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514 results on '"Turecki, G."'

2. Transthyretin orchestrates vitamin B12-induced stress resilience

Author

Stein, G., primary, Aly, J.S., additional, Manzolillo, A., additional, Lange, L., additional, Riege, K., additional, Hussain, I., additional, Heller, E.A., additional, Cubillos, S., additional, Ernst, T., additional, Hübner, C.A., additional, Turecki, G., additional, Hoffmann, S., additional, and Engmann, O., additional

Published
2024
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7. Associations between epigenetic aging and childhood peer victimization, depression, and suicidal ideation in adolescence and adulthood: A study of two population-based samples

Author

Perret, L. C., primary, Geoffroy, M-C., additional, Barr, E., additional, Parnet, F., additional, Provencal, N., additional, Boivin, M., additional, O’Donnell, K. J., additional, Suderman, M., additional, Power, C., additional, Turecki, G., additional, and Ouellet-Morin, I., additional

Published
2023
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20. Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology

Author

Mullins, N. Forstner, A.J. O’Connell, K.S. Coombes, B. Coleman, J.R.I. Qiao, Z. Als, T.D. Bigdeli, T.B. Børte, S. Bryois, J. Charney, A.W. Drange, O.K. Gandal, M.J. Hagenaars, S.P. Ikeda, M. Kamitaki, N. Kim, M. Krebs, K. Panagiotaropoulou, G. Schilder, B.M. Sloofman, L.G. Steinberg, S. Trubetskoy, V. Winsvold, B.S. Won, H.-H. Abramova, L. Adorjan, K. Agerbo, E. Al Eissa, M. Albani, D. Alliey-Rodriguez, N. Anjorin, A. Antilla, V. Antoniou, A. Awasthi, S. Baek, J.H. Bækvad-Hansen, M. Bass, N. Bauer, M. Beins, E.C. Bergen, S.E. Birner, A. Bøcker Pedersen, C. Bøen, E. Boks, M.P. Bosch, R. Brum, M. Brumpton, B.M. Brunkhorst-Kanaan, N. Budde, M. Bybjerg-Grauholm, J. Byerley, W. Cairns, M. Casas, M. Cervantes, P. Clarke, T.-K. Cruceanu, C. Cuellar-Barboza, A. Cunningham, J. Curtis, D. Czerski, P.M. Dale, A.M. Dalkner, N. David, F.S. Degenhardt, F. Djurovic, S. Dobbyn, A.L. Douzenis, A. Elvsåshagen, T. Escott-Price, V. Ferrier, I.N. Fiorentino, A. Foroud, T.M. Forty, L. Frank, J. Frei, O. Freimer, N.B. Frisén, L. Gade, K. Garnham, J. Gelernter, J. Giørtz Pedersen, M. Gizer, I.R. Gordon, S.D. Gordon-Smith, K. Greenwood, T.A. Grove, J. Guzman-Parra, J. Ha, K. Haraldsson, M. Hautzinger, M. Heilbronner, U. Hellgren, D. Herms, S. Hoffmann, P. Holmans, P.A. Huckins, L. Jamain, S. Johnson, J.S. Kalman, J.L. Kamatani, Y. Kennedy, J.L. Kittel-Schneider, S. Knowles, J.A. Kogevinas, M. Koromina, M. Kranz, T.M. Kranzler, H.R. Kubo, M. Kupka, R. Kushner, S.A. Lavebratt, C. Lawrence, J. Leber, M. Lee, H.-J. Lee, P.H. Levy, S.E. Lewis, C. Liao, C. Lucae, S. Lundberg, M. MacIntyre, D.J. Magnusson, S.H. Maier, W. Maihofer, A. Malaspina, D. Maratou, E. Martinsson, L. Mattheisen, M. McCarroll, S.A. McGregor, N.W. McGuffin, P. McKay, J.D. Medeiros, H. Medland, S.E. Millischer, V. Montgomery, G.W. Moran, J.L. Morris, D.W. Mühleisen, T.W. O’Brien, N. O’Donovan, C. Olde Loohuis, L.M. Oruc, L. Papiol, S. Pardiñas, A.F. Perry, A. Pfennig, A. Porichi, E. Potash, J.B. Quested, D. Raj, T. Rapaport, M.H. DePaulo, J.R. Regeer, E.J. Rice, J.P. Rivas, F. Rivera, M. Roth, J. Roussos, P. Ruderfer, D.M. Sánchez-Mora, C. Schulte, E.C. Senner, F. Sharp, S. Shilling, P.D. Sigurdsson, E. Sirignano, L. Slaney, C. Smeland, O.B. Smith, D.J. Sobell, J.L. Søholm Hansen, C. Soler Artigas, M. Spijker, A.T. Stein, D.J. Strauss, J.S. Świątkowska, B. Terao, C. Thorgeirsson, T.E. Toma, C. Tooney, P. Tsermpini, E.-E. Vawter, M.P. Vedder, H. Walters, J.T.R. Witt, S.H. Xi, S. Xu, W. Yang, J.M.K. Young, A.H. Young, H. Zandi, P.P. Zhou, H. Zillich, L. Adolfsson, R. Agartz, I. Alda, M. Alfredsson, L. Babadjanova, G. Backlund, L. Baune, B.T. Bellivier, F. Bengesser, S. Berrettini, W.H. Blackwood, D.H.R. Boehnke, M. Børglum, A.D. Breen, G. Carr, V.J. Catts, S. Corvin, A. Craddock, N. Dannlowski, U. Dikeos, D. Esko, T. Etain, B. Ferentinos, P. Frye, M. Fullerton, J.M. Gawlik, M. Gershon, E.S. Goes, F.S. Green, M.J. Grigoroiu-Serbanescu, M. Hauser, J. Henskens, F. Hillert, J. Hong, K.S. Hougaard, D.M. Hultman, C.M. Hveem, K. Iwata, N. Jablensky, A.V. Jones, I. Jones, L.A. Kahn, R.S. Kelsoe, J.R. Kirov, G. Landén, M. Leboyer, M. Lewis, C.M. Li, Q.S. Lissowska, J. Lochner, C. Loughland, C. Martin, N.G. Mathews, C.A. Mayoral, F. McElroy, S.L. McIntosh, A.M. McMahon, F.J. Melle, I. Michie, P. Milani, L. Mitchell, P.B. Morken, G. Mors, O. Mortensen, P.B. Mowry, B. Müller-Myhsok, B. Myers, R.M. Neale, B.M. Nievergelt, C.M. Nordentoft, M. Nöthen, M.M. O’Donovan, M.C. Oedegaard, K.J. Olsson, T. Owen, M.J. Paciga, S.A. Pantelis, C. Pato, C. Pato, M.T. Patrinos, G.P. Perlis, R.H. Posthuma, D. Ramos-Quiroga, J.A. Reif, A. Reininghaus, E.Z. Ribasés, M. Rietschel, M. Ripke, S. Rouleau, G.A. Saito, T. Schall, U. Schalling, M. Schofield, P.R. Schulze, T.G. Scott, L.J. Scott, R.J. Serretti, A. Shannon Weickert, C. Smoller, J.W. Stefansson, H. Stefansson, K. Stordal, E. Streit, F. Sullivan, P.F. Turecki, G. Vaaler, A.E. Vieta, E. Vincent, J.B. Waldman, I.D. Weickert, T.W. Werge, T. Wray, N.R. Zwart, J.-A. Biernacka, J.M. Nurnberger, J.I. Cichon, S. Edenberg, H.J. Stahl, E.A. McQuillin, A. Di Florio, A. Ophoff, R.A. Andreassen, O.A. HUNT All-In Psychiatry

