Lourdes Fañanás

Centro de Investigación Biomedica En Red del Área de Salud Mental, Madrid, Madrid, Spain

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Publications (183)802.58 Total impact

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    ABSTRACT: Schizophrenia patients typically present a widespread bilateral cortical thinning from the early stages of the illness. However, there is controversy whether this reduction in cortical thickness (CT) is static or progressive over the evolution of the disorder. Disrupted-in-Schizophrenia 1 (DISC1) is one of the main candidates genes for schizophrenia, as it has been found associated to the illness, and to several endophenotypes of the disorder including structural brain differences. This gene is known to be involved in neurodevelopment and brain maturation processes. We therefore hypothesized that variations in this gene modulate different progressions of CT in psychosis. Seventy-nine Caucasian drug-naive patients experiencing a first episode of non-affective psychosis were genotyped for rs6675281 (Leu607Phe) and rs821616 (Ser704Cys) SNPs of the DISC1 gene. Brain MRIs were carried out at baseline and 3 years after initiating the treatment. Other clinical and socio-demographic variables were recorded to rule out possible confounding effects. Patients homozygous for the Leu allele of the rs6675281 SNP had a significant (p < 0.05) descend in CT over the 3-years period, while those carrying the Phe allele presented an increase in CT. When combining the two SNPs we found a synergic effect on CT progression, presenting those patients homozygous for Leu607 +Ser704 a more pronounced cortical thinning. In conclusion, DISC1 gene variations may modulate the longitudinal changes in cortical thickness in patients suffering from a first episode of non-affective psychosis.
    Brain Imaging and Behavior 07/2015; DOI:10.1007/s11682-015-9433-1 · 4.60 Impact Factor
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    ABSTRACT: Schizotypal traits are phenotypic risk factors for schizophrenia, associated with biological changes across a putative schizophrenia spectrum. In this study, we tested the hypothesis that brain structural changes in key brain areas relevant to this spectrum (esp. medial and lateral prefrontal cortex) would vary across different degrees of schizotypal trait expression and/or phenotypic markers of psychosis proneness in healthy non-clinical volunteers. We analysed high-resolution 3Tesla magnetic resonance images (MRI) of 59 healthy volunteers using voxel-based morphometry (VBM), correlating grey matter values to the positive and negative symptom factors of the schizotypal personality questionnaire (SPQ, German version) and a measure of psychosis proneness (community assessment of psychic experiences, CAPE). We found positive correlations between positive SPQ dimension and bilateral inferior and right superior frontal cortices, and positive CAPE dimension and left inferior frontal cortex, as well as CAPE negative dimension and right supplementary motor area (SMA) and left inferior parietal cortex. However, only the positive correlation of the right precuneus with negative schizotypy scores was significant after FWE correction for multiple comparisons. Our findings confirm an effect of schizotypal traits and psychosis proneness on brain structure in healthy subjects, providing further support to a biological continuum model. Copyright © 2015 Elsevier B.V. All rights reserved.
    Schizophrenia Research 07/2015; DOI:10.1016/j.schres.2015.06.017 · 4.43 Impact Factor
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    ABSTRACT: The main aim of the present research was to study the prospective relationships of the five-factor model of personality and the internalizing and externalizing suprafactors of psychopathology. A sample of 323 young adults completed the NEO-FFI at Time 1 and different scales of symptoms 5 years later. Neuroti- cism prospectively predicted the internalizing factor, while extraversion, low agreeableness and low con- scientiousness predicted the externalizing factor. We found additional paths between introversion and social phobia symptoms, and between low agreeableness and psychopathy symptoms. These relation- ships remained significant, even when controlling for previous symptoms, except for extraversion. Gen- der had no moderation effect on the interrelationship between personality and psychopathology factors. The present study extends previous research about personality and psychopathology, and suggests differ- ent ways in which they can be related.
