidal ideation is common among individuals with first episode psychosis (FEP), with prevalence estimates up to 56.5 %. Despite its high prevalence, relatively little is known about how sociodemographic, clinical and/or developmental characteristics contribute to the experience of suicidal ideation in individuals with FEP. Methods: In this cross-sectional study (FEP n = 551 and controls n = 857), univariate logistic regression analyses were performed to study the associations of sociodemographic, clinical, and developmental factors with suicidal ideation in individuals with FEP as well as controls. Suicidal ideation was assessed using the Community Assessment of Psychic Experiences (CAPE). In addition, multivariate logistic regression analyses were conducted based on a stepwise approach. Results: In FEP, only depressive symptoms remained significantly associated with suicidal ideation when all correlates were integrated into one model. In the multivariate model in controls, depressive symptoms, positive symptoms, and traumatic childhood experiences were significantly associated with suicidal ideation. Conclusions: This study showed that depressive symptoms are an important factor relating to suicidal ideation in individuals with FEP, over and above other clinical, sociodemographic, and developmental factors. This underscores the relevance of screening for suicidal ideation in individuals with FEP, and highlights the need for a better understanding of the diagnostic uncertainty and course of mood symptoms in early psychosis. Limitations: Cross-sectional study design, self-reported questionnaires.

Published
2024

2. Mapping genomic loci implicates genes and synaptic biology in schizophrenia

Author

Trubetskoy, V. Pardiñas, A.F. Qi, T. Panagiotaropoulou, G. Awasthi, S. Bigdeli, T.B. Bryois, J. Chen, C.-Y. Dennison, C.A. Hall, L.S. Lam, M. Watanabe, K. Frei, O. Ge, T. Harwood, J.C. Koopmans, F. Magnusson, S. Richards, A.L. Sidorenko, J. Wu, Y. Zeng, J. Grove, J. Kim, M. Li, Z. Voloudakis, G. Zhang, W. Adams, M. Agartz, I. Atkinson, E.G. Agerbo, E. Al Eissa, M. Albus, M. Alexander, M. Alizadeh, B.Z. Alptekin, K. Als, T.D. Amin, F. Arolt, V. Arrojo, M. Athanasiu, L. Azevedo, M.H. Bacanu, S.A. Bass, N.J. Begemann, M. Belliveau, R.A. Bene, J. Benyamin, B. Bergen, S.E. Blasi, G. Bobes, J. Bonassi, S. Braun, A. Bressan, R.A. Bromet, E.J. Bruggeman, R. Buckley, P.F. Buckner, R.L. Bybjerg-Grauholm, J. Cahn, W. Cairns, M.J. Calkins, M.E. Carr, V.J. Castle, D. Catts, S.V. Chambert, K.D. Chan, R.C.K. Chaumette, B. Cheng, W. Cheung, E.F.C. Chong, S.A. Cohen, D. Consoli, A. Cordeiro, Q. Costas, J. Curtis, C. Davidson, M. Davis, K.L. de Haan, L. Degenhardt, F. DeLisi, L.E. Demontis, D. Dickerson, F. Dikeos, D. Dinan, T. Djurovic, S. Duan, J. Ducci, G. Dudbridge, F. Eriksson, J.G. Fañanás, L. Faraone, S.V. Fiorentino, A. Forstner, A. Frank, J. Freimer, N.B. Fromer, M. Frustaci, A. Gadelha, A. Genovese, G. Gershon, E.S. Giannitelli, M. Giegling, I. Giusti-Rodríguez, P. Godard, S. Goldstein, J.I. González Peñas, J. González-Pinto, A. Gopal, S. Gratten, J. Green, M.F. Greenwood, T.A. Guillin, O. Gülöksüz, S. Gur, R.E. Gur, R.C. Gutiérrez, B. Hahn, E. Hakonarson, H. Haroutunian, V. Hartmann, A.M. Harvey, C. Hayward, C. Henskens, F.A. Herms, S. Hoffmann, P. Howrigan, D.P. Ikeda, M. Iyegbe, C. Joa, I. Julià, A. Kähler, A.K. Kam-Thong, T. Kamatani, Y. Karachanak-Yankova, S. Kebir, O. Keller, M.C. Kelly, B.J. Khrunin, A. Kim, S.-W. Klovins, J. Kondratiev, N. Konte, B. Kraft, J. Kubo, M. Kučinskas, V. Kučinskiene, Z.A. Kusumawardhani, A. Kuzelova-Ptackova, H. Landi, S. Lazzeroni, L.C. Lee, P.H. Legge, S.E. Lehrer, D.S. Lencer, R. Lerer, B. Li, M. Lieberman, J. Light, G.A. Limborska, S. and Trubetskoy, V. Pardiñas, A.F. Qi, T. Panagiotaropoulou, G. Awasthi, S. Bigdeli, T.B. Bryois, J. Chen, C.-Y. Dennison, C.A. Hall, L.S. Lam, M. Watanabe, K. Frei, O. Ge, T. Harwood, J.C. Koopmans, F. Magnusson, S. Richards, A.L. Sidorenko, J. Wu, Y. Zeng, J. Grove, J. Kim, M. Li, Z. Voloudakis, G. Zhang, W. Adams, M. Agartz, I. Atkinson, E.G. Agerbo, E. Al Eissa, M. Albus, M. Alexander, M. Alizadeh, B.Z. Alptekin, K. Als, T.D. Amin, F. Arolt, V. Arrojo, M. Athanasiu, L. Azevedo, M.H. Bacanu, S.A. Bass, N.J. Begemann, M. Belliveau, R.A. Bene, J. Benyamin, B. Bergen, S.E. Blasi, G. Bobes, J. Bonassi, S. Braun, A. Bressan, R.A. Bromet, E.J. Bruggeman, R. Buckley, P.F. Buckner, R.L. Bybjerg-Grauholm, J. Cahn, W. Cairns, M.J. Calkins, M.E. Carr, V.J. Castle, D. Catts, S.V. Chambert, K.D. Chan, R.C.K. Chaumette, B. Cheng, W. Cheung, E.F.C. Chong, S.A. Cohen, D. Consoli, A. Cordeiro, Q. Costas, J. Curtis, C. Davidson, M. Davis, K.L. de Haan, L. Degenhardt, F. DeLisi, L.E. Demontis, D. Dickerson, F. Dikeos, D. Dinan, T. Djurovic, S. Duan, J. Ducci, G. Dudbridge, F. Eriksson, J.G. Fañanás, L. Faraone, S.V. Fiorentino, A. Forstner, A. Frank, J. Freimer, N.B. Fromer, M. Frustaci, A. Gadelha, A. Genovese, G. Gershon, E.S. Giannitelli, M. Giegling, I. Giusti-Rodríguez, P. Godard, S. Goldstein, J.I. González Peñas, J. González-Pinto, A. Gopal, S. Gratten, J. Green, M.F. Greenwood, T.A. Guillin, O. Gülöksüz, S. Gur, R.E. Gur, R.C. Gutiérrez, B. Hahn, E. Hakonarson, H. Haroutunian, V. Hartmann, A.M. Harvey, C. Hayward, C. Henskens, F.A. Herms, S. Hoffmann, P. Howrigan, D.P. Ikeda, M. Iyegbe, C. Joa, I. Julià, A. Kähler, A.K. Kam-Thong, T. Kamatani, Y. Karachanak-Yankova, S. Kebir, O. Keller, M.C. Kelly, B.J. Khrunin, A. Kim, S.-W. Klovins, J. Kondratiev, N. Konte, B. Kraft, J. Kubo, M. Kučinskas, V. Kučinskiene, Z.A. Kusumawardhani, A. Kuzelova-Ptackova, H. Landi, S. Lazzeroni, L.C. Lee, P.H. Legge, S.E. Lehrer, D.S. Lencer, R. Lerer, B. Li, M. Lieberman, J. Light, G.A. Limborska, S.

Abstract

Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies. © 2022. The Author(s), under exclusive licence to Springer Nature Limited.

