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2. The effect of polygenic risk score and childhood adversity experiences on transdiagnostic symptom dimensions at first-episode psychosis: evidence for an affective pathway to psychosis

Author

Alameda, Luis, primary, Pérez, Victoria, additional, Forti, Marta di, additional, Spinazzola, Edoardo, additional, Trotta, Giulia, additional, Arango, Celso, additional, Arrojo, Manuel, additional, Bernardo, Miguel, additional, Bobes, Julio, additional, Gayer-Anderson, Charlotte, additional, Del-Ben, Cristina Marta, additional, Sideli, Lucia, additional, Jones, Peter, additional, Kirkbride, James, additional, Cascia, Caterina La, additional, Tripoli, Giada, additional, Ferraro, Laura, additional, Barbera, Daniele La, additional, Lasalvia, Antonio, additional, Tosato, Sarah, additional, Llorca, Pierre Michel, additional, Menezes, Paulo, additional, Os, Jim van, additional, Rutten, Bart, additional, Santos, Jose, additional, Sanjuan, Julio, additional, Selten, Jean-Paul, additional, Szöke, Andrei, additional, Tarricone, Ilaria, additional, Tortelli, Andrea, additional, Velthorst, Eva, additional, Johgsma, Hannah E., additional, Vassos, Evangelos, additional, Quattrone, Diego, additional, Murray, Robin, additional, and Aas, Monica, additional

Published
2024
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3. Methylomic signature of current cannabis use in two first-episode psychosis cohorts

Author

Dempster, Emma, primary, Wong, Chloe, additional, Burrage, Joe, additional, Hannon, Eilis, additional, Quattrone, Diego, additional, Giulia, Trotta, additional, Rodriguez, Victoria, additional, Spinazzola, Edoardo, additional, Tripoli, Giada, additional, Austin-Zimmerman, Isabelle, additional, Li, Z, additional, Gayer-Anderson, Charlotte, additional, Freeman, Tom, additional, Johnson, Emma, additional, Jongsma, Hannah, additional, Simona, Stilo, additional, Cascia, Caterina La, additional, Ferraro, Laura, additional, Barbera, Daniele La, additional, Lasalvia, Antonio, additional, Tosato, Sarah, additional, Tarricone, Ilaria, additional, D’Andrea, Giuseppe, additional, Galatolo, Michela, additional, Tortelli, Andrea, additional, Arango, Celso, additional, Jones, Peter, additional, Pompili, Maurizio, additional, Selten, Jean-Paul, additional, de Haan, Lieuwe, additional, Menezes, Paulo, additional, Del-Ben, Cristina Marta, additional, Santos, José, additional, Arrojo, Manuel, additional, Bobes, Julio, additional, Sanjuan, Julio, additional, Bernardo, Miquel, additional, Breen, Gerome, additional, Mondelli, Valeria, additional, Dazzan, Paola, additional, Iyegbe, Conrad, additional, Vassos, Evangelos, additional, Morgan, Craig, additional, Mukherjee, Diptendu, additional, Os, Jim van, additional, Rutten, Bart, additional, O'Donovan, Michael, additional, Sham, Pak, additional, Mill, Jonathan, additional, Murray, Robin, additional, Forti, Marta di, additional, and Alameda, Luis, additional

Published
2023
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4. Clustering Schizophrenia Genes by Their Temporal Expression Patterns Aids Functional Interpretation.

Author

van der Meer, Dennis, Cheng, Weiqiu, Rokicki, Jaroslav, Fernandez-Cabello, Sara, Shadrin, Alexey, Smeland, Olav B, Ehrhart, Friederike, Gülöksüz, Sinan, Pries, Lotta-Katrin, Lin, Bochao, Rutten, Bart P F, Os, Jim van, O'Donovan, Michael, Richards, Alexander L, Steen, Nils Eiel, Djurovic, Srdjan, Westlye, Lars T, Andreassen, Ole A, Kaufmann, Tobias, and (GROUP), Genetic Risk and Outcome of Psychosis investigators

Subjects
GENETICS of schizophrenia, RISK assessment, CLUSTER analysis (Statistics), RESEARCH funding, FUNCTIONAL assessment, NEURAL development, BRAIN, TRANSCRIPTION factors, CELL cycle, IMMUNE system, GENE expression
Abstract

Background Schizophrenia is a highly heritable brain disorder with a typical symptom onset in early adulthood. The 2-hit hypothesis posits that schizophrenia results from differential early neurodevelopment, predisposing an individual, followed by a disruption of later brain maturational processes that trigger the onset of symptoms. Study design We applied hierarchical clustering to transcription levels of 345 genes previously linked to schizophrenia, derived from cortical tissue samples from 56 donors across the lifespan. We subsequently calculated clustered-specific polygenic risk scores for 743 individuals with schizophrenia and 743 sex- and age-matched healthy controls. Study results Clustering revealed a set of 183 genes that was significantly upregulated prenatally and downregulated postnatally and 162 genes that showed the opposite pattern. The prenatally upregulated set of genes was functionally annotated to fundamental cell cycle processes, while the postnatally upregulated set was associated with the immune system and neuronal communication. We found an interaction between the 2 scores; higher prenatal polygenic risk showed a stronger association with schizophrenia diagnosis at higher levels of postnatal polygenic risk. Importantly, this finding was replicated in an independent clinical cohort of 3233 individuals. Conclusions We provide genetics-based evidence that schizophrenia is shaped by disruptions of separable biological processes acting at distinct phases of neurodevelopment. The modeling of genetic risk factors that moderate each other's effect, informed by the timing of their expression, will aid in a better understanding of the development of schizophrenia. [ABSTRACT FROM AUTHOR]

Published
2024
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5. Synergistic effects of childhood adversity and polygenic risk in first-episode psychosis: the EU-GEI study