    Personality and Individual Differences 06/2015; 79. DOI:10.1016/j.paid.2015.02.002 · 1.86 Impact Factor
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    ABSTRACT: Recent findings indicate that alterations of the amygdalar resting-state fMRI connectivity play an important role in the etiology of depression. While both depression and resting-state brain activity are shaped by genes and environment, the relative contribution of genetic and environmental factors mediating the relationship between amygdalar resting-state connectivity and depression remain largely unexplored. Likewise, novel neuroimaging research indicates that different mathematical representations of resting-state fMRI activity patterns are able to embed distinct information relevant to brain health and disease. The present study analyzed the influence of genes and environment on amygdalar resting-state fMRI connectivity, in relation to depression risk. High-resolution resting-state fMRI scans were analyzed to estimate functional connectivity patterns in a sample of 48 twins (24 monozygotic pairs) informative for depressive psychopathology (6 concordant, 8 discordant and 10 healthy control pairs). A graph-theoretical framework was employed to construct brain networks using two methods: (i) the conventional approach of filtered BOLD fMRI time-series and (ii) analytic components of this fMRI activity. Results using both methods indicate that depression risk is increased by environmental factors altering amygdalar connectivity. When analyzing the analytic components of the BOLD fMRI time-series, genetic factors altering the amygdala neural activity at rest show an important contribution to depression risk. Overall, these findings show that both genes and environment modify different patterns the amygdala resting-state connectivity to increase depression risk. The genetic relationship between amygdalar connectivity and depression may be better elicited by examining analytic components of the brain resting-state BOLD fMRI signals. Hum Brain Mapp, 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Human Brain Mapping 06/2015; DOI:10.1002/hbm.22876 · 6.92 Impact Factor
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    ABSTRACT: Previous research suggests that low birth weight (BW) induces reduced brain cortical surface area (SA) which would persist until at least early adulthood. Moreover, low BW has been linked to psychiatric disorders such as depression and psychological distress, and to altered neurocognitive profiles. We present novel findings obtained by analysing high-resolution structural MRI scans of 48 twins; specifically, we aimed: i) to test the BW-SA association in a middle-aged adult sample; and ii) to assess whether either depression/anxiety disorders or intellectual quotient (IQ) influence the BW-SA link, using a monozygotic (MZ) twin design to separate environmental and genetic effects. Both lower BW and decreased IQ were associated with smaller total and regional cortical SA in adulthood. Within a twin pair, lower BW was related to smaller total cortical and regional SA. In contrast, MZ twin differences in SA were not related to differences in either IQ or depression/anxiety disorders. The present study supports findings indicating that i) BW has a long-lasting effect on cortical SA, where some familial and environmental influences alter both foetal growth and brain morphology; ii) uniquely environmental factors affecting BW also alter SA; iii) higher IQ correlates with larger SA; and iv) these effects are not modified by internalizing psychopathology.
    PLoS ONE 06/2015; 10(6):e0129616. DOI:10.1371/journal.pone.0129616 · 3.23 Impact Factor
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    ABSTRACT: Early Life Stress (ELS) is a known risk factor for suffering psychopathology in adulthood. The hypothalamic-pituitary-adrenal (HPA) axis has been described to be deregulated in both individuals who experienced early psychosocial stress and in patients with a wide range of psychiatric disorders. The NR3C1 gene codes for the glucocorticoid receptor, a key element involved in several steps of HPA axis modulation. In this review, we gather existing evidence linking NR3C1 methylation pattern with either ELS or psychopathology. We summarize that several types of ELS have been frequently associated with NR3C1 hypermethylation whereas hypomethylation has been continuously found to be associated with post-traumatic stress disorder. In light of the reported findings, the main concerns of ongoing research in this field are the lack of methodological consensus and selection of CpG sites. Further studies should target individual CpG site methylation assessment focusing in biologically relevant areas such as transcription factor binding regions whereas widening the examined sequence in order to include all non-coding first exons of the NR3C1 gene in the analysis. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; 55. DOI:10.1016/j.neubiorev.2015.05.016 · 10.28 Impact Factor
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    ABSTRACT: Late and early stressful factors have widely been recognized to play a role in the aetiology of depression. Recent research indicates that such adverse environmental stimuli may alter gene expression in humans via epigenetic modifications. While epigenetic changes such as DNA methylation are likely involved in these processes, it is still unknown what specific genomic loci may be hyper- or hypo-methylated in depression. The association between depressive symptoms during the last 30 days (Brief Symptom Inventory [BSI]) and peripheral-blood DNA methylation levels at genomic loci previously reported as epigenetically altered in saliva and brain of depressive patients was evaluated in a community sample of 34 adult Caucasian MZ twins (17 pairs). Intrapair DNA methylation differences in an intron of DEPDC7 (chr11:33040743) were associated with intrapair differences in current depressive symptoms. Accordingly, a site-specific 10% DNA hypomethylation in a co-twin would correlate with a current depressive symptom score around 3.1 BSI points above the score of his/her less-depressed co-twin. These findings indicate that DEPDC7 hypomethylation in peripheral blood DNA may be associated with recent depressive symptomatology, in line with previous results. Copyright © 2015. Published by Elsevier Masson SAS.
    European Psychiatry 05/2015; DOI:10.1016/j.eurpsy.2015.04.001 · 3.21 Impact Factor
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    ABSTRACT: Depressive disorders have been shown to be highly influenced by environmental pathogenic factors, some of which are believed to exert stress on human brain functioning via epigenetic modifications. Previous genome-wide methylomic studies on depression have suggested that, along with differential DNA methylation, affected co-twins of monozygotic (MZ) pairs have increased DNA methylation variability, probably in line with theories of epigenetic stochasticity. Nevertheless, the potential biological roots of this variability remain largely unexplored. The current study aimed to evaluate whether DNA methylation differences within MZ twin pairs were related to differences in their psychopathological status. Data from the Illumina Infinium HumanMethylation450 Beadchip was used to evaluate peripheral blood DNA methylation of 34 twins (17 MZ pairs). Two analytical strategies were used to identify (a) differentially methylated probes (DMPs) and (b) variably methylated probes (VMPs). Most DMPs were located in genes previously related to neuropsychiatric phenotypes. Remarkably, one of these DMPs (cg01122889) was located in the WDR26 gene, the DNA sequence of which has been implicated in major depressive disorder from genome-wide association studies. Expression of WDR26 has also been proposed as a biomarker of depression in human blood. Complementarily, VMPs were located in genes such as CACNA1C, IGF2 and the p38 MAP kinase MAPK11, showing enrichment for biological processes such as glucocorticoid signaling. These results expand on previous research to indicate that both differential methylation and differential variability have a role in the etiology and clinical manifestation of depression, and provide clues on specific genomic loci of potential interest in the epigenetics of depression.
    Translational Psychiatry 04/2015; 5(4):e557. DOI:10.1038/tp.2015.49 · 4.36 Impact Factor
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    ABSTRACT: Structural brain abnormalities are already present during the early phases of psychosis, but factors underlying brain volume changes are still not well understood. The neuregulin 1 gene (NRG1), influencing neurodevelopment and neuroplasticity, has been associated with schizophrenia. Our aim was to examine whether variations in the NRG1 gene (SNP8NRG221132, SNP8NRG6221533 and SNP8NRG243177 polymorphisms) influence longitudinal changes in the brain during a first episode of psychosis (FEP). A 3-year follow-up magnetic resonance imaging (MRI) study was performed. Fifty-nine minimally medicated patients who were experiencing FEP and 14 healthy control individuals underwent genotyping and structural brain MRI at baseline and at 1- and 3-year follow-up. A comparison of brain volumes, gray matter, white matter (WM), lateral ventricles (LV), cortical cerebrospinal fluid, and thalamus and caudate was made between the groups according to their genotype. In patients, the SNP8NRG6221533 risk C allele was significantly associated with increased LV volume across time. C allele carriers had significantly less WM compared with subjects homozygous for the T allele after the follow-up. No other significant differences were observed among subgroups. No significant changes according to the genotypes were found in healthy individuals. Our findings suggest that variations of neurodevelopment-related genes, such as the NRG1 gene, can contribute to brain abnormalities described in early phases of schizophrenia and progressive changes during the initial years of the illness. To our knowledge, it is the first time that a relation between NRG1 polymorphisms and longitudinal brain changes is reported. © 2015 S. Karger AG, Basel.