Published
2022

3. Evidence, and replication thereof, that molecular-genetic and environmental risks for psychosis impact through an affective pathway

Author

van Os, J., van Os, J., Pries, L.K., ten Have, M., de Graaf, R., van Dorsselaer, S., Delespaul, P., Bak, M., Kenis, G., Lin, B.D., Luykx, J.J., Richards, A.L., Akdede, B., Binbay, T., Altinyazar, V., Yalincetin, B., Gumus-Akay, G., Cihan, B., Soygur, H., Ulas, H., Cankurtaran, E.S., Kaymak, S.U., Mihaljevic, M.M., Petrovic, S.A., Mirjanic, T., Bernardo, M., Mezquida, G., Amoretti, S., Bobes, J., Saiz, P.A., Garcia-Portilla, M.P., Sanjuan, J., Aguilar, E.J., Santos, J.L., Jimenez-Lopez, E., Arrojo, M., Carracedo, A., Lopez, G., Gonzalez-Penas, J., Parellada, M., Maric, N.P., Atbasoglu, C., Ucok, A., Alptekin, K., Saka, M.C., Arango, C., O'Donovan, M., Rutten, B.P.F., Guloksuz, S., van Os, J., van Os, J., Pries, L.K., ten Have, M., de Graaf, R., van Dorsselaer, S., Delespaul, P., Bak, M., Kenis, G., Lin, B.D., Luykx, J.J., Richards, A.L., Akdede, B., Binbay, T., Altinyazar, V., Yalincetin, B., Gumus-Akay, G., Cihan, B., Soygur, H., Ulas, H., Cankurtaran, E.S., Kaymak, S.U., Mihaljevic, M.M., Petrovic, S.A., Mirjanic, T., Bernardo, M., Mezquida, G., Amoretti, S., Bobes, J., Saiz, P.A., Garcia-Portilla, M.P., Sanjuan, J., Aguilar, E.J., Santos, J.L., Jimenez-Lopez, E., Arrojo, M., Carracedo, A., Lopez, G., Gonzalez-Penas, J., Parellada, M., Maric, N.P., Atbasoglu, C., Ucok, A., Alptekin, K., Saka, M.C., Arango, C., O'Donovan, M., Rutten, B.P.F., and Guloksuz, S.

Abstract

Background There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation. Methods We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls. Results The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: -0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465). Conclusions The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.

Published
2022

4. Evidence, and replication thereof, that molecular-genetic and environmental risks for psychosis impact through an affective pathway

Author

van Os, J., Pries, L.K., ten Have, M., de Graaf, R., van Dorsselaer, S., Delespaul, P., Bak, M., Kenis, G., Lin, B.D., Luykx, J.J., Richards, A.L., Akdede, B., Binbay, T., Altinyazar, V., Yalincetin, B., Gumus-Akay, G., Cihan, B., Soygur, H., Ulas, H., Cankurtaran, E.S., Kaymak, S.U., Mihaljevic, M.M., Petrovic, S.A., Mirjanic, T., Bernardo, M., Mezquida, G., Amoretti, S., Bobes, J., Saiz, P.A., Garcia-Portilla, M.P., Sanjuan, J., Aguilar, E.J., Santos, J.L., Jimenez-Lopez, E., Arrojo, M., Carracedo, A., Lopez, G., Gonzalez-Penas, J., Parellada, M., Maric, N.P., Atbasoglu, C., Ucok, A., Alptekin, K., Saka, M.C., Arango, C., O'Donovan, M., Rutten, B.P.F., Guloksuz, S., van Os, J., Pries, L.K., ten Have, M., de Graaf, R., van Dorsselaer, S., Delespaul, P., Bak, M., Kenis, G., Lin, B.D., Luykx, J.J., Richards, A.L., Akdede, B., Binbay, T., Altinyazar, V., Yalincetin, B., Gumus-Akay, G., Cihan, B., Soygur, H., Ulas, H., Cankurtaran, E.S., Kaymak, S.U., Mihaljevic, M.M., Petrovic, S.A., Mirjanic, T., Bernardo, M., Mezquida, G., Amoretti, S., Bobes, J., Saiz, P.A., Garcia-Portilla, M.P., Sanjuan, J., Aguilar, E.J., Santos, J.L., Jimenez-Lopez, E., Arrojo, M., Carracedo, A., Lopez, G., Gonzalez-Penas, J., Parellada, M., Maric, N.P., Atbasoglu, C., Ucok, A., Alptekin, K., Saka, M.C., Arango, C., O'Donovan, M., Rutten, B.P.F., and Guloksuz, S.

Abstract

Background There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation. Methods We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls. Results The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: -0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465). Conclusions The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.

Published
2022

5. Genetic and psychosocial stressors have independent effects on the level of subclinical psychosis: findings from the multinational EU-GEI study

Author

Hersenen-Medisch 1, Brain, Pignon, B, Peyre, H, Ayrolles, A, Kirkbride, J B, Jamain, S, Ferchiou, A, Richard, J R, Baudin, G, Tosato, S, Jongsma, H, de Haan, L, Tarricone, I, Bernardo, M, Velthorst, E, Braca, M, Arango, C, Arrojo, M, Bobes, J, Del-Ben, C M, Di Forti, M, Gayer-Anderson, C, Jones, P B, La Cascia, C, Lasalvia, A, Menezes, P R, Quattrone, D, Sanjuán, J, Selten, J P, Tortelli, A, Llorca, P M, van Os, J, Rutten, B P F, Murray, R M, Morgan, C, Leboyer, M, Szöke, A, Schürhoff, F, Hersenen-Medisch 1, Brain, Pignon, B, Peyre, H, Ayrolles, A, Kirkbride, J B, Jamain, S, Ferchiou, A, Richard, J R, Baudin, G, Tosato, S, Jongsma, H, de Haan, L, Tarricone, I, Bernardo, M, Velthorst, E, Braca, M, Arango, C, Arrojo, M, Bobes, J, Del-Ben, C M, Di Forti, M, Gayer-Anderson, C, Jones, P B, La Cascia, C, Lasalvia, A, Menezes, P R, Quattrone, D, Sanjuán, J, Selten, J P, Tortelli, A, Llorca, P M, van Os, J, Rutten, B P F, Murray, R M, Morgan, C, Leboyer, M, Szöke, A, and Schürhoff, F

Published
2022

6. The Independent Effects of Psychosocial Stressors on Subclinical Psychosis: Findings From the Multinational EU-GEI Study

Author

Pignon, B., Pignon, B., Lajnef, M., Kirkbride, J.B., Peyre, H., Ferchiou, A., Richard, J.R., Baudin, G., Tosato, S., Jongsma, H., de Haan, L., Tarricone, I., Bernardo, M., Velthorst, E., Braca, M., Arango, C., Arrojo, M., Bobes, J., Del-Ben, C.M., Di Forti, M., Gayer-Anderson, C., Jones, P.B., La Cascia, C., Lasalvia, A., Menezes, P.R., Quattrone, D., Sanjuan, J., Selten, J.P., Tortelli, A., Llorca, P.M., van Os, J., Rutten, B.P.F., Murray, R.M., Morgan, C., Leboyer, M., Szoke, A., Schurhoff, F., Pignon, B., Pignon, B., Lajnef, M., Kirkbride, J.B., Peyre, H., Ferchiou, A., Richard, J.R., Baudin, G., Tosato, S., Jongsma, H., de Haan, L., Tarricone, I., Bernardo, M., Velthorst, E., Braca, M., Arango, C., Arrojo, M., Bobes, J., Del-Ben, C.M., Di Forti, M., Gayer-Anderson, C., Jones, P.B., La Cascia, C., Lasalvia, A., Menezes, P.R., Quattrone, D., Sanjuan, J., Selten, J.P., Tortelli, A., Llorca, P.M., van Os, J., Rutten, B.P.F., Murray, R.M., Morgan, C., Leboyer, M., Szoke, A., and Schurhoff, F.

Abstract

The influence of psychosocial stressors on psychosis risk has usually been studied in isolation and after the onset of the disorder, potentially ignoring important confounding relationships or the fact that some stressors that may be the consequence of the disorder rather than preexisting. The study of subclinical psychosis could help to address some of these issues. In this study, we investigated whether there was (i) an association between dimensions of subclinical psychosis and several psychosocial stressors including: childhood trauma, self-reported discrimination experiences, low social capital, and stressful life experiences, and (ii) any evidence of environment-environment (ExE) interactions between these factors. Data were drawn from the EUGEI study, in which healthy controls (N = 1497) and siblings of subjects with a psychotic disorder (N = 265) were included in six countries. The association between psychosocial stressors and subclinical psychosis dimensions (positive, negative and depressive dimension as measured by the Community Assessment of Psychic Experiences (CAPE) scale) and possible ExE interactions were assessed using linear regression models. After adjusting for sex, age, ethnicity, country, and control/sibling status, childhood trauma (beta for positive dimension: 0.13, negative: 0.49, depressive: 0.26) and stressful life events (positive: 0.08, negative: 0.16, depressive: 0.17) were associated with the three dimensions. Lower social capital was associated with the negative and depression dimensions (negative: 0.26, depressive: 0.13), and self-reported discrimination experiences with the positive dimension (0.06). Our findings are in favor of independent, cumulative and non-specific influences of social adversities in subclinical psychosis in non-clinical populations, without arguments for E x E interactions.