Abstract

Bipolar disorder is a heritable mental illness with complex etiology. We performed a genome-wide association study of 41,917 bipolar disorder cases and 371,549 controls of European ancestry, which identified 64 associated genomic loci. Bipolar disorder risk alleles were enriched in genes in synaptic signaling pathways and brain-expressed genes, particularly those with high specificity of expression in neurons of the prefrontal cortex and hippocampus. Significant signal enrichment was found in genes encoding targets of antipsychotics, calcium channel blockers, antiepileptics and anesthetics. Integrating expression quantitative trait locus data implicated 15 genes robustly linked to bipolar disorder via gene expression, encoding druggable targets such as HTR6, MCHR1, DCLK3 and FURIN. Analyses of bipolar disorder subtypes indicated high but imperfect genetic correlation between bipolar disorder type I and II and identified additional associated loci. Together, these results advance our understanding of the biological etiology of bipolar disorder, identify novel therapeutic leads and prioritize genes for functional follow-up studies. © 2021, The Author(s), under exclusive licence to Springer Nature America, Inc.

Published
2021

21. Cybervictimization in adolescence and its association with subsequent suicidal ideation/attempt beyond face-to-face victimization: a longitudinal population-based study

Author

PERRET, L. C., ORRI, Massiliano, Boivin, M., OUELLET-MORIN, I., DENAULT, A. S., COTE, Sylvana M., TREMBLAY, R. E., Renaud, J., Turecki, G., GEOFFROY, M. C., Bordeaux population health (BPH), and Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
education, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, HEALTHY
Abstract

BackgroundCross‐sectional associations have been documented between cybervictimization and suicidal risk; however, prospective associations remain unclear.MethodsParticipants were members of the Quebec Longitudinal Study of Child Development (QLSCD), a prospective birth cohort of 2,120 individuals followed from birth (1997/98) to age 17 years (2014/15). Cybervictimization and face‐to‐face victimization experienced since the beginning of the school year, as well as serious suicidal ideation and/or suicide attempt were self‐reported at ages 13, 15 and 17 years.ResultsIn cross‐sectional analyses at 13, 15 and 17 years, adolescents cybervictimized at least once had, respectively, 2.3 (95% CI = 1.64–3.19), 4.2 (95% CI = 3.27–5.41) and 3.5 (95% CI = 2.57–4.66) higher odds of suicidal ideation/attempt after adjusting for confounders including face‐to‐face victimization, prior mental health symptoms and family hardship. Sensitivity analyses suggested that cybervictimization only and both cyber‐ and face‐to‐face victimization were associated with a higher risk of suicidal ideation/attempt compared to face‐to‐face victimization only and no victimization; however, analyses were based on small n. In prospective analyses, cybervictimization was not associated with suicidal ideation/attempt 2 years later after accounting for baseline suicidal ideation/attempt and other confounders. In contrast, face‐to‐face victimization was associated with suicidal ideation/attempt 2 years later in the fully adjusted model, including cybervictimization.ConclusionsThe cross‐sectional association between cybervictimization and suicidal ideation/attempt is independent from face‐to‐face victimization. The absence of a prospective association suggested short‐term effects of cybervictimization on suicidal ideation/attempt.

