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Childhood socioemotional development and growth mindset preceding schizophrenia: case–control study using prospectively collected data
(Royal College of Psychiatrists, 2026-04-06)
Javiera Vasquez-Nuñez
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José Conejeros
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Camila Díaz-Dellarrossa
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Cristian Mena
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UNDURRAGA FOURCADE, JUAN PABLO
<jats:sec id="S2056472426110047_as1"> <jats:title>Background</jats:title> <jats:p>Understanding premorbid socioemotional trajectories in schizophrenia is crucial for early identification and potential primary prevention. Studies in adults with schizophrenia suggest similar socioemotional premorbid difficulties, but are limited by their retrospective design.</jats:p> </jats:sec> <jats:sec id="S2056472426110047_as2"> <jats:title>Aims</jats:title> <jats:p>To contribute new insights into the premorbid socioemotional characteristics of schizophrenia, beyond the biases of retrospective studies, this research investigates three educational socioemotional dimensions in children who later developed the disorder.</jats:p> </jats:sec> <jats:sec id="S2056472426110047_as3"> <jats:title>Method</jats:title> <jats:p> We conducted a case–control study using prospectively collected data, examining childhood differences in perceived parental support, self-esteem and school motivation, and growth mindset (intelligence can improve through effort) among individuals who later developed schizophrenia ( <jats:italic>n</jats:italic> = 341) and their classmates ( <jats:italic>n</jats:italic> = 20 567). We constructed <jats:italic>z</jats:italic> -normalised indicators based on standardised national tests administered in fourth, eighth and tenth grades in Chile. Mixed linear models accounted for repeated measures and adjusted for educational level, gender, grade point average, school and year. </jats:p> </jats:sec> <jats:sec id="S2056472426110047_as4"> <jats:title>Results</jats:title> <jats:p> Children later diagnosed with schizophrenia reported less parental educational support compared with their classmates ( <jats:italic>β</jats:italic> = −0.276, 95% CI −0.388 to −0.163). Only girls who later developed schizophrenia reported lower self-esteem and school motivation than their peers ( <jats:italic>β</jats:italic> = −0.290, 95% CI −0.498 to −0.131). Contrary to our hypothesis, children who later developed schizophrenia showed a higher growth mindset ( <jats:italic>β</jats:italic> = 0.287, 95% CI 0.077–0.497). </jats:p> </jats:sec> <jats:sec id="S2056472426110047_as5"> <jats:title>Conclusions</jats:title> <jats:p>Our results suggest that premorbid socioemotional characteristics in schizophrenia are detectable in childhood and may vary by gender. These findings highlight the potential of educational settings as platforms for preventive interventions aimed at enhancing parental support and monitoring students’ psycho-emotional well-being, while acknowledging gender-specific developmental trajectories and heterogeneity in premorbid functioning.</jats:p> </jats:sec>
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Quantitative susceptibility mapping of deep brain nuclei in 22q11.2 deletion syndrome
(Frontiers Media SA, 2026-01-09)
Nestor Muñoz
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Marisleydis García
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Analía Cuiza
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Angeles Tepper
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Javiera Vásquez
<jats:sec> <jats:title>Background</jats:title> <jats:p>22q11.2 Deletion Syndrome (22q11.2 DS) confers a high risk to dopamine-related disorders such as schizophrenia and Parkinson’s disease. These disorders have recently been associated with abnormal iron concentrations in deep brain nuclei. In this study we hypothesized that abnormal iron concentrations may also appear in deep brain nuclei of individuals with 22q11.2 DS.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>We analyzed iron concentrations in four dopamine-related nuclei (caudate, putamen, substantia nigra, and globus pallidus) of 32 individuals, including adolescents and adults, carriers of the 22q11.2 DS and 49 healthy controls. For all individuals, we characterized iron concentrations in each region by quantifying R2* values and using a recently developed technique called Quantitative Susceptibility Mapping (QSM). We used linear mixed models to analyze potential differences between 22q11.2 DS individuals and our control group, considering brain region, age, sex, laterality, volume size, and framewise-displacement as fixed-effect covariates and individuals’ intercepts as random effects.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>All individuals showed age-related increases in R2* values and susceptibility within dopaminergic nuclei (caudate, putamen, and substantia nigra). However, individuals with 22q11.2 DS showed a significantly lower rate of increase compared to healthy control group. This suggests that, over time, individuals with 22q11.2 deletion syndrome accumulate less iron in these nuclei than healthy controls.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>Individuals with 22q11.2 DS present lower iron accumulation in dopaminergic areas, such as substantia nigra, caudate and putamen, relative to healthy controls. These findings suggest a possible association between a dopaminergic dysfunction and abnormal iron accumulation.</jats:p> </jats:sec>
1
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Longitudinal changes in striatocortical connectivity in first-episode psychosis associated with the emergence of treatment resistance
(Springer Science and Business Media LLC, 2025-08-16)
Angeles Tepper
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Javiera Vásquez
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Camila Díaz Dellarossa
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Juan Pablo Ramirez-Mahaluf
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Juan Aguirre
1
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Human development, inequality, and their associations with brain structure across 29 countries
(Royal College of Psychiatrists, 2025)
Vicente Medel
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Luz M. Alliende
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Richard Bethlehem
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Jakob Seidlitz
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Grace Ringlein
2
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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
(Cambridge University Press (CUP), 2025)
Jose Conejeros-Pavez
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Javiera Vasquez
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Camila Diaz
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Cristian Mena
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UNDURRAGA FOURCADE, JUAN PABLO
Background 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 (groupxage of -0.03; 95%CI -0.04, -0.01) and steeper quadratic decline than bipolar disorder (groupxage 2 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 (groupxage 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.