Published
2021

7. Cognitive functioning throughout adulthood and illness stages in individuals with psychotic disorders and their unaffected siblings

Author

Velthorst, E, Mollon, J, Murray, RM, de Haan, L, Germeys, IM, Glahn, DC, Arango, C, van der Ven, E, Di Forti, M, Bernardo, M, Guloksuz, S, Delespaul, P, Mezquida, G, Amoretti, S, Bobes, J, Saiz, PA, Garcia-Portilla, MP, Santos, JL, Jimenez-Lopez, E, Sanjuan, J, Aguilar, EJ, Arrojo, M, Carracedo, A, Lopez, G, Gonzalez-Penas, J, Parellada, M, Atbasoglu, C, Saka, MC, Ucok, A, Alptekin, K, Akdede, B, Binbay, T, Altinyazar, V, Ulas, H, Yalincetin, B, Gumus-Akay, G, Beyaz, BC, Soygur, H, Cankurtaran, ES, Kaymak, SU, Maric, NP, Mihaljevic, MM, Petrovic, SA, Mirjanic, T, Del-Ben, CM, Ferraro, L, Gayer-Anderson, C, Jones, PB, Jongsma, HE, Kirkbride, JB, La Cascia, C, Lasalvia, A, Tosato, S, Llorca, P-M, Menezes, PR, Morgan, C, Quattrone, D, Menchetti, M, Selten, J-P, Szoke, A, Tarricone, I, Tortelli, A, McGuire, P, Valmaggia, L, Kempton, MJ, van der Gaag, M, Riecher-Rossler, A, Bressan, RA, Barrantes-Vidal, N, Nelson, B, McGorry, P, Pantelis, C, Krebs, M-O, Ruhrmann, S, Sachs, G, Rutten, BPF, van Os, J, Alizadeh, BZ, van Amelsvoort, T, Bartels-Velthuis, AA, Bruggeman, R, van Beveren, NJ, Luykx, JJ, Cahn, W, Simons, CJP, Kahn, RS, Schirmbeck, F, van Winkel, R, Reichenberg, A, Velthorst, E, Mollon, J, Murray, RM, de Haan, L, Germeys, IM, Glahn, DC, Arango, C, van der Ven, E, Di Forti, M, Bernardo, M, Guloksuz, S, Delespaul, P, Mezquida, G, Amoretti, S, Bobes, J, Saiz, PA, Garcia-Portilla, MP, Santos, JL, Jimenez-Lopez, E, Sanjuan, J, Aguilar, EJ, Arrojo, M, Carracedo, A, Lopez, G, Gonzalez-Penas, J, Parellada, M, Atbasoglu, C, Saka, MC, Ucok, A, Alptekin, K, Akdede, B, Binbay, T, Altinyazar, V, Ulas, H, Yalincetin, B, Gumus-Akay, G, Beyaz, BC, Soygur, H, Cankurtaran, ES, Kaymak, SU, Maric, NP, Mihaljevic, MM, Petrovic, SA, Mirjanic, T, Del-Ben, CM, Ferraro, L, Gayer-Anderson, C, Jones, PB, Jongsma, HE, Kirkbride, JB, La Cascia, C, Lasalvia, A, Tosato, S, Llorca, P-M, Menezes, PR, Morgan, C, Quattrone, D, Menchetti, M, Selten, J-P, Szoke, A, Tarricone, I, Tortelli, A, McGuire, P, Valmaggia, L, Kempton, MJ, van der Gaag, M, Riecher-Rossler, A, Bressan, RA, Barrantes-Vidal, N, Nelson, B, McGorry, P, Pantelis, C, Krebs, M-O, Ruhrmann, S, Sachs, G, Rutten, BPF, van Os, J, Alizadeh, BZ, van Amelsvoort, T, Bartels-Velthuis, AA, Bruggeman, R, van Beveren, NJ, Luykx, JJ, Cahn, W, Simons, CJP, Kahn, RS, Schirmbeck, F, van Winkel, R, and Reichenberg, A

Abstract

Important questions remain about the profile of cognitive impairment in psychotic disorders across adulthood and illness stages. The age-associated profile of familial impairments also remains unclear, as well as the effect of factors, such as symptoms, functioning, and medication. Using cross-sectional data from the EU-GEI and GROUP studies, comprising 8455 participants aged 18 to 65, we examined cognitive functioning across adulthood in patients with psychotic disorders (n = 2883), and their unaffected siblings (n = 2271), compared to controls (n = 3301). An abbreviated WAIS-III measured verbal knowledge, working memory, visuospatial processing, processing speed, and IQ. Patients showed medium to large deficits across all functions (ES range = -0.45 to -0.73, p < 0.001), while siblings showed small deficits on IQ, verbal knowledge, and working memory (ES = -0.14 to -0.33, p < 0.001). Magnitude of impairment was not associated with participant age, such that the size of impairment in older and younger patients did not significantly differ. However, first-episode patients performed worse than prodromal patients (ES range = -0.88 to -0.60, p < 0.001). Adjusting for cannabis use, symptom severity, and global functioning attenuated impairments in siblings, while deficits in patients remained statistically significant, albeit reduced by half (ES range = -0.13 to -0.38, p < 0.01). Antipsychotic medication also accounted for around half of the impairment in patients (ES range = -0.21 to -0.43, p < 0.01). Deficits in verbal knowledge, and working memory may specifically index familial, i.e., shared genetic and/or shared environmental, liability for psychotic disorders. Nevertheless, potentially modifiable illness-related factors account for a significant portion of the cognitive impairment in psychotic disorders.

Published
2021

8. Pre-training inter-rater reliability of clinical instruments in an international psychosis research project

Author

Berendsen, S, Kapitein, P, Schirmbeck, F, van Tricht, MJ, McGuire, P, Morgan, C, Gayer-Anderson, C, Kempton, MJ, Valmaggia, L, Quattrone, D, di Forti, M, van der Gaag, M, Kirkbride, JB, Jongsma, HE, Jones, PB, Parellada, M, Arango, C, Arrojo, M, Bernardo, M, Sanjuan, J, Santos, JL, Szoke, A, Tortelli, A, Llorca, P-M, Tarricone, I, Tripoli, G, Ferraro, L, La Cascia, C, Lasalvia, A, Tosato, S, Menezes, PR, Del-Ben, CM, Nelson, B, Riecher-Rossler, A, Bressan, R, Barrantes-Vidal, N, Krebs, M-O, Nordentoft, M, Ruhrmann, S, Sachs, G, Rutten, BPF, van Os, J, Velthorst, E, de Haan, L, Berendsen, S, Kapitein, P, Schirmbeck, F, van Tricht, MJ, McGuire, P, Morgan, C, Gayer-Anderson, C, Kempton, MJ, Valmaggia, L, Quattrone, D, di Forti, M, van der Gaag, M, Kirkbride, JB, Jongsma, HE, Jones, PB, Parellada, M, Arango, C, Arrojo, M, Bernardo, M, Sanjuan, J, Santos, JL, Szoke, A, Tortelli, A, Llorca, P-M, Tarricone, I, Tripoli, G, Ferraro, L, La Cascia, C, Lasalvia, A, Tosato, S, Menezes, PR, Del-Ben, CM, Nelson, B, Riecher-Rossler, A, Bressan, R, Barrantes-Vidal, N, Krebs, M-O, Nordentoft, M, Ruhrmann, S, Sachs, G, Rutten, BPF, van Os, J, Velthorst, E, and de Haan, L

Published
2021

9. The Independent Effects of Psychosocial Stressors on Subclinical Psychosis: Findings From the Multinational EU-GEI Study

Author

Pignon, B., Lajnef, M., Kirkbride, J.B., Peyre, H., Ferchiou, A., Richard, J.R., Baudin, G., Tosato, S., Jongsma, H., de Haan, L., Tarricone, I., Bernardo, M., Velthorst, E., Braca, M., Arango, C., Arrojo, M., Bobes, J., Del-Ben, C.M., Di Forti, M., Gayer-Anderson, C., Jones, P.B., La Cascia, C., Lasalvia, A., Menezes, P.R., Quattrone, D., Sanjuan, J., Selten, J.P., Tortelli, A., Llorca, P.M., van Os, J., Rutten, B.P.F., Murray, R.M., Morgan, C., Leboyer, M., Szoke, A., Schurhoff, F., Pignon, B., Lajnef, M., Kirkbride, J.B., Peyre, H., Ferchiou, A., Richard, J.R., Baudin, G., Tosato, S., Jongsma, H., de Haan, L., Tarricone, I., Bernardo, M., Velthorst, E., Braca, M., Arango, C., Arrojo, M., Bobes, J., Del-Ben, C.M., Di Forti, M., Gayer-Anderson, C., Jones, P.B., La Cascia, C., Lasalvia, A., Menezes, P.R., Quattrone, D., Sanjuan, J., Selten, J.P., Tortelli, A., Llorca, P.M., van Os, J., Rutten, B.P.F., Murray, R.M., Morgan, C., Leboyer, M., Szoke, A., and Schurhoff, F.