Published
2020

22. Suicide research, prevention, and COVID-19. Towards a global response and the establishment of an international research collaboration

Author

Niederkrotenthaler, T., Gunnell, D., Arensman, E., Pirkis, J., Appleby, L., Hawton, K., John, A., Kapur, N., Khan, M., O'Connor, R. C., Platt, S., Analuisa, P., Ayuso-Mateos, J. L., Bantjes, J., Bertolote, J., Caine, E., Chan, L. F., Chang, S. -S., Chen, Y. -Y., Christensen, H., Dandona, R., de Leo, D., Eddleston, M., Erlangsen, A., Harkavy-Friedman, J., Jollant, F., Kirtley, O. J., Knipe, D., Kolves, K., Konradsen, F., Liu, S., Mcmanus, S., Mehlum, L., Miller, M., Mittendorfer-Rutz, E., Moran, P., Morrissey, J., Moutier, C., Nielsen, E., Nordentoft, M., O'Connor, R., O'Neill, S., Oquendo, M., Osafo, J., Page, A., Phillips, M. R., Polozhy, B., Pompili, M., Qin, P., Rajapakse, T., Rezaeian, M., Schneider, B., Silverman, M. M., Sinyor, M., Stack, S., Townsend, E., Turecki, G., Ueda, M., Vijayakumar, L., Yip, P., and Zalsman, G.

Subjects
betacoronavirus, covid-19, delivery of health care, evidence-based practice, humans, information dissemination, mental health services, research, sars-cov-2, schools, suicide, coronavirus infections, international cooperation, mental health, pandemics, pneumonia, viral, public health, 050103 clinical psychology, Economic growth, Government, medicine.medical_specialty, Evidence-based practice, Public health, 05 social sciences, Psychological intervention, Mental health, Suicide prevention, 030227 psychiatry, 03 medical and health sciences, Psychiatry and Mental health, 0302 clinical medicine, Political science, Pandemic, Global health, medicine, 0501 psychology and cognitive sciences
Abstract

The COVID-19 pandemic of 2020 is a major global health challenge. At the time of writing, over 11.6 million people around the world had been registered as infected and 538,000 had died (Worldometers, 2020, accessed July 7, 2020). Public health responses to COVID-19 need to balance direct efforts to control the disease and its impact on health systems, infected people, and their families with the impacts from associated mitigating interventions. Such impacts include social isolation, school closure, health service disruption stemming from reconfiguring health systems, and diminished economic activity. The primary focus of both the United Nations (UN) and the World Health Organization (WHO) has been on addressing COVID-19 as a physical health crisis, but the need to strengthen mental health action, including suicide prevention, is increasingly recognized, as is the need for mental health research to be an integral part of the recovery plan (UN, 2020a). The impacts of the pandemic on physical and mental health will unfold differently over time and will vary depending on the duration and fluctuating intensity of the disease. Research is needed to help ensure that decision-making regarding all aspects of health, including mental health (Holmes et al., 2020), is informed by the best quality data at each stage of the pandemic. The pandemic poses a prolonged and unique challenge to public mental health, with major implications for suicide and suicide prevention (Gunnell et al., 2020; Reger, Stanley, & Joiner, 2020). A rise in suicide deaths in the wake of the pandemic is not inevitable. There is consensus, however, that the mitigation of risk will be contingent upon a proactive and effective response involving collaborative work between the state, NGOs, academia, and local governments and coordinated leadership across government ministries, including health, education, security, social services, welfare, and finance. Countries have responded in different ways to the pandemic, effectively creating a series of natural experiments. Thus, regions of the world affected later in the pandemic can draw on lessons from countries, such as China and Italy, affected in its early phase. Likewise, lessons learned early in the pandemic (e.g., on the impact of lockdown and physical distancing measures) can be used to inform responses to any future surges in the incidence of COVID-19. Although there are important parallels between countries in the course of the pandemic, some stressors, responses, and priorities are likely to differ between high- and low–middle-income countries and between cultures and regions. As COVID-19 appears to be disproportionately affecting Black, Asian, and minority ethnic communities, the response – and suicide prevention research carried out to inform the response – needs to be sufficiently granular and account for the complexity of risks in these groups (O'Connor et al., 2020). Throughout this editorial, when we refer to suicide and suicidal behavior, we mean to include both fatal and nonfatal suicidal behaviors and self-harm.

Published
2020

26. Br J Psychiatry

Author

LANGEVIN, S., MASCHERETTI, S., COTE, Sylvana, VITARO, F., BOIVIN, M., TURECKI, G., TREMBLAY, R. E., and OUELLET-MORIN, I.

Published
2019

28. Childhood trajectories of peer victimization and prediction of mental health outcomes in midadolescence: a longitudinal population-based study

Author

GEOFFROY, M. C., Boivin, M., ARSENEAULT, L., Renaud, J., PERRET, L. C., Turecki, G., Michel, Gregory, Salla, Julie, VITARO, F., BRENDGEN, M., TREMBLAY, R. E., COTE, Sylvana M., Bordeaux population health (BPH), and Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
education, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, social sciences, HEALTHY, health care economics and organizations
Abstract

BACKGROUND: Exposure to peer victimization is relatively common. However, little is known about its developmental course and its effect on impairment associated with mental illnesses. We aimed to identify groups of children following differential trajectories of peer victimization from ages 6 to 13 years and to examine predictive associations of these trajectories with mental health in adolescence. METHODS: Participants were members of the Quebec Longitudinal Study of Child Development, a prospective cohort of 2120 children born in 1997/98 who were followed until age 15 years. We included 1363 participants with self-reported victimization from ages 6 to 13 years and data available on their mental health status at 15 years. RESULTS: We identified 3 trajectories of peer victimization. The 2 prevailing groups were participants with little or moderate exposure to victimization (441/1685 [26.2%] and 1000/1685 [59.3%], respectively); the third group (244 [14.5%]) had been chronically exposed to the most severe and long-lasting levels of victimization. The most severely victimized individuals had greater odds of reporting debilitating depressive or dysthymic symptoms (odds ratio [OR] 2.56, 95% confidence interval [CI] 1.27-5.17), debilitating generalized anxiety problems (OR 3.27, CI 1.64-6.51) and suicidality (OR 3.46, CI 1.53-7.81) at 15 years than those exposed to the lowest levels of victimization, after adjustment for sex, childhood mental health, family hardship and victimization perpetration. The association with suicidality remained significant after controlling for concurrent symptoms of depression or dysthymia and generalized anxiety problems. INTERPRETATION: Adolescents who were most severely victimized by peers had an increased risk of experiencing severe symptoms consistent with mental health problems. Given that peer victimization trajectories are established early on, interventions to reduce the risk of being victimized should start before enrolment in the formal school system.

