Failure of deactivation in bipolar disorder during performance of an fMRI adapted version of the Stroop task.

INTRODUCTION: Few studies have examined the functional brain correlates of the performance of the Stroop task in bipolar disorder (BD). It is also not known whether it is associated with failure of de-activation in the default mode network, as has been found in studies using other tasks. METHODS: Twenty-four BD patients and 48 age, sex and educationally estimated intellectual quotient (IQ) matched healthy subjects (HS) underwent a functional MRI during performance of the counting Stroop task. Task-related activations (incongruent versus congruent condition) and de-activations (incongruent versus fixation) were examined using whole-brain, voxel-based methodology. RESULTS: Both the BD patients and the HS showed activation in a cluster encompassing the left dorsolateral and ventrolateral prefrontal cortex and the rostral anterior cingulate cortex and supplementary motor area, with no differences between them. The BD patients, however, showed significant failure of de-activation in the medial frontal cortex and the posterior cingulate cortex/precuneus. CONCLUSIONS: The failure to find activation differences between BD patients and controls suggests that the 'regulative' component of cognitive control remains intact in the disorder, at least outside episodes of illness. The failure of de-activation found adds to evidence documenting trait-like default mode network dysfunction in the disorder.

The gut-microbiota-brain axis in a Spanish population in the aftermath of the COVID-19 pandemic: microbiota composition linked to anxiety, trauma, and depression profiles.

The prevalence of anxiety and depression soared following the COVID-19 pandemic. To effectively treat these conditions, a comprehensive understanding of all etiological factors is needed. This study investigated fecal microbial features associated with mental health outcomes (symptoms of anxiety, depression, or posttraumatic stress disorder (PTSD)) in a Spanish cohort in the aftermath of the COVID-19 pandemic. Microbial communities from stool samples were profiled in 198 individuals who completed validated, self-report questionnaires. 16S ribosomal RNA gene V3-4 amplicon sequencing was performed. Microbial diversity and community structure were analyzed, together with relative taxonomic abundance. In our cohort of N=198, 17.17% reported depressive symptoms, 37.37% state anxiety symptoms, 40.90% trait anxiety symptoms, and 8.08% PTSD symptoms, with high levels of comorbidity. Individuals with trait anxiety had lower Simpson's diversity. Fusicatenibacter saccharivorans was reduced in individuals with comorbid PTSD + depression + state and trait anxiety symptoms, whilst an expansion of Proteobacteria and depletion of Synergistetes phyla were noted in individuals with depressive symptoms. The relative abundance of Anaerostipes was positively correlated with childhood trauma, and higher levels of Turicibacter sanguinis and lower levels of Lentisphaerae were found in individuals who experienced life-threatening traumas. COVID-19 infection and vaccination influenced the overall microbial composition and were associated with distinct relative taxonomic abundance profiles. These findings will help lay the foundation for future studies to identify microbial role players in symptoms of anxiety, depression, and PTSD and provide future therapeutic targets to improve mental health outcomes.

Activation and deactivation patterns in schizophrenia during performance of an fMRI adapted version of the stroop task.

The Stroop task, which examines an aspect of executive function/cognitive control, the ability to inhibit prepotent responses, has been relatively little examined in schizophrenia, and the findings have been inconsistent. Whether performance of this task is associated with failure of de-activation in the disorder is also uncertain. We examined 42 schizophrenic patients and 61 healthy controls during performance of an fMRI-adapted version of the Stroop task, the counting Stroop task. Task-related activations (incongruent > congruent condition) and de-activations (baseline > incongruent) were examined using whole-brain, voxel-based methods. In the healthy controls, task performance was found to be associated with activations in the left dorsolateral prefrontal cortex and the dorsal anterior cingulate cortex, among other regions. De-activations were seen in the medial frontal cortex, the middle and posterior cingulate gyrus and cuneus, the parahippocampal gyrus and the hippocampus. The schizophrenic patients did not show reduced activation compared to the healthy controls. They did, however, show failure of de-activation in the medial frontal cortex. Our negative finding with respect to hypoactivation during performance of a task requiring inhibition of prepotent responses suggests that brain functional abnormality in schizophrenia may not affect all aspects of executive function/cognitive control. The finding of medial frontal cortex failure of de-activation adds to existing findings of default mode network dysfunction in the disorder.