Abstract

The influence of psychosocial stressors on psychosis risk has usually been studied in isolation and after the onset of the disorder, potentially ignoring important confounding relationships or the fact that some stressors that may be the consequence of the disorder rather than preexisting. The study of subclinical psychosis could help to address some of these issues. In this study, we investigated whether there was (i) an association between dimensions of subclinical psychosis and several psychosocial stressors including: childhood trauma, self-reported discrimination experiences, low social capital, and stressful life experiences, and (ii) any evidence of environment-environment (ExE) interactions between these factors. Data were drawn from the EUGEI study, in which healthy controls (N = 1497) and siblings of subjects with a psychotic disorder (N = 265) were included in six countries. The association between psychosocial stressors and subclinical psychosis dimensions (positive, negative and depressive dimension as measured by the Community Assessment of Psychic Experiences (CAPE) scale) and possible ExE interactions were assessed using linear regression models. After adjusting for sex, age, ethnicity, country, and control/sibling status, childhood trauma (beta for positive dimension: 0.13, negative: 0.49, depressive: 0.26) and stressful life events (positive: 0.08, negative: 0.16, depressive: 0.17) were associated with the three dimensions. Lower social capital was associated with the negative and depression dimensions (negative: 0.26, depressive: 0.13), and self-reported discrimination experiences with the positive dimension (0.06). Our findings are in favor of independent, cumulative and non-specific influences of social adversities in subclinical psychosis in non-clinical populations, without arguments for E x E interactions.

Published
2021

10. Identifying gene-environment interactions in schizophrenia: Contemporary challenges for integrated, large-scale investigations

Author

Van Os, J. Rutten, B.P. Myin-Germeys, I. Delespaul, P. Viechtbauer, W. Van Zelst, C. Bruggeman, R. Reininghaus, U. Morgan, C. Murray, R.M. Di Forti, M. McGuire, P. Valmaggia, L.R. Kempton, M.J. Gayer-Anderson, C. Hubbard, K. Beards, S. Stilo, S.A. Onyejiaka, A. Bourque, F. Modinos, G. Tognin, S. Calem, M. O'Donovan, M.C. Owen, M.J. Holmans, P. Williams, N. Craddock, N. Richards, A. Humphreys, I. Meyer-Lindenberg, A. Leweke, F.M. Tost, H. Akdeniz, C. Rohleder, C. Bumb, J.M. Schwarz, E. Alptekin, K. Üçok, A. Saka, M.C. Atbagoǧlu, E.C. Gülöksüz, S. Gumus-Akay, G. Cihan, B. Karadaǧ, H. Soygür, H. Cankurtaran, E.S. Ulusoy, S. Akdede, B. Binbay, T. Ayer, A. Noyan, H. Karadayi, G. Akturan, E. Ulaş, H. Arango, C. Parellada, M. Bernardo, M. Sanjuán, J. Bobes, J. Arrojo, M. Santos, J.L. Cuadrado, P. Solano, J.J.R. Carracedo, A. Bernardo, E.G. Roldán, L. López, G. Cabrera, B. Cruz, S. Mesa, E.M.D. Pouso, M. Jiménez, E. Sánchez, T. Rapado, M. González, E. Martínez, C. Sánchez, E. Olmeda, M.S. De Haan, L. Velthorst, E. Van Der Gaag, M. Selten, J.-P. Van Dam, D. Van Der Ven, E. Van Der Meer, F. Messchaert, E. Kraan, T. Burger, N. Leboyer, M. Szoke, A. Schürhoff, F. Llorca, P.-M. Jamain, S. Tortelli, A. Frijda, F. Vilain, J. Galliot, A.-M. Baudin, G. Ferchiou, A. Richard, J.-R. Bulzacka, E. Charpeaud, T. Tronche, A.-M. De Hert, M. Van Winkel, R. Decoster, J. Derom, C. Thiery, E. Stefanis, N.C. Sachs, G. Aschauer, H. Lasser, I. Winklbaur, B. Schlögelhofer, M. Riecher-Rössler, A. Borgwardt, S. Walter, A. Harrisberger, F. Smieskova, R. Rapp, C. Ittig, S. Soguel-Dit-Piquard, F. Studerus, E. Klosterkötter, J. Ruhrmann, S. Paruch, J. Julkowski, D. Hilboll, D. Sham, P.C. Cherny, S.S. Chen, E.Y.H. Campbell, D.D. Li, M. Romeo-Casabona, C.M. Cirión, A.E. Mora, A.U. Jones, P. Kirkbride, J. Cannon, M. Rujescu, D. Tarricone, I. Berardi, D. Bonora, E. Seri, M. Marcacci, T. Chiri, L. Chierzi, F. Storbini, V. Braca, M. Minenna, M.G. Donegani, I. Fioritti, A. La Barbera, D. La Cascia, C.E. Mu and Van Os, J. Rutten, B.P. Myin-Germeys, I. Delespaul, P. Viechtbauer, W. Van Zelst, C. Bruggeman, R. Reininghaus, U. Morgan, C. Murray, R.M. Di Forti, M. McGuire, P. Valmaggia, L.R. Kempton, M.J. Gayer-Anderson, C. Hubbard, K. Beards, S. Stilo, S.A. Onyejiaka, A. Bourque, F. Modinos, G. Tognin, S. Calem, M. O'Donovan, M.C. Owen, M.J. Holmans, P. Williams, N. Craddock, N. Richards, A. Humphreys, I. Meyer-Lindenberg, A. Leweke, F.M. Tost, H. Akdeniz, C. Rohleder, C. Bumb, J.M. Schwarz, E. Alptekin, K. Üçok, A. Saka, M.C. Atbagoǧlu, E.C. Gülöksüz, S. Gumus-Akay, G. Cihan, B. Karadaǧ, H. Soygür, H. Cankurtaran, E.S. Ulusoy, S. Akdede, B. Binbay, T. Ayer, A. Noyan, H. Karadayi, G. Akturan, E. Ulaş, H. Arango, C. Parellada, M. Bernardo, M. Sanjuán, J. Bobes, J. Arrojo, M. Santos, J.L. Cuadrado, P. Solano, J.J.R. Carracedo, A. Bernardo, E.G. Roldán, L. López, G. Cabrera, B. Cruz, S. Mesa, E.M.D. Pouso, M. Jiménez, E. Sánchez, T. Rapado, M. González, E. Martínez, C. Sánchez, E. Olmeda, M.S. De Haan, L. Velthorst, E. Van Der Gaag, M. Selten, J.-P. Van Dam, D. Van Der Ven, E. Van Der Meer, F. Messchaert, E. Kraan, T. Burger, N. Leboyer, M. Szoke, A. Schürhoff, F. Llorca, P.-M. Jamain, S. Tortelli, A. Frijda, F. Vilain, J. Galliot, A.-M. Baudin, G. Ferchiou, A. Richard, J.-R. Bulzacka, E. Charpeaud, T. Tronche, A.-M. De Hert, M. Van Winkel, R. Decoster, J. Derom, C. Thiery, E. Stefanis, N.C. Sachs, G. Aschauer, H. Lasser, I. Winklbaur, B. Schlögelhofer, M. Riecher-Rössler, A. Borgwardt, S. Walter, A. Harrisberger, F. Smieskova, R. Rapp, C. Ittig, S. Soguel-Dit-Piquard, F. Studerus, E. Klosterkötter, J. Ruhrmann, S. Paruch, J. Julkowski, D. Hilboll, D. Sham, P.C. Cherny, S.S. Chen, E.Y.H. Campbell, D.D. Li, M. Romeo-Casabona, C.M. Cirión, A.E. Mora, A.U. Jones, P. Kirkbride, J. Cannon, M. Rujescu, D. Tarricone, I. Berardi, D. Bonora, E. Seri, M. Marcacci, T. Chiri, L. Chierzi, F. Storbini, V. Braca, M. Minenna, M.G. Donegani, I. Fioritti, A. La Barbera, D. La Cascia, C.E. Mu