Published
2018

29. Association of Childhood Irritability and Depressive/Anxious Mood Profiles With Adolescent Suicidal Ideation and Attempts

Author

ORRI, Massiliano, GALERA, Cedric, Turecki, G., FORTE, A., Renaud, J., Boivin, M., TREMBLAY, R. E., COTE, Sylvana M., GEOFFROY, M. C., Bordeaux population health (BPH), and Université de Bordeaux (UB)-Institut de Santé Publique, d'Épidémiologie et de Développement (ISPED)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
mental disorders, [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie, HEALTHY, behavioral disciplines and activities
Abstract

Importance: Suicidal ideation and suicide attempt (suicidality) are common in adolescence and a public health concern. Childhood depression is a key risk factor for later suicidality and often co-occurs with irritability. No study to date has examined the joint association of depressive mood and irritability during childhood with later suicidality. Objective: To investigate the association of childhood irritability and depressive/anxious mood profiles with adolescent suicidality. Design, Setting, and Participants: This population-based cohort study included 1430 participants in the Quebec Longitudinal Study of Child Development. Participants underwent assessment yearly or bi-yearly (5 months to 17 years). Data were collected from March 16, 1998, through July 17, 2015. Exposures: Profiles defined by the joint developmental trajectories of irritability and depressive/anxious mood at 6 to 12 years of age. Main Outcomes and Measures: Self-reported past-year suicidality (ie, serious suicidal ideation or suicide attempt) at 13, 15, and 17 years of age. Irritability and depressive/anxious mood were assessed using teacher report 5 times from 6 to 12 years of age. Results: The study included 1430 participants (676 boys [47.3%] and 754 girls [52.7%]) followed up to 17 years of age. Group-based multitrajectory modeling identified the following profiles: combined no irritability and low depressive/anxious mood with low irritability and low depressive/anxious mood (831 [58.1%]; reference group), moderate irritability and low depressive/anxious mood (353 [24.7%]), high depressive/anxious mood only (94 [6.6%]), and high irritability and depressive/anxious mood (152 [10.6%]). Children with high irritability and high depressive/anxious mood reported higher rates of suicidality (25 of 152 [16.4%]) compared with the group with the lowest symptom levels (91 of 831 [11.0%]). In logistic regression analyses, the high irritability and depressive/anxious mood profile (odds ratio [OR], 2.22; 95% CI, 1.32-3.74; number needed to be exposed [NNE], 18) was associated with suicidality. To a lesser extent, the moderate irritability and low depressive/anxious mood profile was also associated with suicidality (OR, 1.51; 95% CI, 1.02-2.25; NNE = 48). The high depressive/anxious mood only profile was not associated with later suicidality (OR, 0.96; 95% CI, 0.47-1.95; NNE = -320). The high irritability and depressive/anxious mood profile was associated with a higher suicidal risk compared with the depressive/anxious mood only profile (OR, 2.28; 95% CI, 1.02-5.15). Girls with the high irritability and high depressive/anxious mood profile had higher risk for suicidality (OR, 3.07; 95% CI, 1.54-6.12; NNE = 5). Conclusions and Relevance: Children with high irritability and depressive/anxious mood and, to a lesser extent, with moderate irritability only had a higher suicidal risk during adolescence compared with children with low symptom levels. Early manifestation of chronic irritability during childhood, especially when combined with depressive/anxious mood, may be associated with an elevated risk for adolescent suicidality. The putatively causal role of irritability should be investigated.