The relationships between sociodemographic, psychosocial and clinical variables with personal-stigma in patients diagnosed with schizophrenia.

BACKGROUND: Studies suggest that people with a diagnosis of schizophrenia are one of the most stigmatized groups in society. AIM: To comprehensively analyze personal stigma in patients diagnosed with schizophrenia. METHOD: Data were obtained from 89 patients. Patients were evaluated with the following scales: a sociodemographic and clinical questionnaire, the Discrimination and Stigma Scale, the Self-perception of Stigma Questionnaire for People with Schizophrenia, the Positive and Negative Syndrome Scale, the Calgary Depression Scale for Schizophrenia, the Global Assessment of Functioning Scale, and the Brief Social Functioning Scale. RESULTS: Relations between personal stigma and sociodemographic and psychosocial variables were poor. However, clinical variables correlated with different facets of personal stigma. Personal stigma subscales´ correlations were between experienced stigma, anticipated stigma, and self-stigma to each other. 29.5% of the experienced stigma subscale variance was explained by age of onset and level of depression. 20.1% of the anticipated stigma subscale variance was explained by level of depression and gender. 27.3% of the overcoming stigma subscale variance was explained by level of depression and positive and negative psychotic symptoms. 35.8% of the self-stigma scale variance was explained by the level of depression. CONCLUSIONS: Addressing stigma within treatment seems of crucial importance since all stigma facets seem to be highly related to clinical dimensions, especially depression Therefore, including strategies to reduce stigma in care programs may help patients with schizophrenia to better adjust in life and improve their illness process.

Staging of depressive disorders: Relevance of resistance to treatment and residual symptoms.

BACKGROUND: Clinical staging model for depression helps to better define the clinical situation of patients. The objectives of this study are: to correlate the Hetrick's staging model of depression with the severity of depression, associated disability, and resistance to treatment in the established disease stages and to test the modification introduced by our group consisting in the introduction of a substage for recurrence from a previous episode that was stabilized with a complete remission. METHODS: A Cross-sectional study with 133 adult subjects having a current and primary diagnosis of Depressive disorder was developed. Patients were classified according to the model and assessed with: 17-item Hamilton Depression Scale (HAM-D), Clinical Global Impression (CGI); Global Assessment of Function (GAF); Maudsley Staging Method for treatment resistance (MSM) and Sheeham Disability Schedule (SDS). RESULTS: The variable that best contributes to the differentiation between clinical stages, in established Depression, is resistance to treatment evaluated by the MSM. Correlations between MSM and the clinical stages were statistically significant between most pairs of stages. Finally, we showed preliminary data in order to prove that a differential sub-stage for recurrent depression with and without inter-episodic remission in the current heuristic models could be a possible stage for better define depression staging model. CONCLUSIONS: Resistance to treatment should be included in the definition of clinical stages in established depression. Despite the difficulty of establishing a valid model for the staging of depression, it can certainly add great value to diagnosis, therapeutic interventions and clinical research.