Author

European Commission, South-Eastern Norway Regional Health Authority, Brain and Behavior Research Foundation, Aas, Monica [0000-0002-2338-5826], Aas, Monica, Alameda, Luis, Di Forti, Marta, Quattrone, Diego, Dazzan, Paola, Trotta, Antonella, Ferraro, Laura, Rodríguez, Victoria, Vassos, Evangelos, Sham, Pak C., Tripoli, Giada, La Cascia, Caterina, La Barbera, Daniele, Tarricone, Ilaria, Muratori, Roberto, Berardi, Domenico, Lasalvia, Antonio, Tosato, Sarah, Szöke, Andrei, Llorca, Pierre-Michel, Arango, Celso, Tortelli, Andrea, Haan, Lieuwe de, Velthorst, Eva, Bobes, Julio, Bernardo, Miguel, Sanjuán, Julio, Santos, José Luis, Arrojo, Manuel, Del-Ben, Cristina Marta, Menezes, Paulo Rossi, Selten, Jean-Paul, Jones, Peter B., Jongsma, Hannah E., Kirkbride, James B., Rutten, Bart P. F., Os, Jim van, Gayer-Anderson, Charlotte, Murray, Robin M., Morgan, Craig, European Commission, South-Eastern Norway Regional Health Authority, Brain and Behavior Research Foundation, Aas, Monica [0000-0002-2338-5826], Aas, Monica, Alameda, Luis, Di Forti, Marta, Quattrone, Diego, Dazzan, Paola, Trotta, Antonella, Ferraro, Laura, Rodríguez, Victoria, Vassos, Evangelos, Sham, Pak C., Tripoli, Giada, La Cascia, Caterina, La Barbera, Daniele, Tarricone, Ilaria, Muratori, Roberto, Berardi, Domenico, Lasalvia, Antonio, Tosato, Sarah, Szöke, Andrei, Llorca, Pierre-Michel, Arango, Celso, Tortelli, Andrea, Haan, Lieuwe de, Velthorst, Eva, Bobes, Julio, Bernardo, Miguel, Sanjuán, Julio, Santos, José Luis, Arrojo, Manuel, Del-Ben, Cristina Marta, Menezes, Paulo Rossi, Selten, Jean-Paul, Jones, Peter B., Jongsma, Hannah E., Kirkbride, James B., Rutten, Bart P. F., Os, Jim van, Gayer-Anderson, Charlotte, Murray, Robin M., and Morgan, Craig

Abstract

[Background] A history of childhood adversity is associated with psychotic disorder, with an increase in risk according to the number of exposures. However, it is not known why only some exposed individuals go on to develop psychosis. One possibility is pre-existing polygenic vulnerability. Here, we investigated, in the largest sample of first-episode psychosis (FEP) cases to date, whether childhood adversity and high polygenic risk scores for schizophrenia (SZ-PRS) combine synergistically to increase the risk of psychosis, over and above the effect of each alone., [Methods] We assigned a schizophrenia-polygenic risk score (SZ-PRS), calculated from the Psychiatric Genomics Consortium (PGC2), to all participants in a sample of 384 FEP patients and 690 controls from the case–control component of the EU-GEI study. Only participants of European ancestry were included in the study. A history of childhood adversity was collected using the Childhood Trauma Questionnaire (CTQ). Synergistic effects were estimated using the interaction contrast ratio (ICR) [odds ratio (OR)exposure and PRS − ORexposure − ORPRS + 1] with adjustment for potential confounders., [Results] There was some evidence that the combined effect of childhood adversities and polygenic risk was greater than the sum of each alone, as indicated by an ICR greater than zero [i.e. ICR 1.28, 95% confidence interval (CI) −1.29 to 3.85]. Examining subtypes of childhood adversities, the strongest synergetic effect was observed for physical abuse (ICR 6.25, 95% CI −6.25 to 20.88)., [Conclusions] Our findings suggest possible synergistic effects of genetic liability and childhood adversity experiences in the onset of FEP, but larger samples are needed to increase precision of estimates.

Published
2023

6. A Game of Perspectives: An MRI-Based Analysis of Implicit Mind-Brain Models in Schizophrenia

Author

Álvarez Durán, Pedro, Os, Jim van (Thesis Advisor), Álvarez Durán, Pedro, and Os, Jim van (Thesis Advisor)

Abstract

Our exploration of schizophrenia encompassed a multi-dimensional analysis from three distinct perspectives: research, philosophy, and fieldwork. A central focus of our investigation delved into the intricate relationship between the brain and the mind, with particular attention to the enigmatic explanatory gap that has long challenged our comprehension. Within the realm of research, a prevailing paradigm often implies a model in which the mind emerges as a product of the brain. This prevailing model, alongside the disjointed nature of these three perspectives—research, philosophy, and fieldwork—operating in relative isolation, underscores a critical issue. To transcend these constraints and to advance our understanding of schizophrenia, the brain-mind interaction, and the well-being of patients, we advocate resolutely for a holistic approach. Such an approach harmonizes the biological, social, and psychological dimensions of this complex condition, fostering personalized care strategies tailored to individual clinical profiles while addressing the broader needs of patients, including facets of identity, meaning, and resilience. In essence, our analysis underscores the imperative of unifying these distinct realms of inquiry, emphasizing that a holistic perspective holds the key to not only bridging the persistent gap between the brain and the mind but also to vastly improving the quality of care and support for individuals grappling with schizophrenia, thereby revolutionizing the landscape of mental healthcare.

Published
2023

8. The relationship between genetic liability, childhood maltreatment, and IQ: findings from the EU-GEI multicentric case–control study

Author

European Commission, Sao Paulo Research Foundation, Netherlands Organization for Scientific Research, Economic and Social Research Council (UK), Kings College London, Medical Research Council (UK), Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Ciencia e Innovación (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Comunidad de Madrid, National Institute of Mental Health (US), Fundación Familia Alonso, Fundación Alicia Koplowitz, Sideli, Lucia, Aas, Monica, Quattrone, Diego, La Barbera, Daniele, La Cascia, Caterina, Ferraro, Laura, Alameda, Luis, Velthorst, Eva, Trotta, Giulia, Tripoli, Giada, Schimmenti, Adriano, Fontana, Andrea, Gayer-Anderson, Charlotte, Stilo, Simona, Seminerio, Fabio, Sartorio, Crocettarachele, Marrazzo, Giovanna, Lasalvia, Antonio, Tosato, Sarah, Tarricone, Ilaria, Berardi, Domenico, D’Andrea, Giuseppe, EU-GEI WP2 Group, Arango, Celso, Arrojo, Manuel, Bernardo, Miguel, Bobes, Julio, Sanjuán, Julio, Santos, José Luis, Rossi Menezes, Paulo, Del-Ben, Cristina Marta, Jongsma, Hannah E., Jones, Peter B., Kirkbride, James B., Llorca, Pierre-Michel, Tortelli, Andrea, Pignon, Baptiste, Haan, Lieuwe de, Selten, Jean-Paul, Os, Jim van, Rutten, Bart P. F., Bentall, Richard, Di Forti, Marta, Murray, Robin M., Morgan, Craig, Fisher, Helen L., European Commission, Sao Paulo Research Foundation, Netherlands Organization for Scientific Research, Economic and Social Research Council (UK), Kings College London, Medical Research Council (UK), Ministerio de Ciencia, Innovación y Universidades (España), Ministerio de Ciencia e Innovación (España), Agencia Estatal de Investigación (España), Instituto de Salud Carlos III, Comunidad de Madrid, National Institute of Mental Health (US), Fundación Familia Alonso, Fundación Alicia Koplowitz, Sideli, Lucia, Aas, Monica, Quattrone, Diego, La Barbera, Daniele, La Cascia, Caterina, Ferraro, Laura, Alameda, Luis, Velthorst, Eva, Trotta, Giulia, Tripoli, Giada, Schimmenti, Adriano, Fontana, Andrea, Gayer-Anderson, Charlotte, Stilo, Simona, Seminerio, Fabio, Sartorio, Crocettarachele, Marrazzo, Giovanna, Lasalvia, Antonio, Tosato, Sarah, Tarricone, Ilaria, Berardi, Domenico, D’Andrea, Giuseppe, EU-GEI WP2 Group, Arango, Celso, Arrojo, Manuel, Bernardo, Miguel, Bobes, Julio, Sanjuán, Julio, Santos, José Luis, Rossi Menezes, Paulo, Del-Ben, Cristina Marta, Jongsma, Hannah E., Jones, Peter B., Kirkbride, James B., Llorca, Pierre-Michel, Tortelli, Andrea, Pignon, Baptiste, Haan, Lieuwe de, Selten, Jean-Paul, Os, Jim van, Rutten, Bart P. F., Bentall, Richard, Di Forti, Marta, Murray, Robin M., Morgan, Craig, and Fisher, Helen L.