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Cognitive function at first episode in patients subsequently developing treatment-resistant schizophrenia
(Elsevier BV, 2025-02)
Juan M. Aguirre
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Camila Díaz Dellarossa
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Daniella Barbagelata
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Javiera Vásquez
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Cristián Mena
Scopus© Citations 1 3
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Source‐based morphometry reveals structural brain pattern abnormalities in 22q11.2 deletion syndrome
(2024)
Ruiyang Ge
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Christopher R. K. Ching
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Anne S. Bassett
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Leila Kushan
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Kevin M. Antshel
<jats:title>Abstract</jats:title><jats:p>22q11.2 deletion syndrome (22q11DS) is the most frequently occurring microdeletion in humans. It is associated with a significant impact on brain structure, including prominent reductions in gray matter volume (GMV), and neuropsychiatric manifestations, including cognitive impairment and psychosis. It is unclear whether GMV alterations in 22q11DS occur according to distinct structural patterns. Then, 783 participants (470 with 22q11DS: 51% females, mean age [SD] 18.2 [9.2]; and 313 typically developing [TD] controls: 46% females, mean age 18.0 [8.6]) from 13 datasets were included in the present study. We segmented structural T1‐weighted brain MRI scans and extracted GMV images, which were then utilized in a novel source‐based morphometry (SBM) pipeline (SS‐Detect) to generate structural brain patterns (SBPs) that capture co‐varying GMV. We investigated the impact of the 22q11.2 deletion, deletion size, intelligence quotient, and psychosis on the SBPs. Seventeen GMV‐SBPs were derived, which provided spatial patterns of GMV covariance associated with a quantitative metric (i.e., loading score) for analysis. Patterns of topographically widespread differences in GMV covariance, including the cerebellum, discriminated individuals with 22q11DS from healthy controls. The spatial extents of the SBPs that revealed disparities between individuals with 22q11DS and controls were consistent with the findings of the univariate voxel‐based morphometry analysis. Larger deletion size was associated with significantly lower GMV in frontal and occipital SBPs; however, history of psychosis did not show a strong relationship with these covariance patterns. 22q11DS is associated with distinct structural abnormalities captured by topographical GMV covariance patterns that include the cerebellum. Findings indicate that structural anomalies in 22q11DS manifest in a nonrandom manner and in distinct covarying anatomical patterns, rather than a diffuse global process. These SBP abnormalities converge with previously reported cortical surface area abnormalities, suggesting disturbances of early neurodevelopment as the most likely underlying mechanism.</jats:p>
3Scopus© Citations 6
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Robust and replicable functional brain signatures of 22q11.2 deletion syndrome and associated psychosis: a deep neural network-based multi-cohort study
(2024)
Kaustubh Supekar
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Carlo de los Angeles
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Srikanth Ryali
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Leila Kushan
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Charlie Schleifer
Scopus© Citations 2 5
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Correction: Obesity and brain structure in schizophrenia – ENIGMA study in 3021 individuals
(2022)
Sean R. McWhinney
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Katharina Brosch
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Vince D. Calhoun
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Benedicto Crespo-Facorro
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Nicolas A. Crossley
Scopus© Citations 2 1
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Predictors of clozapine discontinuation at 2 years in treatment-resistant schizophrenia
(2021)
Barbara Iruretagoyena
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Carmen Paz Castañeda
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Cristian Mena
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Camila Diaz
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Ruben Nachar
7Scopus© Citations 10

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