Relación entre variables sociodemográficas, psicosociales y clínicas y el estigma personal en pacientes con diagnóstico de esquizofrenia / The relationships between sociodemographic, psychosocial and clinical variables

ANTECEDENTES: Estudios previos sugieren que las personas con esquizofrenia son uno de los grupos más estigmatizados de la sociedad. OBJETIVO: analizar ampliamente el estigma personal en pacientes con esquizofrenia. MÉTODO: Se obtuvieron datos de 89 pacientes. Éstos fueron evaluados con los siguientes instrumentos: características sociodemográficas y clínicas, Escala de Discriminación y Estigma, Cuestionario de Autopercepción del Estigma, Escala de Síndromes positivos y negativos, Escala de depresión de Calgary, Escala de Evaluación de la Actividad Global y Escala Breve de Funcionamiento Social. RESULTADOS: las relaciones entre el estigma personal y las variables sociodemográficas y psicosociales resultaron escasamente significativas. Sin embargo, las variables clínicas correlacionaron significativamente con diferentes facetas del estigma personal. Las correlaciones de las subescalas de estigma personal fueron entre estigma experimentado, estigma anticipado y autoestigma entre sí. El 29,5% de la variación de la subescala "trato injusto" se explicó por la edad de inicio y el nivel de depresión. El 20,1% de la variación de la subescala "autolimitación" se explicó por el nivel de depresión y el género. El 27,3% de la subescala "superación del estigma" se explica por el nivel de depresión y los síntomas psicóticos positivos y negativos. El 35,8% de la variación de la escala de autoestigma se explicó por el nivel de depresión. CONCLUSIONES: Abordar el estigma dentro del tratamiento parece de crucial importancia ya que todas las facetas del estigma están altamente relacionadas con las dimensiones clínicas, especialmente la depresión. Por lo tanto, incluir estrategias para reducir el estigma en los programas de atención puede ayudar a los pacientes con esquizofrenia a una mejor adaptación funcional y proceso evolutivo

BACKGROUND: Studies suggest that people with a diagnosis of schizophrenia are one of the most stigmatized groups in society. AIM: To comprehensively analyze personal stigma in patients diagnosed with schizophrenia. METHOD: Data were obtained from 89 patients. Patients were evaluated with the following scales: a sociodemographic and clinical questionnaire, the Discrimination and Stigma Scale, the Self-perception of Stigma Questionnaire for People with Schizophrenia, the Positive and Negative Syndrome Scale, the Calgary Depression Scale for Schizophrenia, the Global Assessment of Functioning Scale, and the Brief Social Functioning Scale. RESULTS: Relations between personal stigma and socio-demographic and psychosocial variables were poor. However, clinical variables correlated with different facets of personal stigma. Personal stigma subscales ́ correlations were between experienced stigma, anticipated stigma, and self-stigma to each other. 29.5% of the experienced stigma subscale variance was explained by age of onset and level of depression. 20.1% of the anticipated stigma subscale variance was explained by level of depression and gender. 27.3% of the overcoming stigma subscale variance was explained by level of depression and positive and negative psychotic symptoms. 35.8% of the self-stigma scale variance was explained by the level of depression

Ankyrin Repeat and Kinase Domain Containing 1 Gene, and Addiction Vulnerability.

The TaqIA single nucleotide variant (SNV) has been tested for association with addictions in a huge number of studies. TaqIA is located in the ankyrin repeat and kinase domain containing 1 gene (ANKK1) that codes for a receptor interacting protein kinase. ANKK1 maps on the NTAD cluster along with the dopamine receptor D2 (DRD2), the tetratricopeptide repeat domain 12 (TTC12) and the neural cell adhesion molecule 1 (NCAM1) genes. The four genes have been associated with addictions, although TTC12 and ANKK1 showed the strongest associations. In silico and in vitro studies revealed that ANKK1 is functionally related to the dopaminergic system, in particular with DRD2. In antisocial alcoholism, epistasis between ANKK1 TaqIA and DRD2 C957T SNVs has been described. This clinical finding has been supported by the study of ANKK1 expression in peripheral blood mononuclear cells of alcoholic patients and controls. Regarding the ANKK1 protein, there is direct evidence of its location in adult and developing central nervous system. Together, these findings of the ANKK1 gene and its protein suggest that the TaqIA SNV is a marker of brain differences, both in structure and in dopaminergic function, that increase individual risk to addiction development.