Abstract

Recent years have seen considerable progress in epidemiological and molecular genetic research into environmental and genetic factors in schizophrenia, but methodological uncertainties remain with regard to validating environmental exposures, and the population risk conferred by individual molecular genetic variants is small. There are now also a limited number of studies that have investigated molecular genetic candidate gene-environment interactions (G × E), however, so far, thorough replication of findings is rare and G × E research still faces several conceptual and methodological challenges. In this article, we aim to review these recent developments and illustrate how integrated, large-scale investigations may overcome contemporary challenges in G × E research, drawing on the example of a large, international, multi-center study into the identification and translational application of G × E in schizophrenia. While such investigations are now well underway, new challenges emerge for G × E research from late-breaking evidence that genetic variation and environmental exposures are, to a significant degree, shared across a range of psychiatric disorders, with potential overlap in phenotype. © 2014 The Author.

Published
2014

11. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S., Jong, S. de, Mattheisen, M., Costas, J., Demontis, D., Jamain, S., Pietilainen, O.P.H., Lin, K., Papiol, S., Huttenlocher, J., Sigurdsson, E., Vassos, E., Giegling, I., Breuer, R., Fraser, G., Walker, N., Melle, I., Djurovic, S., Agartz, I., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Olsen, L., Hansen, T., Ingason, A., Pirinen, M., Strengman, E., Hougaard, D.M., Orntoft, T., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Etain, B., Bellivier, F., Meary, A., Schurhoff, F., Szoke, A., Ribolsi, M., Magni, V., Siracusano, A., Sperling, S., Rossner, M., Christiansen, C., Kiemeney, B., Franke, B., Berg, L.H. van den, Veldink, J., Curran, S., Bolton, P., Poot, M., Staal, W., Rehnstrom, K., Kilpinen, H., Freitag, C.M., Meyer, J., Magnusson, P., Saemundsen, E., Martsenkovsky, I., Bikshaieva, I., Martsenkovska, I., Vashchenko, O., Raleva, M., Paketchieva, K., Stefanovski, B., Durmishi, N., Milovancevic, M.P., Tosevski, D.L., Silagadze, T., Naneishvili, N., Mikeladze, N., Surguladze, S., Vincent, J.B., Farmer, A., Mitchell, P.B., Wright, A., Schofield, P.R., Fullerton, J.M., Montgomery, G.W., Martin, N.G., Rubino, I.A., Winkel, R. van, Kenis, G., Hert, M. de, Rethelyi, J.M., Bitter, I., Terenius, L., Jonsson, E.G., Bakker, S., Os, J. van, Jablensky, A., Leboyer, M., Bramon, E., et al., Steinberg, S., Jong, S. de, Mattheisen, M., Costas, J., Demontis, D., Jamain, S., Pietilainen, O.P.H., Lin, K., Papiol, S., Huttenlocher, J., Sigurdsson, E., Vassos, E., Giegling, I., Breuer, R., Fraser, G., Walker, N., Melle, I., Djurovic, S., Agartz, I., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Olsen, L., Hansen, T., Ingason, A., Pirinen, M., Strengman, E., Hougaard, D.M., Orntoft, T., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Etain, B., Bellivier, F., Meary, A., Schurhoff, F., Szoke, A., Ribolsi, M., Magni, V., Siracusano, A., Sperling, S., Rossner, M., Christiansen, C., Kiemeney, B., Franke, B., Berg, L.H. van den, Veldink, J., Curran, S., Bolton, P., Poot, M., Staal, W., Rehnstrom, K., Kilpinen, H., Freitag, C.M., Meyer, J., Magnusson, P., Saemundsen, E., Martsenkovsky, I., Bikshaieva, I., Martsenkovska, I., Vashchenko, O., Raleva, M., Paketchieva, K., Stefanovski, B., Durmishi, N., Milovancevic, M.P., Tosevski, D.L., Silagadze, T., Naneishvili, N., Mikeladze, N., Surguladze, S., Vincent, J.B., Farmer, A., Mitchell, P.B., Wright, A., Schofield, P.R., Fullerton, J.M., Montgomery, G.W., Martin, N.G., Rubino, I.A., Winkel, R. van, Kenis, G., Hert, M. de, Rethelyi, J.M., Bitter, I., Terenius, L., Jonsson, E.G., Bakker, S., Os, J. van, Jablensky, A., Leboyer, M., Bramon, E., and et al.

Abstract

Item does not contain fulltext, Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association study, meta-analysis and follow-up (totaling as many as 18 206 cases and 42 536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7469 bipolar disorder cases, 1535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46 160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255[T]; odds ratio=1.08; P=6.6 x 10(-11)). The new variant is located within a 593-kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255[T] is also associated with lower BMI (P=0.0039 in the public GIANT consortium data set; P=0.00047 in 22 651 additional Icelanders).

Published
2014

12. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, OPH, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, L, Hansen, T, Ingason, A, Pirinen, M, Strengman, E, Hougaard, DM, Ørntoft, T, Didriksen, M, Hollegaard, MV, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, Kiemeney, LA, Franke, B, van den Berg, LH, Veldink, J, Curran, S, Bolton, P, Poot, M, Staal, W, Rehnstrom, K, Kilpinen, H, Freitag, CM, Meyer, J, Magnusson, P, Saemundsen, E, Martsenkovsky, I, Bikshaieva, I, Martsenkovska, I, Vashchenko, O, Raleva, M, Paketchieva, K, Stefanovski, B, Durmishi, N, Pejovic Milovancevic, M, Lecic Tosevski, D, Silagadze, T, Naneishvili, N, Mikeladze, N, Surguladze, S, Vincent, JB, Farmer, A, Mitchell, PB ; https://orcid.org/0000-0002-7954-5235, Wright, A, Schofield, PR ; https://orcid.org/0000-0003-2967-9662, Fullerton, JM ; https://orcid.org/0000-0003-4014-4490, Montgomery, GW, Martin, NG, Rubino, IA, van Winkel, R, Kenis, G, De Hert, M, Réthelyi, JM, Bitter, I, Terenius, L, Jönsson, EG, Bakker, S, van Os, J, Jablensky, A, Leboyer, M, Bramon, E, Powell, J, Murray, R, Corvin, A, Gill, M, Morris, D, O'Neill, FA, Kendler, K, Riley, B, Craddock, N, Owen, MJ, O'Donovan, MC, Thorsteinsdottir, U, Kong, A, Ehrenreich, H, Carracedo, A, Golimbet, V, Andreassen, OA, Børglum, AD, Mors, O, Mortensen, PB, Werge, T, Ophoff, RA, Nöthen, MM, Rietschel, M, Cichon, S, Ruggeri, M, Tosato, S, Palotie, A, St Clair, D, Rujescu, D, Collier, DA, Stefansson, H, Stefansson, K, Schofield, Peter, Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, OPH, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, L, Hansen, T, Ingason, A, Pirinen, M, Strengman, E, Hougaard, DM, Ørntoft, T, Didriksen, M, Hollegaard, MV, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, Kiemeney, LA, Franke, B, van den Berg, LH, Veldink, J, Curran, S, Bolton, P, Poot, M, Staal, W, Rehnstrom, K, Kilpinen, H, Freitag, CM, Meyer, J, Magnusson, P, Saemundsen, E, Martsenkovsky, I, Bikshaieva, I, Martsenkovska, I, Vashchenko, O, Raleva, M, Paketchieva, K, Stefanovski, B, Durmishi, N, Pejovic Milovancevic, M, Lecic Tosevski, D, Silagadze, T, Naneishvili, N, Mikeladze, N, Surguladze, S, Vincent, JB, Farmer, A, Mitchell, PB ; https://orcid.org/0000-0002-7954-5235, Wright, A, Schofield, PR ; https://orcid.org/0000-0003-2967-9662, Fullerton, JM ; https://orcid.org/0000-0003-4014-4490, Montgomery, GW, Martin, NG, Rubino, IA, van Winkel, R, Kenis, G, De Hert, M, Réthelyi, JM, Bitter, I, Terenius, L, Jönsson, EG, Bakker, S, van Os, J, Jablensky, A, Leboyer, M, Bramon, E, Powell, J, Murray, R, Corvin, A, Gill, M, Morris, D, O'Neill, FA, Kendler, K, Riley, B, Craddock, N, Owen, MJ, O'Donovan, MC, Thorsteinsdottir, U, Kong, A, Ehrenreich, H, Carracedo, A, Golimbet, V, Andreassen, OA, Børglum, AD, Mors, O, Mortensen, PB, Werge, T, Ophoff, RA, Nöthen, MM, Rietschel, M, Cichon, S, Ruggeri, M, Tosato, S, Palotie, A, St Clair, D, Rujescu, D, Collier, DA, Stefansson, H, Stefansson, K, and Schofield, Peter