Published
2018

30. Analysis of shared heritability in common disorders of the brain

Author

Anttila, V. Bulik-Sullivan, B. Finucane, H.K. Walters, R.K. Bras, J. Duncan, L. Escott-Price, V. Falcone, G.J. Gormley, P. Malik, R. Patsopoulos, N.A. Ripke, S. Wei, Z. Yu, D. Lee, P.H. Turley, P. Grenier-Boley, B. Chouraki, V. Kamatani, Y. Berr, C. Letenneur, L. Hannequin, D. Amouyel, P. Boland, A. Deleuze, J.-F. Duron, E. Vardarajan, B.N. Reitz, C. Goate, A.M. Huentelman, M.J. Ilyas Kamboh, M. Larson, E.B. Rogaeva, E. George-Hyslop, P.S. Hakonarson, H. Kukull, W.A. Farrer, L.A. Barnes, L.L. Beach, T.G. Yesim Demirci, F. Head, E. Hulette, C.M. Jicha, G.A. Kauwe, J.S.K. Kaye, J.A. Leverenz, J.B. Levey, A.I. Lieberman, A.P. Pankratz, V.S. Poon, W.W. Quinn, J.F. Saykin, A.J. Schneider, L.S. Smith, A.G. Sonnen, J.A. Stern, R.A. Van Deerlin, V.M. Van Eldik, L.J. Harold, D. Russo, G. Rubinsztein, D.C. Bayer, A. Tsolaki, M. Proitsi, P. Fox, N.C. Hampel, H. Owen, M.J. Mead, S. Passmore, P. Morgan, K. Nöthen, M.M. Rossor, M. Lupton, M.K. Hoffmann, P. Kornhuber, J. Lawlor, B. McQuillin, A. Al-Chalabi, A. Bis, J.C. Ruiz, A. Boada, M. Seshadri, S. Beiser, A. Rice, K. Van Der Lee, S.J. De Jager, P.L. Geschwind, D.H. Riemenschneider, M. Riedel-Heller, S. Rotter, J.I. Ransmayr, G. Hyman, B.T. Cruchaga, C. Alegret, M. Winsvold, B. Palta, P. Farh, K.-H. Cuenca-Leon, E. Furlotte, N. Kurth, T. Ligthart, L. Terwindt, G.M. Freilinger, T. Ran, C. Gordon, S.D. Borck, G. Adams, H.H.H. Lehtimäki, T. Wedenoja, J. Buring, J.E. Schürks, M. Hrafnsdottir, M. Hottenga, J.-J. Penninx, B. Artto, V. Kaunisto, M. Vepsäläinen, S. Martin, N.G. Montgomery, G.W. Kurki, M.I. Hämäläinen, E. Huang, H. Huang, J. Sandor, C. Webber, C. Muller-Myhsok, B. Schreiber, S. Salomaa, V. Loehrer, E. Göbel, H. Macaya, A. Pozo-Rosich, P. Hansen, T. Werge, T. Kaprio, J. Metspalu, A. Kubisch, C. Ferrari, M.D. Belin, A.C. Van Den Maagdenberg, A.M.J.M. Zwart, J.-A. Boomsma, D. Eriksson, N. Olesen, J. Chasman, D.I. Nyholt, D.R. Avbersek, A. Baum, L. Berkovic, S. Bradfield, J. Buono, R. Catarino, C.B. Cossette, P. De Jonghe, P. Depondt, C. Dlugos, D. Ferraro, T.N. French, J. Hjalgrim, H. Jamnadas-Khoda, J. Kälviäinen, R. Kunz, W.S. Lerche, H. Leu, C. Lindhout, D. Lo, W. Lowenstein, D. McCormack, M. Møller, R.S. Molloy, A. Ng, P.-W. Oliver, K. Privitera, M. Radtke, R. Ruppert, A.-K. Sander, T. Schachter, S. Schankin, C. Scheffer, I. Schoch, S. Sisodiya, S.M. Smith, P. Sperling, M. Striano, P. Surges, R. Neil Thomas, G. Visscher, F. Whelan, C.D. Zara, F. Heinzen, E.L. Marson, A. Becker, F. Stroink, H. Zimprich, F. Gasser, T. Gibbs, R. Heutink, P. Martinez, M. Morris, H.R. Sharma, M. Ryten, M. Mok, K.Y. Pulit, S. Bevan, S. Holliday, E. Attia, J. Battey, T. Boncoraglio, G. Thijs, V. Chen, W.-M. Mitchell, B. Rothwell, P. Sharma, P. Sudlow, C. Vicente, A. Markus, H. Kourkoulis, C. Pera, J. Raffeld, M. Silliman, S. Perica, V.B. Thornton, L.M. Huckins, L.M. William Rayner, N. Lewis, C.M. Gratacos, M. Rybakowski, F. Keski-Rahkonen, A. Raevuori, A. Hudson, J.I. Reichborn-Kjennerud, T. Monteleone, P. Karwautz, A. Mannik, K. Baker, J.H. O'Toole, J.K. Trace, S.E. Davis, O.S.P. Helder, S.G. Ehrlich, S. Herpertz-Dahlmann, B. Danner, U.N. Van Elburg, A.A. Clementi, M. Forzan, M. Docampo, E. Lissowska, J. Hauser, J. Tortorella, A. Maj, M. Gonidakis, F. Tziouvas, K. Papezova, H. Yilmaz, Z. Wagner, G. Cohen-Woods, S. Herms, S. Julia, A. Rabionet, R. Dick, D.M. Ripatti, S. Andreassen, O.A. Espeseth, T. Lundervold, A.J. Steen, V.M. Pinto, D. Scherer, S.W. Aschauer, H. Schosser, A. Alfredsson, L. Padyukov, L. Halmi, K.A. Mitchell, J. Strober, M. Bergen, A.W. Kaye, W. Szatkiewicz, J.P. Cormand, B. Ramos-Quiroga, J.A. Sánchez-Mora, C. Ribasés, M. Casas, M. Hervas, A. Arranz, M.J. Haavik, J. Zayats, T. Johansson, S. Williams, N. Dempfle, A. Rothenberger, A. Kuntsi, J. Oades, R.D. Banaschewski, T. Franke, B. Buitelaar, J.K. Vasquez, A.A. Doyle, A.E. Reif, A. Lesch, K.