Abstract

This study investigated if the association between childhood maltreatment and cognition among psychosis patients and community controls was partially accounted for by genetic liability for psychosis. Patients with first-episode psychosis (N = 755) and unaffected controls (N = 1219) from the EU-GEI study were assessed for childhood maltreatment, intelligence quotient (IQ), family history of psychosis (FH), and polygenic risk score for schizophrenia (SZ-PRS). Controlling for FH and SZ-PRS did not attenuate the association between childhood maltreatment and IQ in cases or controls. Findings suggest that these expressions of genetic liability cannot account for the lower levels of cognition found among adults maltreated in childhood.

Published
2023

9. Age-Related Social Cognitive Performance in Individuals With Psychotic Disorders and Their First-Degree Relatives.

Author

Velthorst, Eva, Socrates, Adam, Investigators, GROUP, Alizadeh, Behrooz Z, Amelsvoort, Therese van, Bartels-Velthuis, Agna A, Bruggeman, Richard, Cahn, Wiepke, Haan, Lieuwe de, Schirmbeck, Frederike, Simons, Claudia J P, Os, Jim van, and Fett, Anne-Kathrin

Subjects
THOUGHT & thinking, SOCIAL perception, CONFIDENCE intervals, PSYCHOSES, CROSS-sectional method, SENSORY perception, AGING, DESCRIPTIVE statistics, RESEARCH funding, CHI-squared test, SOCIAL skills, SOCIODEMOGRAPHIC factors, EMOTIONS, LONGITUDINAL method
Abstract

Background Social cognitive impairment is a recognized feature of psychotic disorders. However, potential age-related differences in social cognitive impairment have rarely been studied. Study Design Data came from 905 individuals with a psychotic disorder, 966 unaffected siblings, and 544 never-psychotic controls aged 18–55 who participated in the Genetic Risk and Outcome of Psychosis (GROUP) study. Multilevel linear models were fitted to study group main effects and the interaction between group and age on emotion perception and processing (EPP; degraded facial affect recognition) and theory of mind (ToM; hinting task) performance. Age-related differences in the association between socio-demographic and clinical factors, and EPP and ToM were also explored. Study Results Across groups, EPP performance was associated with age (β = −0.02, z = −7.60, 95% CI: −0.02, −0.01, P <.001), with older participants performing worse than younger ones. A significant group-by-age interaction on ToM (X 2(2) = 13.15, P =.001) indicated that older patients performed better than younger ones, while no age-related difference in performance was apparent among siblings and controls. In patients, the association between negative symptoms and ToM was stronger for younger than older patients (z = 2.16, P =.03). Conclusions The findings point to different age-related performance patterns on tests of 2 key social cognitive domains. ToM performance was better in older individuals, although this effect was only observed for patients. EPP was less accurate in older compared with younger individuals. These findings have implications with respect to when social cognitive training should be offered to patients. [ABSTRACT FROM AUTHOR]

Published
2023
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10. Exploring the mediation of DNA methylation across the epigenome between childhood adversity and First Episode of Psychosis – findings from the EU-GEI study

Author

Alameda, Luis, primary, Liu, Zhonghua, additional, Sham, Pak, additional, Monica, AAS, additional, Giulia, Trotta, additional, Victoria, Rodriguez, additional, Forti, Marta di, additional, Simona, Stilo, additional, Radhika, Kandaswamy, additional, Arango, Celso, additional, Arrojo, Manuel, additional, Bernardo, Miquel, additional, Bobes, Julio, additional, de Haan, Lieuwe, additional, Del-Ben, Cristina, additional, Gayer-Anderson, Charlotte, additional, Lucia, Sideli, additional, Jones, Peter, additional, Jongsma, Hannah, additional, Kirkbride, James, additional, Cascia, Caterina La, additional, Lasalvia, Antonio, additional, Tosato, Sarah, additional, Llorca, Pierre Michel, additional, Menezes, Paulo, additional, Os, Jim van, additional, Diego, Quattrone, additional, Rutten, Bart, additional, Santos, José, additional, Sanjuan, Julio, additional, Selten, Jean-Paul, additional, Szöke, Andrei, additional, Tarricone, Ilaria, additional, Tortelli, Andrea, additional, Velthorst, Eva, additional, Morgan, Craig, additional, Dempster, Emma, additional, Hannon, Eilis, additional, Burrage, Joe, additional, Mill, Jonathan, additional, Murray, Robin, additional, and Wong, Chloe, additional

Published
2022
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11. Genetic and psychosocial stressors have independent effects on the level of subclinical psychosis: findings from the multinational EU-GEI study

Author

Pignon, Baptiste, primary, Peyre, Hugo, additional, Ayrolles, Anaël, additional, Kirkbride, James, additional, Jamain, Stéphane, additional, ferchiou, AZIZ, additional, Richard, Jean-Romain, additional, Baudin, Grégoire, additional, Tosato, Sarah, additional, Jongsma, Hannah, additional, De Haan, Lieuwe, additional, Tarricone, Ilaria, additional, Bernardo, Miquel, additional, Velthorst, Eva, additional, braca, mauro, additional, Arango, Celso, additional, Arrojo, Manuel, additional, Bobes, Julio, additional, Del-Ben, Cristina, additional, Forti, Marta di, additional, Gayer-Anderson, Charlotte, additional, Jones, Peter, additional, Lasalvia, Antonio, additional, Menezes, Paulo, additional, Quattrone, Diego, additional, Sanjuan, Julio, additional, Selten, Jean-Paul, additional, Tortelli, Andrea, additional, Llorca, Pierre Michel, additional, Os, Jim van, additional, Rutten, Bart, additional, Murray, Robin, additional, Morgan, Craig, additional, Leboyer, Marion, additional, Szoke, Andrei, additional, and Schurhof, Franck, additional