Hypothalamic-pituitary axis response to a 0.25-MG dexamethasone test in women with fibromyalgia.

Fibromyalgia has been reported as having some clinical overlap with both depression and emotionally-unstable disorders, although both types of disorders present different cortisol suppression response to dexamethasone. In this study we investigated the hypothalamic-pituitary-adrenal system (HPA) in the fibromyalgic syndrome (FMS) using a dexamethasone suppression test (DST) of 0.25 mg designed to specifically detect cortisol hypersuppression. We studied 59 women (20 patients and 39 healthy controls) to whom the DST was administered together with a battery of psychometric tests. In our results, patients with FMS had significant lower levels of basal cortisol pre- and post-DST compared with control subjects. However, cortisol suppression rate in patients after DST was not significantly different than in controls. As other syndromes like post-traumatic stress disorder or emotionally unstable personality disorders, also related with high incidence of severe trauma, FMS patients presented significant low basal cortisol. However, they did not have cortisol hypersuppression as is commonly found in the mentioned disorders. The relation of FMS with lifetime traumas and with emotional instability should be further investigated in order to improve psychological treatment approaches for these patients.LAY SUMMARYPatients with fibromyalgic syndrome have basal hypocortisoism but no cortisol hypersuppression after dexamethasone infusion compared to control subjects, as other trauma-related syndromes.

Diez años de investigación traslacional colaborativa en enfermedades mentales: el CIBERSAM / CIBERSAM: Ten years of collaborative translational research in mental disorders

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The Addiction-Related Protein ANKK1 is Differentially Expressed During the Cell Cycle in Neural Precursors.

TaqIA is a polymorphism associated with addictions and dopamine-related traits. It is located in the ankyrin repeat and kinase domain containing 1 gene (ANKK1) nearby the gene for the dopamine D2 receptor (D2R). Since ANKK1 function is unknown, TaqIA-associated traits have been explained only by differences in D2R. Here we report ANKK1 studies in mouse and human brain using quantitative real-time PCR, Western blot, immunohistochemistry, and flow cytometry. ANKK1 mRNA and protein isoforms vary along neurodevelopment in the human and mouse brain. In mouse adult brain ANKK1 is located in astrocytes, nuclei of postmitotic neurons and neural precursors from neurogenic niches. In both embryos and adults, nuclei of neural precursors show significant variation of ANKK1 intensity. We demonstrate a correlation between ANKK1 and the cell cycle. Cell synchronization experiments showed a significant increment of ANKK1-kinase in mitotic cells while ANKK1-kinase overexpression affects G1 and M phase that were found to be modulated by ANKK1 alleles and apomorphine treatment. Furthermore, during embryonic neurogenesis ANKK1 was expressed in slow-dividing neuroblasts and rapidly dividing precursors which are mitotic cells. These results suggest a role of ANKK1 during the cell cycle in neural precursors thus providing biological support to brain structure involvement in the TaqIA-associated phenotypes.

The Microbiota and Gut-Brain Axis: Contributions to the Immunopathogenesis of Schizophrenia.

BACKGROUND: The underlying pathophysiology of schizophrenia still remains elusive. Thus, there is a pressing need to identify novel targets for the development of new interventions and elucidate related biomarkers for the identification and monitoring of potentially responsive patients. In this sense, several hypotheses involving immune/inflammatory changes and the consequent oxidative/nitrosative stress, as well as a dysregulation in the immuno-inflammatory response have come into sight. METHODS: Considering the great amount of genes encoded by the microbiome and the evidences pointing to the potential role of the gut microbiota on several neurologic and psychiatric diseases, the aim of this review is to evaluate the possible role of these organisms in the immunopathogenesis of schizophrenia. To that end, we will focus not only on gut microbiota dysbiosis but also on bacterial translocation as an inductor of neuroinflammation. RESULTS: Studies have shown that the gut microbiota may play a key role in the immunopathogenesis of schizophrenia and that essential pathways implicated in the etiopathophysiology of schizophrenia are also regulated by the microbiota-gut-brain (MGB) axis. Moreover, studies also indicate a possible role of the innate immunity through the Toll-like receptors (TLRs) and their activation by bacterial translocation, as a consequence of intestinal dysfunction, in the pathophysiology of psychotic disorders. CONCLUSION: This is a promising area of investigation with huge potential to offer advances in the realm of personalized medicine and accordingly, future research should examine several microbiota-targeted therapies in order to improve symptoms and to decrease the immune dysregulation seen in patients with schizophrenia.