-P. Freitag, C. Rivero, O. Palmason, H. Romanos, M. Langley, K. Rietschel, M. Witt, S.H. Dalsgaard, S. Børglum, A.D. Waldman, I. Wilmot, B. Molly, N. Bau, C.H.D. Crosbie, J. Schachar, R. Loo, S.K. McGough, J.J. Grevet, E.H. Medland, S.E. Robinson, E. Weiss, L.A. Bacchelli, E. Bailey, A. Bal, V. Battaglia, A. Betancur, C. Bolton, P. Cantor, R. Celestino-Soper, P. Dawson, G. De Rubeis, S. Duque, F. Green, A. Klauck, S.M. Leboyer, M. Levitt, P. Maestrini, E. Mane, S. Moreno-De-Luca, D. Parr, J. Regan, R. Reichenberg, A. Sandin, S. Vorstman, J. Wassink, T. Wijsman, E. Cook, E. Santangelo, S. Delorme, R. Roge, B. Magalhaes, T. Arking, D. Schulze, T.G. Thompson, R.C. Strohmaier, J. Matthews, K. Melle, I. Morris, D. Blackwood, D. McIntosh, A. Bergen, S.E. Schalling, M. Jamain, S. Maaser, A. Fischer, S.B. Reinbold, C.S. Fullerton, J.M. Guzman-Parra, J. Mayoral, F. Schofield, P.R. Cichon, S. Mühleisen, T.W. Degenhardt, F. Schumacher, J. Bauer, M. Mitchell, P.B. Gershon, E.S. Rice, J. Potash, J.B. Zandi, P.P. Craddock, N. Nicol Ferrier, I. Alda, M. Rouleau, G.A. Turecki, G. Ophoff, R. Pato, C. Anjorin, A. Stahl, E. Leber, M. Czerski, P.M. Cruceanu, C. Jones, I.R. Posthuma, D. Andlauer, T.F.M. Forstner, A.J. Streit, F. Baune, B.T. Air, T. Sinnamon, G. Wray, N.R. MacIntyre, D.J. Porteous, D. Homuth, G. Rivera, M. Grove, J. Middeldorp, C.M. Hickie, I. Pergadia, M. Mehta, D. Smit, J.H. Jansen, R. De Geus, E. Dunn, E. Li, Q.S. Nauck, M. Schoevers, R.A. Beekman, A.T.F. Knowles, J.A. Viktorin, A. Arnold, P. Barr, C.L. Bedoya-Berrio, G. Joseph Bienvenu, O. Brentani, H. Burton, C. Camarena, B. Cappi, C. Cath, D. Cavallini, M. Cusi, D. Darrow, S. Denys, D. Derks, E.M. Dietrich, A. Fernandez, T. Figee, M. Freimer, N. Gerber, G. Grados, M. Greenberg, E. Hanna, G.L. Hartmann, A. Hirschtritt, M.E. Hoekstra, P.J. Huang, A. Huyser, C. Illmann, C. Jenike, M. Kuperman, S. Leventhal, B. Lochner, C. Lyon, G.J. Macciardi, F. Madruga-Garrido, M. Malaty, I.A. Maras, A. McGrath, L. Miguel, E.C. Mir, P. Nestadt, G. Nicolini, H. Okun, M.S. Pakstis, A. Paschou, P. Piacentini, J. Pittenger, C. Plessen, K. Ramensky, V. Ramos, E.M. Reus, V. Richter, M.A. Riddle, M.A. Robertson, M.M. Roessner, V. Rosário, M. Samuels, J.F. Sandor, P. Stein, D.J. Tsetsos, F. Van Nieuwerburgh, F. Weatherall, S. Wendland, J.R. Wolanczyk, T. Worbe, Y. Zai, G. Goes, F.S. McLaughlin, N. Nestadt, P.S. Grabe, H.-J. Depienne, C. Konkashbaev, A. Lanzagorta, N. Valencia-Duarte, A. Bramon, E. Buccola, N. Cahn, W. Cairns, M. Chong, S.A. Cohen, D. Crespo-Facorro, B. Crowley, J. Davidson, M. DeLisi, L. Dinan, T. Donohoe, G. Drapeau, E. Duan, J. Haan, L. Hougaard, D. Karachanak-Yankova, S. Khrunin, A. Klovins, J. Kučinskas, V. Keong, J.L.C. Limborska, S. Loughland, C. Lönnqvist, J. Maher, B. Mattheisen, M. McDonald, C. Murphy, K.C. Nenadic, I. Van Os, J. Pantelis, C. Pato, M. Petryshen, T. Quested, D. Roussos, P. Sanders, A.R. Schall, U. Schwab, S.G. Sim, K. So, H.-C. Stögmann, E. Subramaniam, M. Toncheva, D. Waddington, J. Walters, J. Weiser, M. Cheng, W. Cloninger, R. Curtis, D. Gejman, P.V. Henskens, F. Mattingsdal, M. Oh, S.-Y. Scott, R. Webb, B. Breen, G. Churchhouse, C. Bulik, C.M. Daly, M. Dichgans, M. Faraone, S.V. Guerreiro, R. Holmans, P. Kendler, K.S. Koeleman, B. Mathews, C.A. Price, A. Scharf, J. Sklar, P. Williams, J. Wood, N.W. Cotsapas, C. Palotie, A. Smoller, J.W. Sullivan, P. Rosand, J. Corvin, A. Neale, B.M. The Brainstorm Consortium