Published
2022
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12. Interaction Testing and Polygenic Risk Scoring to Estimate the Association of Common Genetic Variants With Treatment Resistance in Schizophrenia

Author

Pardiñas, Antonio F., Smart, Sophie E., Corvin, Aiden, Freimer, Nelson B., Friedl, Marion, Friedman, Joseph I., Fromer, Menachem, Genovese, Giulio, Georgieva, Lyudmila, Gershon, Elliot S., Giegling, Ina, Giusti-Rodríguez, Paola, Godard, Stephanie, Fanous, Ayman H., Goldstein, Jacqueline I., Golimbet, Vera, Gopal, Srihari, Gratten, Jacob, Haan, Lieuwe de, Hammer, Christian, Hamshere, Marian L., Hansen, Mark, Hansen, Thomas, Haroutunian, Vahram, Frank, Josef, Hartmann, Annette M., Henskens, Frans A., Herms, Stefan, Hirschhorn, Joel N., Hoffmann, Per, Hofman, Andrea, Hollegaard, Mads V., Hougaard, David M., Ikeda, Masashi, Joa, Inge, Kelly, Brian, Julià, Antonio, Kahn, René S., Kalaydjieva, Luba, Karachanak-Yankova, Sena, Karjalainen, Juha, Kavanagh, David, Keller, Matthew C., Kennedy, James L., Khrunin, Andrey, Kim, Yunjung, McQuillin, Andrew, Klovins, Janis, Knowles, James A., Konte, Bettina, Kucinskas, Vaidutis, Kucinskiene, Zita Ausrele, Kuzelova-Ptackova, Hana, Kähler, Anna K., Laurent, Claudine, Keong, Jimmy Lee Chee, Lee, S. Hong, Melle, Ingrid, Lerer, Bernard, Li, Miaoxin, Li, Tao, Liang, Kung-Yee, Lieberman, Jeffrey, Limborska, Svetlana, Loughland, Carmel M., Lubinski, Jan, Lönnqvist, Jouko, Macek, Milan, Mortensen, Preben B., Magnusson, Patrik K. E., Maher, Brion S., Maier, Wolfgang, Mallet, Jacques, Marsal, Sara, Mattheisen, Manuel, Mattingsdal, Morten, McCarley, Robert W., McDonald, Colm, McIntosh, Andrew M., Mowry, Bryan J., Meier, Sandra, Meijer, Carin J., Melegh, Bela, Mesholam-Gately, Raquelle I., Metspalu, Andres, Michie, Patricia T., Milani, Lili, Milanova, Vihra, Mokrab, Younes, Pato, Carlos N., Morris, Derek W., Mors, Ole, Murphy, Kieran C., Myin-Germeys, Inez, Müller-Myhsok, Bertram, Nelis, Mari, Nenadic, Igor, Nertney, Deborah A., Nestadt, Gerald, Nicodemus, Kristin K., Periyasamy, Sathish, Nikitina-Zake, Liene, Nisenbaum, Laura, Nordin, Annelie, O’Callaghan, Eadbhard, O’Dushlaine, Colm, O’Neill, F. Anthony, Oh, Sang-Yun, Olincy, Ann, Olsen, Line, Os, Jim Van, Willcocks, Isabella R., Rietschel, Marcella, Pantelis, Christos, Papadimitriou, George N., Papiol, Sergi, Parkhomenko, Elena, Pato, Michele T., Paunio, Tiina, Pejovic-Milovancevic, Milica, Perkins, Diana O., Pietiläinen, Olli, Pimm, Jonathan, Rujescu, Dan, Pocklington, Andrew J., Powell, John, Price, Alkes, Pulver, Ann E., Purcell, Shaun M., Quested, Digby, Rasmussen, Henrik B., Reichenberg, Abraham, Reimers, Mark A., Richards, Alexander L., Simonsen, Carmen, Roffman, Joshua L., Roussos, Panos, Ruderfer, Douglas M., Salomaa, Veikko, Sanders, Alan R., Schall, Ulrich, Schubert, Christian R., Schulze, Thomas G., Schwab, Sibylle G., Scolnick, Edward M., St Clair, David, Scott, Rodney J., Seidman, Larry J., Shi, Jianxin, Sigurdsson, Engilbert, Silagadze, Teimuraz, Silverman, Jeremy M., Sim, Kang, Slominsky, Petr, Smoller, Jordan W., So, Hon-Cheong, Tooney, Paul, Spencer, Chris C. A., Stahl, Eli A., Stefansson, Hreinn, Steinberg, Stacy, Stogmann, Elisabeth, Straub, Richard E., Strengman, Eric, Strohmaier, Jana, Stroup, T. Scott, Subramaniam, Mythily, Wu, Jing Qin, Suvisaari, Jaana, Svrakic, Dragan M., Szatkiewicz, Jin P., Söderman, Erik, Thirumalai, Srinivas, Toncheva, Draga, Tosato, Sarah, Veijola, Juha, Waddington, John, Walsh, Dermot, Andreassen, Ole A., Wang, Dai, Wang, Qiang, Webb, Bradley T., Weiser, Mark, Wildenauer, Dieter B., Williams, Nigel M., Williams, Stephanie, Witt, Stephanie H., Wolen, Aaron R., Wong, Emily H. M., Kowalec, Kaarina, Wormley, Brandon K., Xi, Hualin Simon, Zai, Clement C., Zheng, Xuebin, Zimprich, Fritz, Wray, Naomi R., Stefansson, Kari, Visscher, Peter M., Adolfsson, Rolf, Blackwood, Douglas H. R., Sullivan, Patrick