CORTICAL THICKNESS AND SUBCORTICAL VOLUMES IN SCHIZOPHRENIA AND BIPOLAR DISORDER

2010 ◽  
Vol 117 (2-3) ◽  
pp. 459 ◽  
Author(s):  
Lars M. Rimol ◽  
Cecilie Hartberg ◽  
Ragnar Nesvåg ◽  
Christine Fennema-Notestine ◽  
Don Hagler ◽  
...  
2010 ◽  
Vol 68 (1) ◽  
pp. 41-50 ◽  
Author(s):  
Lars M. Rimol ◽  
Cecilie B. Hartberg ◽  
Ragnar Nesvåg ◽  
Christine Fennema-Notestine ◽  
Donald J. Hagler ◽  
...  

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Gaelle E. Doucet ◽  
Dongdong Lin ◽  
Yuhui Du ◽  
Zening Fu ◽  
David C. Glahn ◽  
...  

AbstractBipolar disorder and schizophrenia are associated with brain morphometry alterations. This study investigates inter-individual variability in brain structural profiles, both within diagnostic groups and between patients and healthy individuals. Brain morphometric measures from three independent samples of patients with schizophrenia (n = 168), bipolar disorder (n = 122), and healthy individuals (n = 180) were modeled as single vectors to generated individualized profiles of subcortical volumes and regional cortical thickness. These profiles were then used to compute a person-based similarity index (PBSI) for subcortical volumes and for regional cortical thickness, to quantify the within-group similarity of the morphometric profile of each individual to that of the other participants in the same diagnostic group. There was no effect of diagnosis on the PBSI for subcortical volumes. In contrast, compared to healthy individuals, the PBSI for cortical thickness was lower in patients with schizophrenia (effect size = 0.4, p ≤ 0.0002), but not in patients with bipolar disorder. The results were robust and reproducible across samples. We conclude that disease mechanisms for these disorders produce modest inter-individual variations in brain morphometry that should be considered in future studies attempting to cluster patients in subgroups.


2018 ◽  
Vol 28 (1) ◽  
pp. 37-47 ◽  
Author(s):  
Cecilie Bhandari Hartberg ◽  
Elisabeth H. Lange ◽  
Trine Vik Lagerberg ◽  
Unn K. Haukvik ◽  
Ole A. Andreassen ◽  
...  

2021 ◽  
pp. 1-12
Author(s):  
Simon Schmitt ◽  
Tina Meller ◽  
Frederike Stein ◽  
Katharina Brosch ◽  
Kai Ringwald ◽  
...  

Abstract Background MRI-derived cortical folding measures are an indicator of largely genetically driven early developmental processes. However, the effects of genetic risk for major mental disorders on early brain development are not well understood. Methods We extracted cortical complexity values from structural MRI data of 580 healthy participants using the CAT12 toolbox. Polygenic risk scores (PRS) for schizophrenia, bipolar disorder, major depression, and cross-disorder (incorporating cumulative genetic risk for depression, schizophrenia, bipolar disorder, autism spectrum disorder, and attention-deficit hyperactivity disorder) were computed and used in separate general linear models with cortical complexity as the regressand. In brain regions that showed a significant association between polygenic risk for mental disorders and cortical complexity, volume of interest (VOI)/region of interest (ROI) analyses were conducted to investigate additional changes in their volume and cortical thickness. Results The PRS for depression was associated with cortical complexity in the right orbitofrontal cortex (right hemisphere: p = 0.006). A subsequent VOI/ROI analysis showed no association between polygenic risk for depression and either grey matter volume or cortical thickness. We found no associations between cortical complexity and polygenic risk for either schizophrenia, bipolar disorder or psychiatric cross-disorder when correcting for multiple testing. Conclusions Changes in cortical complexity associated with polygenic risk for depression might facilitate well-established volume changes in orbitofrontal cortices in depression. Despite the absence of psychopathology, changed cortical complexity that parallels polygenic risk for depression might also change reward systems, which are also structurally affected in patients with depressive syndrome.


2009 ◽  
Vol 2 (2) ◽  
Author(s):  
Thomas Martin Doring ◽  
Tadeu Takao Almodovar Kubo ◽  
Juliana Rodrigues Doring ◽  
Jiosef Fainberg ◽  
Mario Juruena ◽  
...  

2019 ◽  
Vol 22 ◽  
pp. 101695
Author(s):  
Nefize Yalin ◽  
Aybala Saricicek ◽  
Ceren Hidiroglu ◽  
Andre Zugman ◽  
Nese Direk ◽  
...  

CNS Spectrums ◽  
2019 ◽  
Vol 25 (6) ◽  
pp. 790-796
Author(s):  
Celia Maria de Araujo ◽  
Walter Swardfager ◽  
Andre Zugman ◽  
Hugo Cogo-Moreira ◽  
Sintia I. Belangero ◽  
...  

AbstractObjectiveMental disorders can have a major impact on brain development. Peripheral blood concentrations of brain-derived neurotrophic factor (BDNF) are lower in adult psychiatric disorders. Serum BDNF concentrations and BDNF genotype have been associated with cortical maturation in children and adolescents. In 2 large independent samples, this study tests associations between serum BDNF concentrations, brain structure, and psychopathology, and the effects of BDNF genotype on BDNF serum concentrations in late childhood and early adolescence.MethodsChildren and adolescents (7-14 years old) from 2 cities (n = 267 in Porto Alegre; n = 273 in São Paulo) were evaluated as part of the Brazilian high-risk cohort (HRC) study. Serum BDNF concentrations were quantified by sandwich ELISA. Genotyping was conducted from blood or saliva samples using the SNParray Infinium HumanCore Array BeadChip. Subcortical volumes and cortical thickness were quantified using FreeSurfer. The Development and Well-Being Behavior Assessment was used to identify the presence of a psychiatric disorder.ResultsSerum BDNF concentrations were not associated with subcortical volumes or with cortical thickness. Serum BDNF concentration did not differ between participants with and without mental disorders, or between Val homozygotes and Met carriers.ConclusionsNo evidence was found to support serum BDNF concentrations as a useful marker of developmental differences in brain and behavior in early life. Negative findings were replicated in 2 of the largest independent samples investigated to date.


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