Abstract

Disorders of the brain can exhibit considerable epidemiological comorbidity and often share symptoms, provoking debate about their etiologic overlap. We quantified the genetic sharing of 25 brain disorders from genome-wide association studies of 265,218 patients and 784,643 control participants and assessed their relationship to 17 phenotypes from 1,191,588 individuals. Psychiatric disorders share common variant risk, whereas neurological disorders appear more distinct from one another and from the psychiatric disorders. We also identified significant sharing between disorders and a number of brain phenotypes, including cognitive measures. Further, we conducted simulations to explore how statistical power, diagnostic misclassification, and phenotypic heterogeneity affect genetic correlations. These results highlight the importance of common genetic variation as a risk factor for brain disorders and the value of heritability-based methods in understanding their etiology. © 2018 American Association for the Advancement of Science. All rights reserved.

Published
2018

32. Examining the role of mother-child interactions and DNA methylation of the oxytocin receptor gene in understanding child controlling attachment behaviors.

Author

Lecompte, V., Robins, S., King, L., Solomonova, E., Khan, N., Moss, E., Nagy, C., Feeley, N., Gold, I., Hayton, B., Turecki, G., and Zelkowitz, P.

Subjects
ATTACHMENT behavior, CELL receptors, CHILD behavior, GENES, MOTHER-child relationship, MOTHERHOOD, OXYTOCIN, PARENTING, DNA methylation
Abstract

This study examined mother-child interactions and DNA methylation of the oxytocin receptor (OXTR) gene in the child, in relation with controlling-attachment behaviors at early preschool age. Maternal interactive behaviors were coded using the Emotional Availability Scales, and child attachment behaviors were assessed with the Separation-Reunion procedure and coded with the Preschool Attachment Rating Scales. DNA methylation data were captured from exon 3 of the OXTR. Results indicated that lower maternal sensitivity was associated with more controlling-caregiving behaviors, and that less maternal structuring was associated with more controlling-punitive behaviors. Hypomethylation of the OXTR gene was associated with greater maternal structuring behaviors, and with more child controlling-caregiving behaviors. The moderating role of the OXTR gene was examined in the association between interactive behaviors and child controlling behaviors, but no interaction effect was found. These results suggest that maternal interactive behaviors and OXTR methylation are independently associated with child controlling attachment. [ABSTRACT FROM AUTHOR]

Published
2021
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34. Rare susceptibility variants for bipolar disorder suggest a role for G protein-coupled receptors

Author

Cruceanu, C, primary, Schmouth, J-F, additional, Torres-Platas, S G, additional, Lopez, J P, additional, Ambalavanan, A, additional, Darcq, E, additional, Gross, F, additional, Breton, B, additional, Spiegelman, D, additional, Rochefort, D, additional, Hince, P, additional, Petite, J M, additional, Gauthier, J, additional, Lafrenière, R G, additional, Dion, P A, additional, Greenwood, C M, additional, Kieffer, B L, additional, Alda, M, additional, Turecki, G, additional, and Rouleau, G A, additional

Published
2017
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36. VGF function in depression and antidepressant efficacy

Author

Jiang, C, primary, Lin, W-J, additional, Sadahiro, M, additional, Labonté, B, additional, Menard, C, additional, Pfau, M L, additional, Tamminga, C A, additional, Turecki, G, additional, Nestler, E J, additional, Russo, S J, additional, and Salton, S R, additional

Published
2017
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37. Cocaine-induced chromatin modifications are associated with increased gene expression and DNA-DNA interactions of autism-candidate 2

Author

Engmann, O., primary, Labonte, B., additional, Mitchell, A., additional, Bashtrykov, P., additional, Calipari, E., additional, Rosenbluh, C., additional, Loh, Y., additional, Walker, D., additional, Burek, D., additional, Hamilton, P., additional, Issler, O., additional, Neve, R., additional, Turecki, G., additional, Hurd, Y., additional, Chess, A., additional, Shen, L., additional, Jeltsch, A., additional, Akbarian, S., additional, and Nestler, E., additional

Published
2017
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39. Brain microglia in psychiatric disorders

Author

Mondelli, Valeria, Vernon, Anthony C, Turkheimer, Federico, Dazzan, Paola, Pariante, Carmine M, Frost, JL, Schafer, DP, Banati, RB, Newcombe, J, Gunn, RN, al., et, Tang, Y, Le, W, Estes, ML, McAllister, AK, Ransohoff, RM, Davalos, D, Grutzendler, J, Yang, G, Peferoen, LA, Vogel, DY, Ummenthum, K, Norden, DM, Trojanowski, PJ, Villanueva, E, Navarro, E, Godbout, JP, Kreisel, T, Frank, MG, Licht, T, Wachholz, S, Eßlinger, M, Plümper, J, Manitz, MP, Juckel, G, Friebe, A, Trépanier, MO, Hopperton, KE, Mizrahi, R, Mechawar, N, Bazinet, RP, Torres-Platas, SG, Cruceanu, C, Chen, GG, Turecki, G, Steiner, J, Bielau, H, Brisch, R, Schnieder, TP, Trencevska, I, Rosoklija, G, Fillman, SG, Cloonan, N, Catts, VS, Rupprecht, R, Papadopoulos, V, Rammes, G, Qiu, ZK, Li, MS, He, JL, Hannestad, J, Gallezot, JD, Schafbauer, T, Israel, I, Ohsiek, A, Al-Momani, E, Mirzaei, N, Tang, SP, Ashworth, S, Gulyás, B, Makkai, B, Kása, P, Turkheimer, FE, Rizzo, G, Bloomfield, PS, Owen, DR, Yeo, AJ, DellaGioia, N, Setiawan, E, Wilson, AA, Su, L, Faluyi, YO, Hong, YT, Haarman, BC, Lek, RF Riemersma-Van der, Groot, JC de, Berckel, BN van, Bossong, MG, Boellaard, R, Doorduin, J, Vries, EF de, Willemsen, AT, Dierckx, RA, Klein, HC, Takano, A, Arakawa, R, Ito, H, Kenk, M, Selvanathan, T, Rao, N, Selvaraj, S, Veronese, M, Coughlin, JM, Wang, Y, Ambinder, EB, Doef, TF van der, Witte, LD de, Sutterland, AL, Hafizi, S, Tseng, HH, Holmes, SE, Hinz, R, Drake, RJ, Yaqub, M, Schuitemaker, A, Edison, P, Pavese, N, Lockhart, A, Davis, B, Matthews, JC, Quarantelli, M, Laule, C, Vavasour, IM, Kolind, SH, Pasternak, O, Sochen, N, Gur, Y, Intrator, N, Assaf, Y, Andreasen, NC, Ehrhardt, JC, Swayze, VW, Supprian, T, Hofmann, E, Warmuth-Metz, M, Franzek, E, Becker, T, Pfefferbaum, A, Sullivan, EV, Hedehus, M, Moseley, M, Lim, KO, Mandl, RC, Schnack, HG, Luigjes, J, Cahn, W, Bagary, MS, Symms, MR, Barker, GJ, Mutsatsa, SH, Joyce, EM, Ron, MA, Foong, J, Maier, M, Brocklehurst, S, Miller, DH, Kubicki, M, Park, H, Westin, CF, Bouix, S, Dahlben, B, Oestreich, LK, Shenton, ME, Amato, D, Beasley, CL, Hahn, MK, Vernon, AC, Natesan, S, Modo, M, Kapur, S, Mondelli, V, Reininghaus, U, Kempton, MJ, Valmaggia, L, Baumeister, D, Lightman, SL, Pariante, CM, Danese, A, Moffitt, TE, Ambler, A, Poulton, R, Caspi, A, Akhtar, R, Ciufolini, S, Meyer, U, So, PW, Lythgoe, DJ, Cotel, MC, Lenartowicz, EM, Anacker, C, Calcia, MA, Bonsall, DR, Barichello, T, Howes, OD, Burke, NN, Fan, CY, Trang, T, McMahon, SB, Russa, F La, Bennett, DL, Püntener, U, Booth, SG, Perry, VH, Teeling, JL, Hahn, YK, Podhaizer, EM, Farris, SP, Miles, MF, Hauser, KF, Knapp, PE, Notter, T, Gschwind, T, Varga, B, Markó, K, Hádinger, N, Cattaneo, A, Ferrari, C, Uher, R, Belvederi, Murri M, Sandiego, CM, Pittman, B, Weber, MD, Sheridan, JF, Raison, CL, Rutherford, RE, Woolwine, BJ, Möller, T, Boddeke, HW, O'Connor, JC, Lawson, MA, André, C, Hinwood, M, Morandini, J, Day, TA, Walker, FR, Bard, F, Bhattacharya, A, Pae, CU, Marks, DM, Han, C, Patkar, AA, Oya, K, Kishi, T, Iwata, N, Pathology, NCA - Neuroinflamation, Molecular cell biology and Immunology, Gastroenterology and hepatology, CCA - Disease profiling, ICaR - Heartfailure and pulmonary arterial hypertension, ICaR - Ischemia and repair, NCA - Brain imaging technology, Radiology and nuclear medicine, Amsterdam Neuroscience - Brain Imaging, Otolaryngology / Head & Neck Surgery, EMGO - Quality of care, AII - Infectious diseases, CCA - Imaging, and Neurology