F., Bramon, Elvira, Buxbaum, Joseph D., Børglum, Anders D., Cichon, Sven, Darvasi, Ariel, Domenici, Enrico, Ehrenreich, Hannelore, Esko, Tõnu, Gejman, Pablo V., Gill, Michael, Murray, Robin M., Gurling, Hugh, Hultman, Christina M., Iwata, Nakao, Jablensky, Assen V., Jönsson, Erik G., Kendler, Kenneth S., Kirov, George, Knight, Jo, Lencz, Todd, Levinson, Douglas F., Holmans, Peter A., Owen, Michael J., Li, Qingqin S., Liu, Jianjun, Malhotra, Anil K., McCarroll, Steven A., Moran, Jennifer L., Nöthen, Markus M., Ophoff, Roel A., Palotie, Aarno, Petryshen, Tracey L., MacCabe, James H., Posthuma, Danielle, Riley, Brien P., Sham, Pak C., Sklar, Pamela, Clair, David St, Weinberger, Daniel R., Wendland, Jens R., Werge, Thomas, Daly, Mark J., Agbedjro, Deborah, O’Donovan, Michael C., Stahl, Daniel, Kapur, Shitij, Millgate, Edward, Kepinska, Adrianna, Kravariti, Eugenia, Ajnakina, Olesya, Alameda, Luis, Barnes, Thomas R. E., Berardi, Domenico, Bonora, Elena, Walters, James T. R., Camporesi, Sara, Cleusix, Martine, Conus, Philippe, Crespo-Facorro, Benedicto, D’Andrea, Giuseppe, Demjaha, Arsime, Do, Kim Q., Doody, Gillian A., Eap, Chin B., Ferchiou, Aziz, Ripke, Stephan, Di Forti, Marta, Guidi, Lorenzo, Homman, Lina, Jenni, Raoul, Joyce, Eileen M., Kassoumeri, Laura, Khadimallah, Inès, Lastrina, Ornella, Muratori, Roberto, Noyan, Handan, Neale, Benjamin M., O’Neill, Francis A., Pignon, Baptiste, Restellini, Romeo, Richard, Jean-Romain, Schürhoff, Franck, Španiel, Filip, Szöke, Andrei, Tarricone, Ilaria, Tortelli, Andrea, Üçok, Alp, Farh, Kai-How, Vázquez-Bourgon, Javier, Lee, Phil, Bulik-Sullivan, Brendan, Collier, David A., Dennison, Charlotte A., Huang, Hailiang, Pers, Tune H., Agartz, Ingrid, Agerbo, Esben, Albus, Margot, Alexander, Madeline, Amin, Farooq, Bacanu, Silviu A., Begemann, Martin, Belliveau, Richard A ., Lynham, Amy J., Bene, Judit, Bergen, Sarah E., Bevilacqua, Elizabeth, Black, Donald W., Bruggeman, Richard, Buccola, Nancy G., Buckner, Randy L., Byerley, William, Cahn, Wiepke, Cai, Guiqing, Legge, Sophie E., Campion, Dominique, Cantor, Rita M., Carr, Vaughan J., Carrera, Noa, Catts, Stanley V., Chambert, Kimberly D., Chan, Raymond C. K., Chen, Ronald Y. L., Chen, Eric Y. H., Cheng, Wei, Baune, Bernhard T., Cheung, Eric F. C., Chong, Siow Ann, Cloninger, C. Robert, Cohen, David, Cohen, Nadine, Cormican, Paul, Craddock, Nick, Crowley, James J., Curtis, David, Davidson, Michael, Bigdeli, Tim B., Davis, Kenneth L., Degenhardt, Franziska, Favero, Jurgen Del, DeLisi, Lynn E., Demontis, Ditte, Dikeos, Dimitris, Dinan, Timothy, Djurovic, Srdjan, Donohoe, Gary, Drapeau, Elodie, Cairns, Murray J., Duan, Jubao, Dudbridge, Frank, Durmishi, Naser, Eichhammer, Peter, Eriksson, Johan, Escott-Price, Valentina, Essioux, Laurent, Farrell, Martilias S., Franke, Lude, Freedman, Robert, Genetics Workstream of the Schizophrenia Treatment Resistance and Therapeutic Advances (STRATA) Consortium and the Schizophrenia Working Group of the Psychiatric Genomics Consortium (PGC), Ripke, S., Neale, B.M., Farh, K.H., Lee, P., Bulik-Sullivan, B., Collier, D.A., Huang, H., Pers, T.H., Agartz, I., Agerbo, E., Albus, M., Alexander, M., Amin, F., Bacanu, S.A., Begemann, M., Belliveau, R.A., Bene, J., Bergen, S.E., Bevilacqua, E., Black, D.W., Bruggeman, R., Buccola, N.G., Buckner, R.L., Byerley, W., Cahn, W., Cai, G., Campion, D., Cantor, R.M., Carr, V.J., Carrera, N., Catts, S.V., Chambert, K.D., Chan, RCK, Chen, RYL, Chen, EYH, Cheng, W., Cheung, EFC, Chong, S.A., Cloninger, C.R., Cohen, D., Cohen, N., Cormican, P., Craddock, N., Crowley, J.J., Curtis, D., Davidson, M., Davis, K.L., Degenhardt, F., Favero, J.D., DeLisi, L.E., Demontis, D., Dikeos, D., Dinan, T., Djurovic, S., Donohoe, G., Drapeau, E., Duan, J., Dudbridge, F., Durmishi, N., Eichhammer, P., Eriksson, J., Escott-Price, V., Essioux, L., Farrell, M.S., Franke, L., Freedman, R., Freimer, N.B., Friedl, M., Friedman, J.I., Fromer, M., Genovese, G., Georgieva, L., Gershon, E.S., Giegling, I., Giusti-Rodríguez, P., Godard, S., Goldstein, J.I., Golimbet, V., Gopal, S., Gratten, J., Haan, L., Hammer, C., Hamshere, M.L., Hansen, M., Hansen, T., Haroutunian, V., Hartmann, A.M., Henskens, F.A., Herms, S., Hirschhorn, J.N., Hoffmann, P., Hofman, A., Hollegaard, M.V., Hougaard, D.M., Ikeda, M., Joa, I., Julià, A., Kahn, R.S., Kalaydjieva, L., Karachanak-Yankova, S., Karjalainen, J., Kavanagh, D., Keller, M.C., Kennedy, J.L., Khrunin, A., Kim, Y., Klovins, J., Knowles, J.A., Konte, B., Kucinskas, V., Kucinskiene, Z.A., Kuzelova-Ptackova, H., Kähler, A.K., Laurent, C., Keong, JLC, Lee, S.H., Lerer, B., Li, M., Li, T., Liang, K.Y., Lieberman, J., Limborska, S., Loughland, C.M., Lubinski, J., Lönnqvist, J., Macek, M., Magnusson, PKE, Maher, B.S., Maier, W., Mallet, J., Marsal, S., Mattheisen, M., Mattingsdal, M., McCarley, R.W., McDonald, C., McIntosh, A.M., Meier, S., Meijer, C.J., Melegh, B., Melle, I., Mesholam-Gately, R.I., Metspalu, A., Michie, P.T., Milani, L., Milanova, V., Mokrab, Y., Morris, D.W., Mors, O., Murphy, K.C., Myin-Germeys, I., Müller-Myhsok, B., Nelis, M., Nenadic, I., Nertney, D.A., Nestadt, G., Nicodemus, K.K., Nikitina-Zake, L., Nisenbaum, L., Nordin, A., O'Callaghan, E., O'Dushlaine, C., O'Neill, F.A., Oh, S.Y., Olincy, A., Olsen, L., Os, J.V., Pantelis, C., Papadimitriou, G.N., Papiol, S., Parkhomenko, E., Pato, M.T., Paunio, T., Pejovic-Milovancevic, M., Perkins, D.O., Pietiläinen, O., Pimm, J., Pocklington, A.J., Powell, J., Price, A., Pulver, A.E., Purcell, S.M., Quested, D., Rasmussen, H.B., Reichenberg, A., Reimers, M.A., Richards, A.L., Roffman, J.L., Roussos, P., Ruderfer, D.M., Salomaa, V., Sanders, A.R., Schall, U., Schubert, C.R., Schulze, T.G., Schwab, S.G., Scolnick, E.M., Scott, R.J., Seidman, L.J., Shi, J., Sigurdsson, E., Silagadze, T., Silverman, J.M., Sim, K., Slominsky, P., Smoller, J.W., So, H.C., Spencer, CCA, Stahl, E.A., Stefansson, H., Steinberg, S., Stogmann, E., Straub, R.E., Strengman, E., Strohmaier, J., Stroup, T.S., Subramaniam, M., Suvisaari, J., Svrakic, D.M., Szatkiewicz, J.P., Söderman, E., Thirumalai, S., Toncheva, D., Tosato, S., Veijola, J., Waddington, J., Walsh, D., Wang, D., Wang, Q., Webb, B.T., Weiser, M., Wildenauer, D.B., Williams, N.M., Williams, S., Witt, S.H., Wolen, A.R., Wong, EHM, Wormley, B.K., Xi, H.S., Zai, C.C., Zheng, X., Zimprich, F., Wray, N.R., Stefansson, K., Visscher, P.M., Adolfsson, R., Blackwood, DHR, Bramon, E., Buxbaum, J.D., Børglum, A.D., Cichon, S., Darvasi, A., Domenici, E., Ehrenreich, H., Esko, T., Gejman, P.V., Gill, M., Gurling, H., Hultman, C.M., Iwata, N., Jablensky, A.V., Jönsson, E.G., Kendler, K.S., Kirov, G., Knight, J., Lencz, T., Levinson, D.F., Li, Q.S., Liu, J., Malhotra, A.K., McCarroll, S.A., Moran, J.L., Mortensen, P.B., Nöthen, M.M., Ophoff, R.A., Palotie, A., Petryshen, T.L., Posthuma, D., Riley, B.P., Sham, P.C., Sklar, P., Clair, D.S., Weinberger, D.R., Wendland, J.R., Werge, T., Daly, M.J., Agbedjro, D., Stahl, D., Kapur, S., Millgate, E., Kepinska, A., Kravariti, E., Medical Research Council (UK), Cardiff University, Welsh Government, Health and Care Research Wales, European Commission, Academy of Medical Sciences (UK), Research Council of Norway, K. G. Jebsen Centres for Medical Research, National Institute for Health Research (UK), University College London, Government of Canada, University of Manitoba, Swedish Research Council, National Institute of Mental Health (US), Kings College London, Public Health Agency (Northern Ireland), The Psychiatry Research Trust, Maudsley Charity, Swiss National Science Foundation, Fondation Alamaya, Ministry of Health of the Czech Republic, Instituto de Salud Carlos III, Plan Nacional sobre Drogas (España), Fundació Seny, Fundación Marques de Valdecilla, Ministerio de Economía y Competitividad (España), Wellcome Trust, and Universidad de Cantabria

