Publications by authors named "Josep Salavert"
Background: Schizophrenic symptoms are known to segregate into reality distortion, negative and disorganization syndromes, but the correlates of these syndromes with regional brain structural change are not well established. Cognitive impairment is a further clinical feature of schizophrenia, whose brain structural correlates are the subject of conflicting findings.
Methods: 165 patients with schizophrenia were rated for symptoms using the PANSS, and cognitive impairment was indexed by estimated premorbid-current IQ discrepancy.
Article Synopsis
- Schizophrenia may arise from evolutionary changes that affect how human brains develop, particularly through Human Accelerated Regions (HARs) that enhance neurodevelopmental processes.
- A study compared 128 schizophrenia patients with 115 controls, analyzing polygenic risk scores focused on HARs and their impact on brain structure.
- Results showed that higher polygenic loads from fetal HARs are linked to reduced surface area in specific brain regions in patients, indicating the significance of prenatal transcriptional regulation in schizophrenia risk.
Article Synopsis
- The study examines the differences in the morphology of the human cerebral cortex across various psychiatric disorders, suggesting that early growth patterns in the cortex may influence later variations in surface area and mental health outcomes.
- Using data from over 27,000 MRI scans, researchers identified significant differences in cortical area among individuals with conditions like ADHD, schizophrenia, and major depression, particularly in association cortices linked to cognitive processing.
- The findings indicate a correlation between these structural differences and prenatal gene expression related to cell types important for brain development, highlighting how prenatal factors may play a crucial role in the risk of developing mental illnesses.
Previous studies have shown that the gene encoding the adhesion G protein-coupled receptor L3 (ADGRL3; formerly latrophilin 3, LPHN3) is associated with Attention-Deficit/Hyperactivity Disorder (ADHD). Conversely, no studies have investigated the anatomical or functional brain substrates of ADGRL3 risk variants. We examined here whether individuals with different ADGRL3 haplotypes, including both patients with ADHD and healthy controls, showed differences in brain anatomy and function.
View Article and Find Full Text PDFBackground: An alteration in self/other differentiation has been proposed as a basis for several symptoms in schizophrenia, including delusions of reference and social functioning deficits. Dysfunction of the right temporo-parietal junction (TPJ), a region linked with social cognition, has been proposed as the basis of this alteration. However, imaging studies of self- and other-processing in schizophrenia have shown, so far, inconsistent results.
View Article and Find Full Text PDFBackground: The brain functional correlates of autobiographical recall are well established, but have been little studied in schizophrenia. Additionally, autobiographical memory is one of a small number of cognitive tasks that activates rather than de-activates the default mode network, which has been found to be dysfunctional in this disorder.
Methods: Twenty-seven schizophrenic patients and 30 healthy controls underwent functional magnetic resonance imaging while viewing cue words that evoked autobiographical memories.
The purpose of this study was to determine whether platelet serotonin-2A (5-HT2A) binding sites and inositol 1,4,5 trisphosphate (IP3) concentrations before treatment can identify olanzapine-responsive patients. The study included 21 never medicated, first-episode schizophrenia patients (antipsychotic-naïve) and 21 patients with a DSM-IV-TR diagnosis of paranoid schizophrenia who had not received depot antipsychotic treatment in the previous 6 months or oral antipsychotic or antidepressant treatment in the previous 2 months (antipsychotic-free). In the antipsychotic-naïve group, olanzapine responders had a significantly lower number of 5-HT2A receptors and lower IP3 concentrations at baseline than non-responders.
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