Elevated midline-parietal gamma band noise power in schizophrenia but not in bipolar patients.

Gamma oscillations are key in coordinating brain activity and seem to be altered in schizophrenia. In previous work, we studied the spatial distribution of a noise power measure (scalp-recorded electroencephalographic activity unlocked to stimuli) and found higher magnitudes in the gamma band related to symptoms and cognition in schizophrenia. In the current study, we sought to replicate those findings and to study its specificity for schizophrenia in a completely independent sample. A principal component analysis (PCA) was used to determine the factorial structure of gamma noise power acquired with an electroencephalographic recording during an odd-ball P300 paradigm in the 250- to 550-ms window in 70 patients with schizophrenia (16 patients with first episode), 45 bipolar patients and 65 healthy controls. Clinical and cognitive correlates of the resulting factors were also assessed. Three factors arose from the PCA. The first displayed a midline-parietal distribution (roughly corresponding to the default mode network), the second was centro-temporal and the third anterior-frontal. Schizophrenia but not bipolar patients showed higher gamma noise power loadings in the first factor in comparison with controls. Scores for this factor were significantly and directly associated with positive and total symptoms in patients and inversely associated with global cognition in all participants. The results of this study replicate those of our previous publication and suggest an elevated midline-parietal gamma noise power specific to schizophrenia. The gamma noise power measure seems to be a useful tool for studying background oscillatory activity during performance of cognitive tasks.

Facial affect recognition in early and late-stage schizophrenia patients.

Prior studies have shown deficits in social cognition and emotion perception in first-episode psychosis (FEP) and multi-episode schizophrenia (MES) patients. These studies compared patients at different stages of the illness with only a single control group which differed in age from at least one clinical group. The present study provides new evidence of a differential pattern of deficit in facial affect recognition in FEP and MES patients using a double age-matched control design. Compared to their controls, FEP patients only showed impaired recognition of fearful faces (p=.007). In contrast to this, the MES patients showed a more generalized deficit compared to their age-matched controls, with impaired recognition of angry, sad and fearful faces (ps<.01) and an increased misattribution of emotional meaning to neutral faces. PANSS scores of FEP patients on Depressed factor correlated positively with the accuracy to recognize fearful expressions (r=.473). For the MES group fear recognition correlated positively with negative PANSS factor (r=.498) and recognition of sad and neutral expressions was inversely correlated with disorganized PANSS factor (r=-.461 and r=-.541, respectively). These results provide evidence that a generalized impairment of affect recognition is observed in advanced-stage patients and is not characteristic of the early stages of schizophrenia. Moreover, the finding that anomalous attribution of emotional meaning to neutral faces is observed only in MES patients suggests that an increased attribution of salience to social stimuli is a characteristic of social cognition in advanced stages of the disorder.

The Addiction-Related Gene Ankk1 is Oppositely Regulated by D1R- and D2R-Like Dopamine Receptors.