Subjects
Male, endocrine system, Multifactorial Inheritance, animal structures, Psychiatry and Behavioral Health, Online First, Humans, Genetic Predisposition to Disease, ddc:610, Neurogenetics, Medicinsk genetik, Original Investigation, Research, Schizophrenia Sprectum and Other Psychotic Disorders, Featured, Genetics and genomics, Psychiatry and Mental health, Neurology, Psychotic Disorders, Schizophrenia, Female, Medical Genetics, hormones, hormone substitutes, and hormone antagonists, Comments, Genome-Wide Association Study
Abstract

[Importance] About 20% to 30% of people with schizophrenia have psychotic symptoms that do not respond adequately to first-line antipsychotic treatment. This clinical presentation, chronic and highly disabling, is known as treatment-resistant schizophrenia (TRS). The causes of treatment resistance and their relationships with causes underlying schizophrenia are largely unknown. Adequately powered genetic studies of TRS are scarce because of the difficulty in collecting data from well-characterized TRS cohorts., [Objective] To examine the genetic architecture of TRS through the reassessment of genetic data from schizophrenia studies and its validation in carefully ascertained clinical samples., [Design, Setting, and Participants] Two case-control genome-wide association studies (GWASs) of schizophrenia were performed in which the case samples were defined as individuals with TRS (n = 10 501) and individuals with non-TRS (n = 20 325). The differences in effect sizes for allelic associations were then determined between both studies, the reasoning being such differences reflect treatment resistance instead of schizophrenia. Genotype data were retrieved from the CLOZUK and Psychiatric Genomics Consortium (PGC) schizophrenia studies. The output was validated using polygenic risk score (PRS) profiling of 2 independent schizophrenia cohorts with TRS and non-TRS: a prevalence sample with 817 individuals (Cardiff Cognition in Schizophrenia [CardiffCOGS]) and an incidence sample with 563 individuals (Genetics Workstream of the Schizophrenia Treatment Resistance and Therapeutic Advances [STRATA-G])., [Main Outcomes and Measures] GWAS of treatment resistance in schizophrenia. The results of the GWAS were compared with complex polygenic traits through a genetic correlation approach and were used for PRS analysis on the independent validation cohorts using the same TRS definition., [Results] The study included a total of 85 490 participants (48 635 [56.9%] male) in its GWAS stage and 1380 participants (859 [62.2%] male) in its PRS validation stage. Treatment resistance in schizophrenia emerged as a polygenic trait with detectable heritability (1% to 4%), and several traits related to intelligence and cognition were found to be genetically correlated with it (genetic correlation, 0.41-0.69). PRS analysis in the CardiffCOGS prevalence sample showed a positive association between TRS and a history of taking clozapine (r2 = 2.03%; P = .001), which was replicated in the STRATA-G incidence sample (r2 = 1.09%; P = .04)., [Conclusions and Relevance] In this GWAS, common genetic variants were differentially associated with TRS, and these associations may have been obscured through the amalgamation of large GWAS samples in previous studies of broadly defined schizophrenia. Findings of this study suggest the validity of meta-analytic approaches for studies on patient outcomes, including treatment resistance., This work was supported by Medical Research Council Centre grant MR/L010305/1, Medical Research Council Program grant MR/P005748/1, and Medical Research Council Project grants MR/L011794/1 and MC_PC_17212 to Cardiff University and by the National Centre for Mental Health, funded by the Welsh Government through Health and Care Research Wales. This work acknowledges the support of the Supercomputing Wales project, which is partially funded by the European Regional Development Fund via the Welsh Government. Dr Pardiñas was supported by an Academy of Medical Sciences Springboard Award (SBF005\1083). Dr Andreassen was supported by the Research Council of Norway (grants 283798, 262656, 248980, 273291, 248828, 248778, and 223273); KG Jebsen Stiftelsen, South-East Norway Health Authority, and the European Union’s Horizon 2020 Research and Innovation Programme (grant 847776). Dr Ajnakina was supported by an National Institute for Health Research postdoctoral fellowship (PDF-2018-11-ST2-020). Dr Joyce was supported by the University College London Hospitals/UCL University College London Biomedical Research Centre. Dr Kowalec received funding from the European Union’s Horizon 2020 Research and Innovation Programme under the Marie Skłodowska-Curie grant agreement (793530) from the government of Canada Banting postdoctoral fellowship programme and the University of Manitoba. Dr Sullivan was supported by the Swedish Research Council (Vetenskapsrådet, D0886501), the European Union’s Horizon 2020 programme (COSYN, 610307) and the US National Institute of Mental Health (U01 MH109528 and R01 MH077139). The Psychiatric Genomics Consortium was partly supported by the National Institute Of Mental Health (grants R01MH124873). The Sweden Schizophrenia Study was supported by the National Institute Of Mental Health (grant R01MH077139). The STRATA consortium was supported by a Stratified Medicine Programme grant to Dr MacCabe from the Medical Research Council (grant MR/L011794/1), which funded the research and supported Drs Pardiñas, Smart, Kassoumeri, Murray, Walters, and MacCabe. Dr Smart was supported by a Collaboration for Leadership in Applied Health Research and Care South London at King’s College Hospital National Health Service Foundation Trust. The AESOP (US) cohort was funded by the UK Medical Research Council (grant G0500817). The Belfast (UK) cohort was funded by the Research and Development Office of Northern Ireland. The Bologna (Italy) cohort was funded by the European Community’s Seventh Framework program (HEALTH-F2-2010–241909, project EU-GEI). The Genetics and Psychosis project (London, UK) cohort was funded by the UK National Institute of Health Research Specialist Biomedical Research Centre for Mental Health, South London and the Maudsley National Health Service Mental Health Foundation Trust (SLAM) and the Institute of Psychiatry, Psychology, and Neuroscience at King’s College London; Psychiatry Research Trust; Maudsley Charity Research Fund; and the European Community’s Seventh Framework program (HEALTH-F2-2009-241909, project EU-GEI). The Lausanne (Switzerland) cohort was funded by the Swiss National Science Foundation (grants 320030_135736/1, 320030-120686, 324730-144064, 320030-173211, and 171804); the National Center of Competence in Research Synaptic Bases of Mental Diseases from the Swiss National Science Foundation (grant 51AU40_125759); and Fondation Alamaya. The Oslo (Norway) cohort was funded by the Research Council of Norway (grant 223273/F50, under the Centers of Excellence funding scheme, 300309, 283798) and the South-Eastern Norway Regional Health Authority (grants 2006233, 2006258, 2011085, 2014102, 2015088, and 2017-112). The Paris (France) cohort was funded by European Community’s Seventh Framework program (HEALTH-F2-2010–241909, project EU-GEI). The Prague (Czech Republic) cohort was funded by the Ministry of Health of the Czech Republic (grant NU20-04-00393). The Santander (Spain) cohort was funded by the following grants to Dr Crespo-Facorro: Instituto de Salud Carlos III (grants FIS00/3095, PI020499, PI050427, and PI060507), Plan Nacional de Drogas Research (grant 2005-Orden sco/3246/2004), SENY Fundatio Research (grant 2005-0308007), Fundacion Marques de Valdecilla (grant A/02/07, API07/011) and Ministry of Economy and Competitiveness and the European Fund for Regional Development (grants SAF2016-76046-R and SAF2013-46292-R). The West London (UK) cohort was funded by The Wellcome Trust (grants 042025, 052247, and 064607).

Published
2022
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13. Impact of adverse childhood experiences on educational achievements in young people at clinical high risk of developing psychosis.

Author

Tognin, Stefania, Catalan, Ana, Kempton, Matthew J., Nelson, Barnaby, McGorry, Patrick, Riecher-Rössler, Anita, Bressan, Rodrigo, Barrantes-Vidal, Neus, Krebs, Marie-Odile, Nordentoft, Merete, Ruhrmann, Stephan, Sachs, Gabriele, Rutten, Bart P. F., Os, Jim van, de Haan, Lieuwe, van der Gaag, Mark, McGuire, Philip, and Valmaggia, Lucia R.

Subjects
YOUNG adults, ADVERSE childhood experiences, ACADEMIC achievement, PHYSICAL abuse, PSYCHOSES, EMPLOYMENT statistics, INTELLIGENCE tests, PSYCHOLOGICAL abuse
Abstract

Background. Adverse childhood experiences (ACE) can affect educational attainments, but little is known about their impact on educational achievements in people at clinical high risk of psychosis (CHR). Methods. In total, 344 CHR individuals and 67 healthy controls (HC) were recruited as part of the European Community’s Seventh Framework Programme-funded multicenter study the European Network of National Schizophrenia Networks Studying Gene–Environment Interactions (EU-GEI). The brief version of the Child Trauma Questionnaire was used to measure ACE, while educational attainments were assessed using a semi-structured interview. Results. At baseline, compared with HC, the CHR group spent less time in education and had higher rates of ACE, lower rates of employment, and lower estimated intelligence quotient (IQ). Across both groups, the total number of ACE was associated with fewer days in education and lower level of education. Emotional abuse was associated with fewer days in education in HC. Emotional neglect was associated with a lower level of education in CHR, while sexual abuse was associated with a lower level of education in HC. In the CHR group, the total number of ACE, physical abuse, and neglect was significantly associated with unemployment, while emotional neglect was associated with employment.Conclusions. ACE are strongly associated with developmental outcomes such as educational achievement. Early intervention for psychosis programs should aim at integrating specific interventions to support young CHR people in their educational and vocational recovery. More generally, public health and social interventions focused on the prevention of ACE (or reduce their impact if ACE occur) are recommended. [ABSTRACT FROM AUTHOR]

Published
2023
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14. The relationship between daily positive future thinking and past-week suicidal ideation in youth: An experience sampling study.