Subjects
0301 basic medicine, medicine.medical_specialty, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, Humans, Psychology, In patient, Psychiatry, Biological Psychiatry, Neuroinflammation, Inflammation, Microglia, business.industry, Macrophages, Mental Disorders, Brain, Magnetic Resonance Imaging, Psychiatry and Mental health, 030104 developmental biology, medicine.anatomical_structure, Psychosocial stress, Treatment strategy, Autopsy, business, Neuroscience, 030217 neurology & neurosurgery, Stress, Psychological, Immune activation
Abstract

SummaryThe role of immune activation in psychiatric disorders has attracted considerable attention over the past two decades, contributing to the rise of a new era for psychiatry. Microglia, the macrophages of the brain, are progressively becoming the main focus of the research in this field. In this Review, we assess the literature on microglia activation across different psychiatric disorders, including post-mortem and in-vivo studies in humans and experimental studies in animals. Although microglia activation has been noted in all types of psychiatric disorder, no association was seen with specific diagnostic categories. Furthermore, the findings from these studies highlight that not all psychiatric patients have microglial activation. Therefore, the cause of the neuroinflammation in these cohorts and its implications are unclear. We discuss psychosocial stress as one of the main factors determining microglial activation in patients with psychiatric disorders, and explore the relevance of these findings for future treatment strategies.

Published
2016

45. Animal models to improve our understanding and treatment of suicidal behavior

Author

Gould, T D, primary, Georgiou, P, additional, Brenner, L A, additional, Brundin, L, additional, Can, A, additional, Courtet, P, additional, Donaldson, Z R, additional, Dwivedi, Y, additional, Guillaume, S, additional, Gottesman, I I, additional, Kanekar, S, additional, Lowry, C A, additional, Renshaw, P F, additional, Rujescu, D, additional, Smith, E G, additional, Turecki, G, additional, Zanos, P, additional, Zarate, C A, additional, Zunszain, P A, additional, and Postolache, T T, additional

Published
2017
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50. Role of Tet1 and 5-hydroxymethylcytosine in cocaine action

Author

Feng, J, Shao, N, Szulwach, KE, Vialou, VF, Huynh, J, Zhong, C, Le, T, Ferguson, D, Cahill, ME, Li, Y, Koo, J, Ribeiro, E, Labonté, B, Laitman, BM, Estey, D, Stockman, V, Kennedy, PJ, Couroussé, T, Mensah, I, Turecki, G, Faull, KF, Ming, G, Song, H, Fan, G, Casaccia, P, Jin, P, and Nestler, EJ

Abstract

© 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. Ten-eleven translocation (TET) enzymes mediate the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), which is enriched in brain, and its ultimate DNA demethylation. However, the influence of TET and 5hmC on gene transcription in brain remains elusive. We found that ten-eleven translocation protein 1 (TET1) was downregulated in mouse nucleus accumbens (NAc), a key brain reward structure, by repeated cocaine administration, which enhanced behavioral responses to cocaine. We then identified 5hmC induction in putative enhancers and coding regions of genes that have pivotal roles in drug addiction. Such induction of 5hmC, which occurred similarly following TET1 knockdown alone, correlated with increased expression of these genes as well as with their alternative splicing in response to cocaine administration. In addition, 5hmC alterations at certain loci persisted for at least 1 month after cocaine exposure. Together, these reveal a previously unknown epigenetic mechanism of cocaine action and provide new insight into how 5hmC regulates transcription in brain in vivo.

Published
2015

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