Abstract

Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association study, meta-analysis and follow-up (totaling as many as 18 206 cases and 42 536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7469 bipolar disorder cases, 1535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46 160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255T; odds ratio=1.08; P=6.6 × 10 -11). The new variant is located within a 593-kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255T is also associated with lower BMI (P=0.0039 in the public GIANT consortium data set; P=0.00047 in 22 651 additional Icelanders). © 2014 Macmillan Publishers Limited.

Published
2014

13. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S., Jong, S. de, Mattheisen, M., Costas, J., Demontis, D., Jamain, S., Pietilainen, O.P.H., Lin, K., Papiol, S., Huttenlocher, J., Sigurdsson, E., Vassos, E., Giegling, I., Breuer, R., Fraser, G., Walker, N., Melle, I., Djurovic, S., Agartz, I., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Olsen, L., Hansen, T., Ingason, A., Pirinen, M., Strengman, E., Hougaard, D.M., Orntoft, T., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Etain, B., Bellivier, F., Meary, A., Schurhoff, F., Szoke, A., Ribolsi, M., Magni, V., Siracusano, A., Sperling, S., Rossner, M., Christiansen, C., Kiemeney, B., Franke, B., Berg, L.H. van den, Veldink, J., Curran, S., Bolton, P., Poot, M., Staal, W., Rehnstrom, K., Kilpinen, H., Freitag, C.M., Meyer, J., Magnusson, P., Saemundsen, E., Martsenkovsky, I., Bikshaieva, I., Martsenkovska, I., Vashchenko, O., Raleva, M., Paketchieva, K., Stefanovski, B., Durmishi, N., Milovancevic, M.P., Tosevski, D.L., Silagadze, T., Naneishvili, N., Mikeladze, N., Surguladze, S., Vincent, J.B., Farmer, A., Mitchell, P.B., Wright, A., Schofield, P.R., Fullerton, J.M., Montgomery, G.W., Martin, N.G., Rubino, I.A., Winkel, R. van, Kenis, G., Hert, M. de, Rethelyi, J.M., Bitter, I., Terenius, L., Jonsson, E.G., Bakker, S., Os, J. van, Jablensky, A., Leboyer, M., Bramon, E., et al., Steinberg, S., Jong, S. de, Mattheisen, M., Costas, J., Demontis, D., Jamain, S., Pietilainen, O.P.H., Lin, K., Papiol, S., Huttenlocher, J., Sigurdsson, E., Vassos, E., Giegling, I., Breuer, R., Fraser, G., Walker, N., Melle, I., Djurovic, S., Agartz, I., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Olsen, L., Hansen, T., Ingason, A., Pirinen, M., Strengman, E., Hougaard, D.M., Orntoft, T., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Etain, B., Bellivier, F., Meary, A., Schurhoff, F., Szoke, A., Ribolsi, M., Magni, V., Siracusano, A., Sperling, S., Rossner, M., Christiansen, C., Kiemeney, B., Franke, B., Berg, L.H. van den, Veldink, J., Curran, S., Bolton, P., Poot, M., Staal, W., Rehnstrom, K., Kilpinen, H., Freitag, C.M., Meyer, J., Magnusson, P., Saemundsen, E., Martsenkovsky, I., Bikshaieva, I., Martsenkovska, I., Vashchenko, O., Raleva, M., Paketchieva, K., Stefanovski, B., Durmishi, N., Milovancevic, M.P., Tosevski, D.L., Silagadze, T., Naneishvili, N., Mikeladze, N., Surguladze, S., Vincent, J.B., Farmer, A., Mitchell, P.B., Wright, A., Schofield, P.R., Fullerton, J.M., Montgomery, G.W., Martin, N.G., Rubino, I.A., Winkel, R. van, Kenis, G., Hert, M. de, Rethelyi, J.M., Bitter, I., Terenius, L., Jonsson, E.G., Bakker, S., Os, J. van, Jablensky, A., Leboyer, M., Bramon, E., and et al.

Abstract

Item does not contain fulltext, Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association study, meta-analysis and follow-up (totaling as many as 18 206 cases and 42 536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7469 bipolar disorder cases, 1535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46 160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255[T]; odds ratio=1.08; P=6.6 x 10(-11)). The new variant is located within a 593-kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255[T] is also associated with lower BMI (P=0.0039 in the public GIANT consortium data set; P=0.00047 in 22 651 additional Icelanders).

Published
2014

14. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S., Jong, S. de, Mattheisen, M., Costas, J., Demontis, D., Jamain, S., Pietilainen, O.P.H., Lin, K., Papiol, S., Huttenlocher, J., Sigurdsson, E., Vassos, E., Giegling, I., Breuer, R., Fraser, G., Walker, N., Melle, I., Djurovic, S., Agartz, I., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Olsen, L., Hansen, T., Ingason, A., Pirinen, M., Strengman, E., Hougaard, D.M., Orntoft, T., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Etain, B., Bellivier, F., Meary, A., Schurhoff, F., Szoke, A., Ribolsi, M., Magni, V., Siracusano, A., Sperling, S., Rossner, M., Christiansen, C., Kiemeney, B., Franke, B., Berg, L.H. van den, Veldink, J., Curran, S., Bolton, P., Poot, M., Staal, W., Rehnstrom, K., Kilpinen, H., Freitag, C.M., Meyer, J., Magnusson, P., Saemundsen, E., Martsenkovsky, I., Bikshaieva, I., Martsenkovska, I., Vashchenko, O., Raleva, M., Paketchieva, K., Stefanovski, B., Durmishi, N., Milovancevic, M.P., Tosevski, D.L., Silagadze, T., Naneishvili, N., Mikeladze, N., Surguladze, S., Vincent, J.B., Farmer, A., Mitchell, P.B., Wright, A., Schofield, P.R., Fullerton, J.M., Montgomery, G.W., Martin, N.G., Rubino, I.A., Winkel, R. van, Kenis, G., Hert, M. de, Rethelyi, J.M., Bitter, I., Terenius, L., Jonsson, E.G., Bakker, S., Os, J. van, Jablensky, A., Leboyer, M., Bramon, E., et al., Steinberg, S., Jong, S. de, Mattheisen, M., Costas, J., Demontis, D., Jamain, S., Pietilainen, O.P.H., Lin, K., Papiol, S., Huttenlocher, J., Sigurdsson, E., Vassos, E., Giegling, I., Breuer, R., Fraser, G., Walker, N., Melle, I., Djurovic, S., Agartz, I., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Olsen, L., Hansen, T., Ingason, A., Pirinen, M., Strengman, E., Hougaard, D.M., Orntoft, T., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Etain, B., Bellivier, F., Meary, A., Schurhoff, F., Szoke, A., Ribolsi, M., Magni, V., Siracusano, A., Sperling, S., Rossner, M., Christiansen, C., Kiemeney, B., Franke, B., Berg, L.H. van den, Veldink, J., Curran, S., Bolton, P., Poot, M., Staal, W., Rehnstrom, K., Kilpinen, H., Freitag, C.M., Meyer, J., Magnusson, P., Saemundsen, E., Martsenkovsky, I., Bikshaieva, I., Martsenkovska, I., Vashchenko, O., Raleva, M., Paketchieva, K., Stefanovski, B., Durmishi, N., Milovancevic, M.P., Tosevski, D.L., Silagadze, T., Naneishvili, N., Mikeladze, N., Surguladze, S., Vincent, J.B., Farmer, A., Mitchell, P.B., Wright, A., Schofield, P.R., Fullerton, J.M., Montgomery, G.W., Martin, N.G., Rubino, I.A., Winkel, R. van, Kenis, G., Hert, M. de, Rethelyi, J.M., Bitter, I., Terenius, L., Jonsson, E.G., Bakker, S., Os, J. van, Jablensky, A., Leboyer, M., Bramon, E., and et al.