Author

Kirtley, Olivia J., Lafit, Ginette, Vaessen, Thomas, Decoster, Jeroen, Derom, Catherine, Gülöksüz, Sinan, De Hert, Marc, Jacobs, Nele, Menne-Lothmann, Claudia, Rutten, Bart P. F., Thiery, Evert, Os, Jim van, van Winkel, Ruud, Wichers, Marieke, and Myin-Germeys, Inez

Subjects
SUICIDAL ideation, OPTIMISM, SUICIDAL behavior, AFFECT (Psychology), COMMUNITIES
Abstract

Reduced positive future thinking has been associated with suicidal ideation and behavior in adults, and appears to be exacerbated by negative affect. Yet, this has received little attention in youth. Prior research has also focused on longer-term future thinking, e.g., months and years, and relied on lab-based assessments. Using the experience sampling method (ESM), we investigated whether short-term future thinking in daily life was associated with suicidal ideation in youth and explored the role of affect in the future thinking-suicidal ideation relationship. A community sample of N = 722 adolescent twins and their non-twin siblings completed ESM as part of the TwinssCan study (n = 55 with, and n = 667 without, past-week suicidal ideation). Participants completed self-report questionnaires, including on past-week suicidal ideation as part of the SCL-90. Subsequently, daily future thinking was assessed each morning for six days with ESM. To investigate the relationship between daily positive future thinking and past-week suicidal ideation, we estimated a mixed-effects linear regression model with a random intercept for participant, including age and sex as covariates. The relationship between daily positive future thinking, past-week suicidal ideation, and average positive and negative affect from the previous day was investigated by estimating two separate mixed-effects linear regression models (one for negative affect, one for positive affect), with a random intercept for participant, and random slopes for average positive and negative affect. Our results showed that participants reporting higher past-week suicidal ideation also reported significantly less daily positive future thinking during the ESM period, and this association remained significant when controlling for previous-day average positive and negative affect. Higher average positive affect from the previous day was significantly associated with higher positive future thinking. Although average negative affect from the previous day was associated with lower positive future thinking, this association was not statistically significant. Our findings indicate that short-term future thinking relates to suicidal ideation among a non-clinical sample of adolescents. Future research should investigate the directionality of the future thinking-suicidal ideation relationship, in order to investigate whether impaired future thinking may be an early warning signal for escalating suicidal ideation in youth. [ABSTRACT FROM AUTHOR]

Published
2022
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15. Movement Disorders and Mortality in Severely Mentally Ill Patients: The Curacao Extrapyramidal Syndromes Study XIV.

Author

Willems, Anne E, Mentzel, Charlotte L, Bakker, Pieter Roberto, Os, Jim Van, Tenback, Diederik E, Gelan, Petra, Daantjes, Erna, Matroos, Glenn E, Hoek, Hans W, and Harten, Peter N Van

Subjects
MORTALITY risk factors, MORTALITY prevention, BASAL ganglia diseases, LIFE expectancy, MOVEMENT disorders, RISK assessment, TARDIVE akathisia, DISABILITIES, PARKINSONIAN disorders, MENTAL illness, LONGITUDINAL method, PROPORTIONAL hazards models, DISEASE complications
Abstract

Background and Hypothesis There is a substantial gap in life expectancy between patients with severe mental illness (SMI) and the general population and it is important to understand which factors contribute to this difference. Research suggests an association between tardive dyskinesia (TD) and mortality; however, results are inconclusive. In addition, studies investigating associations between parkinsonism or akathisia and mortality are rare. We hypothesized that TD would be a risk factor for mortality in patients with SMI. Study Design We studied a cohort of 157 patients diagnosed predominantly with schizophrenia on the former Netherlands Antilles. TD, parkinsonism, and akathisia were assessed with rating scales on eight occasions over a period of 18 years. Twenty-four years after baseline, survival status and if applicable date of death were determined. Associations between movement disorders and survival were analyzed using Cox regression. Sex, age, antipsychotics, antidepressants and benzodiazepines at each measurement occasion were tested as covariates. Study Results Parkinsonism was a significant risk factor with an HR of 1.02 per point on the motor subscale of the Unified Parkinson's Disease Rating Scale (range 0–56). TD and akathisia were not significantly associated with mortality. Conclusions Parkinsonism may be an important risk factor for mortality in SMI patients. This finding calls for more follow-up and intervention studies to confirm this finding and to explore whether treatment or prevention of parkinsonism can reduce excess mortality. [ABSTRACT FROM AUTHOR]

Published
2022
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16. Impact of Comorbid Affective Disorders on Longitudinal Clinical Outcomes in Individuals at Ultra-high Risk for Psychosis.

Author

Schirmbeck, Frederike, Burg, Nadine C van der, Blankers, Matthijs, Vermeulen, Jentien M, McGuire, Philip, Valmaggia, Lucia R, Kempton, Matthew J, van der Gaag, Mark, Riecher-Rössler, Anita, Bressan, Rodrigo A, Barrantes-Vidal, Neus, Nelson, Barnaby, Amminger, G Paul, McGorry, Patrick, Pantelis, Christos, Krebs, Marie-Odile, Ruhrmann, Stephan, Sachs, Gabriele, Rutten, Bart P F, and Os, Jim van

Subjects
CONFIDENCE intervals, PSYCHOSES, TREATMENT effectiveness, AFFECTIVE disorders, MENTAL depression, DESCRIPTIVE statistics, ANXIETY, LOGISTIC regression analysis, ODDS ratio, DATA analysis software, COMORBIDITY, PROPORTIONAL hazards models
Abstract

Introduction Diagnoses of anxiety and/or depression are common in subjects at Ultra-High Risk for Psychosis (UHR) and associated with extensive functional impairment. Less is known about the impact of affective comorbidities on the prospective course of attenuated psychotic symptoms (APS). Method Latent class mixed modelling identified APS trajectories in 331 UHR subjects assessed at baseline, 6, 12, and 24 months follow-up. The prognostic value of past, baseline, and one-year DSM-IV depressive or anxiety disorders on trajectories was investigated using logistic regression, controlling for confounders. Cox proportional hazard analyses investigated associations with transition risk. Results 46.8% of participants fulfilled the criteria for a past depressive disorder, 33.2% at baseline, and 15.1% at one-year follow-up. Any past, baseline, or one-year anxiety disorder was diagnosed in 42.9%, 37.2%, and 27.0%, respectively. Participants were classified into one of three latent APS trajectory groups: (1) persistently low, (2) increasing, and (3) decreasing. Past depression was associated with a higher risk of belonging to the increasing trajectory group, compared to the persistently low (OR = 3.149, [95%CI: 1.298–7.642]) or decreasing group (OR = 3.137, [1.165–8.450]). In contrast, past (OR =.443, [.179–1.094]) or current (OR =.414, [.156–1.094]) anxiety disorders showed a trend-level association with a lower risk of belonging to the increasing group compared to the persistently low group. Past depression was significantly associated with a higher risk of transitioning to psychosis (HR = 2.123, [1.178–3.828]). Conclusion A past depressive episode might be a particularly relevant risk factor for an unfavorable course of APS in UHR individuals. Early affective disturbances may be used to advance detection, prognostic, and clinical strategies. [ABSTRACT FROM AUTHOR]

Published
2022
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