The ankyrin repeat and kinase domain containing 1 (ANKK1) TaqIA polymorphism has been extensively studied as a marker of the gene for dopamine receptor D2 (DRD2) in addictions and other dopamine-associated traits. In vitro mRNA and protein studies have shown a potential connection between ANKK1 and the dopaminergic system functioning. Here, we have investigated whether Ankk1 expression in the brain is regulated by treatment with dopaminergic agonists. We used quantitative RT-PCR of total brain and Western blots of specific brain areas to study Ankk1 in murine brain after dopaminergic treatments. We found that Ankk1 mRNA was upregulated after activation of D1R-like dopamine receptors with SKF38393 (2.660 ± 1.035-fold; t: 4.066, df: 11, P = 0.002) and apomorphine (2.043 ± 0.595-fold; t: 3.782, df: 8, P = 0.005). The D2R-like agonist quinelorane has no effect upon Ankk1 mRNA (1.004 ± 0.580-fold; t: 0.015, df: 10, P = 0.9885). In contrast, mice treatment with the D2R-like agonists 7-OH-DPAT and aripiprazole caused a significant Ankk1 mRNA downregulation (0.606 ± 0.057-fold; t: 2.786, df: 10, P = 0.02 and 0.588 ± 0.130-fold; t: 2.394, df: 11, P = 0.036, respectively). With respect the Ankk1 proteins profile, no effects were found after SKF38393 (t: 0.54, df: 2, P = 0.643) and Quinelorane (t: 0.286, df: 8, P = 0.782) treatments. In contrast, the D2R-like agonist 7-OH-DPAT (±) caused a significant increment of Ankk1 in the striatum (t: 2.718, df: 7; P = 0.03) when compared to the prefrontal cortex. The activation of D1R-like and D2-R-like leads to opposite transcriptional regulation of Ankk1 by specific pathways.

Are negative symptoms really related to cognition in schizophrenia?

Previous studies have generally found a relationship between negative and cognitive symptoms in schizophrenia. The present study investigated the relationship between the 5 PANSS factors of a recent consensus model developed by NIMH researchers, and cognitive performance as assessed with the MATRICS Consensus Cognitive Battery (MCCB) in 80 patients with schizophrenia using correlation and regression analyses. The PANSS Cognitive factor showed a small to moderate significant association with MCCB Speed of processing, Working memory, Verbal learning, the Neurocognitive composite score, and the Overall composite score. Notably, however, no relationship was found between the PANSS Negative factor and any of the MCCB scores. The Positive, Excited and Depressed factors also did not show associations with the MCCB. These results highlight the need for refined assessment instruments and support the relative independence of cognition from other domains of psychopathology, including negative symptoms, in patients with schizophrenia.

Patterns of Emotion Attribution are Affected in Patients with Schizophrenia.

Deficits in facial affect recognition have been repeatedly reported in schizophrenia patients. The hypothesis that this deficit is caused by poorly differentiated cognitive representation of facial expressions was tested in this study. To this end, performance of patients with schizophrenia and controls was compared in a new emotion-rating task. This novel approach allowed the participants to rate each facial expression at different times in terms of different emotion labels. Results revealed that patients tended to give higher ratings to emotion labels that did not correspond to the portrayed emotion, especially in the case of negative facial expressions (p < .001, η 2 = .131). Although patients and controls gave similar ratings when the emotion label matched with the facial expression, patients gave higher ratings on trials with "incorrect" emotion labels (p s < .05). Comparison of patients and controls in a summary index of expressive ambiguity showed that patients perceived angry, fearful and happy faces as more emotionally ambiguous than did the controls (p < .001, η 2 = .135). These results are consistent with the idea that the cognitive representation of emotional expressions in schizophrenia is characterized by less clear boundaries and a less close correspondence between facial configurations and emotional states.

