Browsing by Author "Gonzalez, Alfonso"
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Publication Correction: Obesity and brain structure in schizophrenia - ENIGMA study in 3021 individuals(2022) McWhinney, Sean; Brosch, Katharina; Calhoun, Vince; Crespo, Benedicto; Crossley, Nicolas; Dannlowski, Udo; Dickie, Erin; Dietze, Lorielle; Donohoe, Gary; Du Plessis, Stefan; Ehrlich, Stefan; Emsley, Robin; Furstova, Petra; Glahn, David; Gonzalez, Alfonso; Grotegerd, Dominik; Holleran, Laurena; Kircher, Tilo; Knytl, Pavel; Kolenic, Marian; Lencer, Rebekka; Nenadić, Igor; Opel, Nils; Pfarr, Julia; Rodrigue, Amanda; Rootes, Kelly; Ross, Alex; Sim, Kang; Škoch, Antonín; Spaniel, Filip; Stein, Frederike; Švancer, Patrik; Tordesillas, Diana; Undurraga, Juan; Vázquez, Javier; Voineskos, Aristotle; Walton, Esther; Weickert, Thomas; Weickert, Cynthia; Thompson, Paul; M Van Erp, Theo; Turner, Jessica; Hajek, TomasCorrección de: Molecular Psychiatry https://doi-org.udd.idm.oclc.org/10.1038/s41380-022-01616-5 , publicado en línea el 14 de junio de 2022 El nombre de uno de los coautores (Javier Vázquez-Bourgon) había sido escrito incorrectamente en el pasado, lo que ya ha sido corregido. The article “Obesity and brain structure in schizophrenia – ENIGMA study in 3021 individuals”, written by Sean R. McWhinney, Katharina Brosch, Vince D. Calhoun, Benedicto Crespo-Facorro, Nicolas A. Crossley, Udo Dannlowski, Erin Dickie, Lorielle M. F. Dietze, Gary Donohoe, Stefan Plessis, Stefan Ehrlich, Robin Emsley, Petra Furstova, David C. Glahn, Alfonso Gonzalez- Valderrama, Dominik Grotegerd, Laurena Holleran, Tilo T. J. Kircher, Pavel Knytl, Marian Kolenic, Rebekka Lencer, Igor Nenadić, Nils Opel, JuliaKatharina Pfarr, Amanda L. Rodrigue, Kelly Rootes-Murdy, Alex J. Ross, Kang Sim, Antonín Škoch, Filip Spaniel, Frederike Stein, Patrik Švancer, Diana Tordesillas-Gutiérrez, Juan Undurraga, Javier Váquez-Bourgon, Aristotle Voineskos, Esther Walton, Thomas W. Weickert, Cynthia Shannon Weickert, Paul M. Thompson, Theo G. M. Erp, Jessica A. Turner, Tomas Hajek, was originally published electronically on the publisher’s internet portal on 14 June 2022 without open access. With the author(s)’ decision to opt for Open Choice the copyright of the article changed on 20 May 2022 to © The Author(s) 2022 and the article is forthwith distributed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/ licenses/by/4.0/.Publication Obesity and brain structure in schizophrenia - ENIGMA study in 3021 individuals(2022) McWhinney, Sean; Brosch, Katharina; Calhoun, Vince; Crespo, Benedicto; Crossley, Nicolas; Dannlowski, Udo; Dickie, Erin; Dietze, Lorielle; Donohoe, Gary; Du Plessis, Stefan; Ehrlich, Stefan; Emsley, Robin; Furstova. Petra; Glahn, David; Gonzalez, Alfonso; Grotegerd, Dominik; Nenadić , Igor; Ope, Nils; Pfarr, Julia; Rodrigue, Amanda; Stein, Frederike; Švance, Patrik; Tordesillas, Diana; Undurraga, Juan; Vázquez-Bourgon, Javier; Voineskos, Aristotle; Walton, Esther; Weickert, Thomas; Shannon, Cynthia; Thompson, Paul; Van Erp, Theo; Turner, Jessica; Hajek, TomasSchizophrenia is frequently associated with obesity, which is linked with neurostructural alterations. Yet, we do not understand how the brain correlates of obesity map onto the brain changes in schizophrenia. We obtained MRI-derived brain cortical and subcortical measures and body mass index (BMI) from 1260 individuals with schizophrenia and 1761 controls from 12 independent research sites within the ENIGMA-Schizophrenia Working Group. We jointly modeled the statistical effects of schizophrenia and BMI using mixed effects. BMI was additively associated with structure of many of the same brain regions as schizophrenia, but the cortical and subcortical alterations in schizophrenia were more widespread and pronounced. Both BMI and schizophrenia were primarily associated with changes in cortical thickness, with fewer correlates in surface area. While, BMI was negatively associated with cortical thickness, the significant associations between BMI and surface area or subcortical volumes were positive. Lastly, the brain correlates of obesity were replicated among large studies and closely resembled neurostructural changes in major depressive disorders. We confirmed widespread associations between BMI and brain structure in individuals with schizophrenia. People with both obesity and schizophrenia showed more pronounced brain alterations than people with only one of these conditions. Obesity appears to be a relevant factor which could account for heterogeneity of brain imaging findings and for differences in brain imaging outcomes among people with schizophrenia.Publication Premorbid school performance trajectories in patients with treatment-resistant schizophrenia prescribed clozapine in the public health system in Chile: a case-control study, 2007-2020(2025) Conejeros, Jose; Vasquez, Javiera; Diaz, Camila; Mena, Cristian; Undurraga, Juan; Gonzalez, Alfonso; Claro, Susana; Undurraga, Eduardo; Crossley, NicolasBackground: The premorbid phase of treatment-resistant schizophrenia (TRS) may reveal underlying mechanisms and inform early interventions. According to the neurodevelopmental hypothesis, treatment resistance may be linked to pronounced developmental impairments. We examined school grades and attendance trajectories in children who later developed TRS. Methods: This case-control study analyzed school grade point average and attendance among all individuals born after 1990 and started on clozapine in Chile's public health system as a proxy for TRS. Control groups included children later diagnosed with treatment-responsive schizophrenia, bipolar disorder, and unaffected classmates. Linear mixed models accounted for individual and school-level confounders. Results: We included 1072 children (9929 observations, 29.3% female) subsequently diagnosed with TRS, 323 (2802 observations, 25.7% female) with schizophrenia, 175 (1784 observations, 53.8% female) bipolar disorder, and 273,260 (533,335 observations, 47% female) unaffected classmates. Children who later developed TRS had worse grades across levels than their classmates (-0.26 SD [-0.2, -0.4]), but not treatment-responsive schizophrenia. All severe mental illness groups showed grade declines in later school levels, with TRS showing steeper linear decline than treatment-responsive schizophrenia (group×age of -0.03; 95%CI -0.04, -0.01) and steeper quadratic decline than bipolar disorder (group×age2 of -0.005; -0.01, -0.001). Attendance declined over time in the two groups developing schizophrenia compared to their classmates. Those developing TRS experienced the sharpest drop (group×age compared to schizophrenia -0.03; -0.05, -0.01 and bipolar disorder -0.027; -0.049, -0.006). Conclusions: TRS may stem from a more aggressive pathological process or pronounced late-maturation abnormality, rather than an early premorbid impairment, suggesting an intervention target