Abstract

Item does not contain fulltext, Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association study, meta-analysis and follow-up (totaling as many as 18 206 cases and 42 536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7469 bipolar disorder cases, 1535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46 160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255[T]; odds ratio=1.08; P=6.6 x 10(-11)). The new variant is located within a 593-kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255[T] is also associated with lower BMI (P=0.0039 in the public GIANT consortium data set; P=0.00047 in 22 651 additional Icelanders).

Published
2014

15. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, O P H, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, Line, Hansen, Thomas Folkmann, Ingason, A, Pirinen, M, Strengman, E, Hougaard, D M, Orntoft, T, Didriksen, M, Hollegaard, M V, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, Werge, T, Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, O P H, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, Line, Hansen, Thomas Folkmann, Ingason, A, Pirinen, M, Strengman, E, Hougaard, D M, Orntoft, T, Didriksen, M, Hollegaard, M V, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, and Werge, T

Abstract

Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association study, meta-analysis and follow-up (totaling as many as 18 206 cases and 42 536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7469 bipolar disorder cases, 1535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46 160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255[T]; odds ratio=1.08; P=6.6 × 10(-11)). The new variant is located within a 593-kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255[T] is also associated with lower BMI (P=0.0039 in the public GIANT consortium data set; P=0.00047 in 22 651 additional Icelanders).

Published
2014

16. Common variant at 16p11.2 conferring risk of psychosis

Author

Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, O P H, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, Line, Hansen, Thomas Folkmann, Ingason, A, Pirinen, M, Strengman, E, Hougaard, D M, Orntoft, T, Didriksen, M, Hollegaard, M V, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, Werge, T, Steinberg, S, de Jong, S, Mattheisen, M, Costas, J, Demontis, D, Jamain, S, Pietiläinen, O P H, Lin, K, Papiol, S, Huttenlocher, J, Sigurdsson, E, Vassos, E, Giegling, I, Breuer, R, Fraser, G, Walker, N, Melle, I, Djurovic, S, Agartz, I, Tuulio-Henriksson, A, Suvisaari, J, Lönnqvist, J, Paunio, T, Olsen, Line, Hansen, Thomas Folkmann, Ingason, A, Pirinen, M, Strengman, E, Hougaard, D M, Orntoft, T, Didriksen, M, Hollegaard, M V, Nordentoft, M, Abramova, L, Kaleda, V, Arrojo, M, Sanjuán, J, Arango, C, Etain, B, Bellivier, F, Méary, A, Schürhoff, F, Szoke, A, Ribolsi, M, Magni, V, Siracusano, A, Sperling, S, Rossner, M, Christiansen, C, and Werge, T

Abstract

Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association study, meta-analysis and follow-up (totaling as many as 18 206 cases and 42 536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7469 bipolar disorder cases, 1535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46 160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255[T]; odds ratio=1.08; P=6.6 × 10(-11)). The new variant is located within a 593-kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255[T] is also associated with lower BMI (P=0.0039 in the public GIANT consortium data set; P=0.00047 in 22 651 additional Icelanders).

Published
2014

17. Modelling a quantitative ensilability index adapted to forages from wet temperate areas

Author

Martínez Fernández, A., Soldado Cabezuelo, Ana Belén, Roza Delgado, María Begoña de la, Argamentería Gutiérrez, Alejandro, González Arrojo, M. A., Martínez Fernández, A., Soldado Cabezuelo, Ana Belén, Roza Delgado, María Begoña de la, Argamentería Gutiérrez, Alejandro, and González Arrojo, M. A.

Abstract

Forage ensilability mainly depends on dry matter (DM), water soluble carbohydrates (WSC) and buffer capacity (BC) values at harvest time. According to these parameters, and based on a collection of 208 forages of known ensilability characteristics including short and long term meadows for grazing, italian ryegrass, maize, triticale, soybean, faba bean crops, and samples coming from cereal-legume associations, the objective of this study has been to define a quantitative ensilability index (EI) based on a relationship between DM, WSC and BC contents at harvest date, adapted to the characteristics of fodder from wet temperate areas. For this purpose, a discriminant procedure was used to define this EI based on a linear combination of DM, WSC and BC of forages at harvest time. The quantitative calculated indexes distinguish five successive ranges of ensilability: high ensilability (EI > +28), medium high ensilability (+9 < EI . +28), medium ensilability (.28 < EI . +9), medium low ensilability (.47 . EI . .28) and low ensilability (EI < .47). This quantitative index was externally evaluated and 100% of samples were successfully classified.

Published
2013

18. Common variants at VRK2 and TCF4 conferring risk of schizophrenia

Author

Steinberg, S., Jong, S. de, Andreassen, O.A., Werge, T., Borglum, A.D., Mors, O., Mortensen, P.B., Gustafsson, O., Costas, J., Pietilainen, O.P.H., Demontis, D., Papiol, S., Huttenlocher, J., Mattheisen, M., Breuer, R., Vassos, E., Giegling, I., Fraser, G., Walker, N., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Agartz, I., Melle, I., Djurovic, S., Strengman, E., Jurgens, G., Glenthoj, B., Terenius, L., Hougaard, D.M., Orntoft, T., Wiuf, C., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Winkel, R. van, Kenis, G., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Sperling, S., Rossner, M., Ribolsi, M., Magni, V., Siracusano, A., Christiansen, C., Kiemeney, L.A.L.M., Veldink, J., Berg, L. van den, Ingason, A., Muglia, P., Murray, R., Nothen, Markus, Sigurdsson, E., Petursson, H., Thorsteinsdottir, U., Kong, A., Rubino, I.A., Hert, M. de, Rethelyi, J.M., Bitter, I., Jonsson, E.G., Golimbet, V., Carracedo, A., Ehrenreich, H., Craddock, N., Owen, M.J., O'Donovan, M.C., Ruggeri, M., Tosato, S., Peltonen, L., Ophoff, R.A., Collier, D.A., St Clair, D., Rietschel, M., Cichon, S., Stefansson, H., Rujescu, D., Stefansson, K., Steinberg, S., Jong, S. de, Andreassen, O.A., Werge, T., Borglum, A.D., Mors, O., Mortensen, P.B., Gustafsson, O., Costas, J., Pietilainen, O.P.H., Demontis, D., Papiol, S., Huttenlocher, J., Mattheisen, M., Breuer, R., Vassos, E., Giegling, I., Fraser, G., Walker, N., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Agartz, I., Melle, I., Djurovic, S., Strengman, E., Jurgens, G., Glenthoj, B., Terenius, L., Hougaard, D.M., Orntoft, T., Wiuf, C., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Winkel, R. van, Kenis, G., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Sperling, S., Rossner, M., Ribolsi, M., Magni, V., Siracusano, A., Christiansen, C., Kiemeney, L.A.L.M., Veldink, J., Berg, L. van den, Ingason, A., Muglia, P., Murray, R., Nothen, Markus, Sigurdsson, E., Petursson, H., Thorsteinsdottir, U., Kong, A., Rubino, I.A., Hert, M. de, Rethelyi, J.M., Bitter, I., Jonsson, E.G., Golimbet, V., Carracedo, A., Ehrenreich, H., Craddock, N., Owen, M.J., O'Donovan, M.C., Ruggeri, M., Tosato, S., Peltonen, L., Ophoff, R.A., Collier, D.A., St Clair, D., Rietschel, M., Cichon, S., Stefansson, H., Rujescu, D., and Stefansson, K.

Abstract

Contains fulltext : 97739.pdf (publisher's version ) (Closed access), Common sequence variants have recently joined rare structural polymorphisms as genetic factors with strong evidence for association with schizophrenia. Here we extend our previous genome-wide association study and meta-analysis (totalling 7 946 cases and 19 036 controls) by examining an expanded set of variants using an enlarged follow-up sample (up to 10 260 cases and 23 500 controls). In addition to previously reported alleles in the major histocompatibility complex region, near neurogranin (NRGN) and in an intron of transcription factor 4 (TCF4), we find two novel variants showing genome-wide significant association: rs2312147[C], upstream of vaccinia-related kinase 2 (VRK2) [odds ratio (OR) = 1.09, P = 1.9 x 10(-9)] and rs4309482[A], between coiled-coiled domain containing 68 (CCDC68) and TCF4, about 400 kb from the previously described risk allele, but not accounted for by its association (OR = 1.09, P = 7.8 x 10(-9)).