Desarrollo profesional en investigación traslacional en neurociencias y salud mental: educación y formación dentro del Centro de Investigación Biomédica en Red en Salud Mental / Building up careers in translational neuroscience and mental health research: Education and training in the Centre for Biomedical Research in Mental Health

Aumenta el número de redes de investigación colaborativas en salud mental y con ello la importancia de los programas de formación como parte esencial de la especialización de sus miembros. A continuación revisamos de un modo crítico la implementación específica de un programa de formación en investigación traslacional en salud mental y neurociencias en el Centro de Investigación Biomédica en Red en Salud Mental, con el fin de informar sobre la integración estratégica de la investigación básica dentro de la práctica clínica y lograr un impacto positivo en los sistemas de salud mental y la sociedad. Se examinan las actividades de formación y los programas específicos desarrollados por la red de investigación, así como los desafíos de su implementación. El Centro de Investigación Biomédica en Red en Salud Mental ha centrado su formación a través de diferentes actividades que han dado lugar al desarrollo de un máster interuniversitario y a un programa de posgrado en Investigación en Salud Mental, certificado por la Agencia Nacional de Evaluación de la Calidad y Acreditación. La consolidación de los programas de formación dentro del Centro de Investigación Biomédica en Red en Salud Mental ha supuesto un avance considerable para la formación de los investigadores, a fin de satisfacer las necesidades actuales de competencia en materia de investigación. El máster constituye una oportunidad única para el desarrollo de las habilidades necesarias en investigación en neurociencia y salud mental dentro del marco oficial de los programas universitarios en España (AU)

The number of large collaborative research networks in mental health is increasing. Training programs are an essential part of them. We critically review the specific implementation of a research training program in a translational Centre for Biomedical Research in Mental Health in order to inform the strategic integration of basic research into clinical practice to have a positive impact in the mental health system and society. Description of training activities, specific educational programs developed by the research network, and challenges on its implementation are examined. The Centre for Biomedical Research in Mental Health has focused on training through different activities which have led to the development of an interuniversity master's degree postgraduate program in mental health research, certified by the National Spanish Agency for Quality Evaluation and Accreditation. Consolidation of training programs within the Centre for Biomedical Research in Mental Health has considerably advanced the training of researchers to meet competency standards on research. The master's degree constitutes a unique opportunity to accomplish neuroscience and mental health research career-building within the official framework of university programs in Spain (AU)

Building up careers in translational neuroscience and mental health research: Education and training in the Centre for Biomedical Research in Mental Health.

The number of large collaborative research networks in mental health is increasing. Training programs are an essential part of them. We critically review the specific implementation of a research training program in a translational Centre for Biomedical Research in Mental Health in order to inform the strategic integration of basic research into clinical practice to have a positive impact in the mental health system and society. Description of training activities, specific educational programs developed by the research network, and challenges on its implementation are examined. The Centre for Biomedical Research in Mental Health has focused on training through different activities which have led to the development of an interuniversity master's degree postgraduate program in mental health research, certified by the National Spanish Agency for Quality Evaluation and Accreditation. Consolidation of training programs within the Centre for Biomedical Research in Mental Health has considerably advanced the training of researchers to meet competency standards on research. The master's degree constitutes a unique opportunity to accomplish neuroscience and mental health research career-building within the official framework of university programs in Spain.

Patterns of emotion attribution are affected in patients with schizophrenia

Deficits in facial affect recognition have been repeatedly reported in schizophrenia patients. The hypothesis that this deficit is caused by poorly differentiated cognitive representation of facial expressions was tested in this study. To this end, performance of patients with schizophrenia and controls was compared in a new emotion-rating task. This novel approach allowed the participants to rate each facial expression at different times in terms of different emotion labels. Results revealed that patients tended to give higher ratings to emotion labels that did not correspond to the portrayed emotion, especially in the case of negative facial expressions (p < .001, η2 = .131). Although patients and controls gave similar ratings when the emotion label matched with the facial expression, patients gave higher ratings on trials with "incorrect" emotion labels (ps < .05). Comparison of patients and controls in a summary index of expressive ambiguity showed that patients perceived angry, fearful and happy faces as more emotionally ambiguous than did the controls (p < .001, η2 = .135). These results are consistent with the idea that the cognitive representation of emotional expressions in schizophrenia is characterized by less clear boundaries and a less close correspondence between facial configurations and emotional states (AU)

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