Published
2011

19. Common variants at VRK2 and TCF4 conferring risk of schizophrenia

Author

Steinberg, S., Jong, S. de, Andreassen, O.A., Werge, T., Borglum, A.D., Mors, O., Mortensen, P.B., Gustafsson, O., Costas, J., Pietilainen, O.P.H., Demontis, D., Papiol, S., Huttenlocher, J., Mattheisen, M., Breuer, R., Vassos, E., Giegling, I., Fraser, G., Walker, N., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Agartz, I., Melle, I., Djurovic, S., Strengman, E., Jurgens, G., Glenthoj, B., Terenius, L., Hougaard, D.M., Orntoft, T., Wiuf, C., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Winkel, R. van, Kenis, G., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Sperling, S., Rossner, M., Ribolsi, M., Magni, V., Siracusano, A., Christiansen, C., Kiemeney, L.A.L.M., Veldink, J., Berg, L. van den, Ingason, A., Muglia, P., Murray, R., Nothen, Markus, Sigurdsson, E., Petursson, H., Thorsteinsdottir, U., Kong, A., Rubino, I.A., Hert, M. de, Rethelyi, J.M., Bitter, I., Jonsson, E.G., Golimbet, V., Carracedo, A., Ehrenreich, H., Craddock, N., Owen, M.J., O'Donovan, M.C., Ruggeri, M., Tosato, S., Peltonen, L., Ophoff, R.A., Collier, D.A., St Clair, D., Rietschel, M., Cichon, S., Stefansson, H., Rujescu, D., Stefansson, K., Steinberg, S., Jong, S. de, Andreassen, O.A., Werge, T., Borglum, A.D., Mors, O., Mortensen, P.B., Gustafsson, O., Costas, J., Pietilainen, O.P.H., Demontis, D., Papiol, S., Huttenlocher, J., Mattheisen, M., Breuer, R., Vassos, E., Giegling, I., Fraser, G., Walker, N., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Agartz, I., Melle, I., Djurovic, S., Strengman, E., Jurgens, G., Glenthoj, B., Terenius, L., Hougaard, D.M., Orntoft, T., Wiuf, C., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Winkel, R. van, Kenis, G., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Sperling, S., Rossner, M., Ribolsi, M., Magni, V., Siracusano, A., Christiansen, C., Kiemeney, L.A.L.M., Veldink, J., Berg, L. van den, Ingason, A., Muglia, P., Murray, R., Nothen, Markus, Sigurdsson, E., Petursson, H., Thorsteinsdottir, U., Kong, A., Rubino, I.A., Hert, M. de, Rethelyi, J.M., Bitter, I., Jonsson, E.G., Golimbet, V., Carracedo, A., Ehrenreich, H., Craddock, N., Owen, M.J., O'Donovan, M.C., Ruggeri, M., Tosato, S., Peltonen, L., Ophoff, R.A., Collier, D.A., St Clair, D., Rietschel, M., Cichon, S., Stefansson, H., Rujescu, D., and Stefansson, K.

Abstract

Contains fulltext : 97739.pdf (publisher's version ) (Closed access), Common sequence variants have recently joined rare structural polymorphisms as genetic factors with strong evidence for association with schizophrenia. Here we extend our previous genome-wide association study and meta-analysis (totalling 7 946 cases and 19 036 controls) by examining an expanded set of variants using an enlarged follow-up sample (up to 10 260 cases and 23 500 controls). In addition to previously reported alleles in the major histocompatibility complex region, near neurogranin (NRGN) and in an intron of transcription factor 4 (TCF4), we find two novel variants showing genome-wide significant association: rs2312147[C], upstream of vaccinia-related kinase 2 (VRK2) [odds ratio (OR) = 1.09, P = 1.9 x 10(-9)] and rs4309482[A], between coiled-coiled domain containing 68 (CCDC68) and TCF4, about 400 kb from the previously described risk allele, but not accounted for by its association (OR = 1.09, P = 7.8 x 10(-9)).

Published
2011

20. Common variants at VRK2 and TCF4 conferring risk of schizophrenia

Author

Steinberg, S., Jong, S. de, Andreassen, O.A., Werge, T., Borglum, A.D., Mors, O., Mortensen, P.B., Gustafsson, O., Costas, J., Pietilainen, O.P.H., Demontis, D., Papiol, S., Huttenlocher, J., Mattheisen, M., Breuer, R., Vassos, E., Giegling, I., Fraser, G., Walker, N., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Agartz, I., Melle, I., Djurovic, S., Strengman, E., Jurgens, G., Glenthoj, B., Terenius, L., Hougaard, D.M., Orntoft, T., Wiuf, C., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Winkel, R. van, Kenis, G., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Sperling, S., Rossner, M., Ribolsi, M., Magni, V., Siracusano, A., Christiansen, C., Kiemeney, L.A.L.M., Veldink, J., Berg, L. van den, Ingason, A., Muglia, P., Murray, R., Nothen, Markus, Sigurdsson, E., Petursson, H., Thorsteinsdottir, U., Kong, A., Rubino, I.A., Hert, M. de, Rethelyi, J.M., Bitter, I., Jonsson, E.G., Golimbet, V., Carracedo, A., Ehrenreich, H., Craddock, N., Owen, M.J., O'Donovan, M.C., Ruggeri, M., Tosato, S., Peltonen, L., Ophoff, R.A., Collier, D.A., St Clair, D., Rietschel, M., Cichon, S., Stefansson, H., Rujescu, D., Stefansson, K., Steinberg, S., Jong, S. de, Andreassen, O.A., Werge, T., Borglum, A.D., Mors, O., Mortensen, P.B., Gustafsson, O., Costas, J., Pietilainen, O.P.H., Demontis, D., Papiol, S., Huttenlocher, J., Mattheisen, M., Breuer, R., Vassos, E., Giegling, I., Fraser, G., Walker, N., Tuulio-Henriksson, A., Suvisaari, J., Lonnqvist, J., Paunio, T., Agartz, I., Melle, I., Djurovic, S., Strengman, E., Jurgens, G., Glenthoj, B., Terenius, L., Hougaard, D.M., Orntoft, T., Wiuf, C., Didriksen, M., Hollegaard, M.V., Nordentoft, M., Winkel, R. van, Kenis, G., Abramova, L.I., Kaleda, V., Arrojo, M., Sanjuan, J., Arango, C., Sperling, S., Rossner, M., Ribolsi, M., Magni, V., Siracusano, A., Christiansen, C., Kiemeney, L.A.L.M., Veldink, J., Berg, L. van den, Ingason, A., Muglia, P., Murray, R., Nothen, Markus, Sigurdsson, E., Petursson, H., Thorsteinsdottir, U., Kong, A., Rubino, I.A., Hert, M. de, Rethelyi, J.M., Bitter, I., Jonsson, E.G., Golimbet, V., Carracedo, A., Ehrenreich, H., Craddock, N., Owen, M.J., O'Donovan, M.C., Ruggeri, M., Tosato, S., Peltonen, L., Ophoff, R.A., Collier, D.A., St Clair, D., Rietschel, M., Cichon, S., Stefansson, H., Rujescu, D., and Stefansson, K.

Abstract

Contains fulltext : 97739.pdf (publisher's version ) (Closed access), Common sequence variants have recently joined rare structural polymorphisms as genetic factors with strong evidence for association with schizophrenia. Here we extend our previous genome-wide association study and meta-analysis (totalling 7 946 cases and 19 036 controls) by examining an expanded set of variants using an enlarged follow-up sample (up to 10 260 cases and 23 500 controls). In addition to previously reported alleles in the major histocompatibility complex region, near neurogranin (NRGN) and in an intron of transcription factor 4 (TCF4), we find two novel variants showing genome-wide significant association: rs2312147[C], upstream of vaccinia-related kinase 2 (VRK2) [odds ratio (OR) = 1.09, P = 1.9 x 10(-9)] and rs4309482[A], between coiled-coiled domain containing 68 (CCDC68) and TCF4, about 400 kb from the previously described risk allele, but not accounted for by its association (OR = 1.09, P = 7.8 x 10(-9)).

Published
2011

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