    Neuropsychobiology 04/2015; 71(2):103-111. DOI:10.1159/000370075 · 2.30 Impact Factor
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    ABSTRACT: Schizotypal personality disorder (SPD) symptoms or features are common in patients with psychosis and their healthy relatives. However, the long-term stability of these SPD features and therefore their constituting enduring traits underlying vulnerability to psychosis remain to be clarified. Thirty-two patients with psychotic disorders and 29 of their healthy siblings were included from the long-term follow-up study of 89 nuclear families. Participants were clinically assessed by means of a semi-structured diagnostic interview, whereas the Schizotypal Personality Questionnaire-Brief (SPQ-B) was applied for the self-assessment of SPD symptoms. The assessments were carried out upon admission to the study and at follow-up, about 10 years later. The patients had higher scores than their siblings on the SPQ-B both at baseline and follow-up. In addition, self-reported SPD symptoms remained stable over time in total scores and in all the SPQ-B subscores, except for the SPQ-B Disorganization subscale. Self-reported SPD symptoms were stable over the long term among patients with psychotic disorders and their healthy siblings. This finding provides new support for including the SPD construct as a trait measure for studies addressing both vulnerability to psychosis in first-degree relatives of patients with psychosis and long-term persistence of symptoms in patients suffering from psychosis. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    03/2015; 227(2-3). DOI:10.1016/j.psychres.2015.02.020
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    Dataset: PAID def
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    ABSTRACT: 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 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. Copyright © 2014 SEP y SEPB. Published by Elsevier España. All rights reserved.
    Revista de Psiquiatría Biológica y Salud Mental 02/2015; 8(2). DOI:10.1016/j.rpsm.2014.09.003 · 1.60 Impact Factor
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    ABSTRACT: Background Few studies have analyzed the course of neurocognition in treated children and adolescents with early-onset bipolar disorder (EOBD) and shown improvements in attention, working memory, and verbal memory after treatment. The aim of this study was to determine the progress over two years in neuropsychological performance of a sample of medicated adolescents with EOBD compared to healthy controls (HC). Methods Twenty adolescents, diagnosed in clinical setting as DSM-IV bipolar disorder, treated for two years, euthymic, and 20 gender and age-matched HC were assessed at two moments in reasoning, verbal and visual memory, working memory, speed, visual-motor skills and executive function. Multivariate analyses of variance was carried out to analyze the differences between groups over time, and to monitor the influence of psychotic symptoms and type of mood-stabilizer. Results The entire sample improved on verbal and visual memory tests (verbal recall p<0.01; visual recall p<0.001). Moreover, patients improved more than controls in verbal reasoning (p<0.01), working memory (p<0.01), processing speed (p<0.01) and visual-motor skills (p<0.001). Psychotic symptoms and treatment with lithium were associated with poorer development in executive control tasks. Limitations Sample size was small and groups were re-evaluated in slight different follow-up periods. Doses of antipsychotics drugs over time were not controlled. Conclusions Processing speed and visual-motor skills in the EOBD group normalized during follow-up. Executive functioning, working memory, and verbal and visual memory remained impaired in patients versus controls. The knowledge of cognitive deficits due to normal course of illness or to drug effects allows better therapeutic strategies.
    Journal of Affective Disorders 02/2015; 172:48–54. DOI:10.1016/j.jad.2014.09.041 · 3.71 Impact Factor
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    Personality and Individual Differences 01/2015; · 1.86 Impact Factor
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    ABSTRACT: Though cognitive abilities in adulthood are largely influenced by individual genetic background, they have also been shown to be importantly influenced by environmental factors. Some of these influences are mediated by epigenetic mechanisms. Accordingly, polymorphic variants in the epigenetic gene DNMT3B have been linked to neurocognitive performance. Since monozygotic (MZ) twins may show larger or smaller intrapair phenotypic differences depending on whether their genetic background is more or less sensitive to environmental factors, a twin design was implemented to determine if particular polymorphisms in the DNMT3B gene may be linked to a better (worse) response to enriched (deprived) environmental factors.
    European Psychiatry 12/2014; 30(2). DOI:10.1016/j.eurpsy.2014.11.011 · 3.44 Impact Factor
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    ABSTRACT: Season of birth (SOB) has been shown to modify the risk of several health outcomes, including a number of neuropsychiatric disorders. Empirical evidence indicates that subclinical forms of psychosis in the general population share some risk factors with categorical diagnoses of psychosis. Hence, by systematically reviewing and meta-analyzing new and existing data, the current work aimed to determine whether there is evidence of an association between winter SOB and subclinical psychosis in the general population. Our meta-analytic results do not indicate an association between winter SOB and schizotypy in adult populations, although they indicate winter SOB may be a risk factor for psychotic experiences or symptoms in children around 12-15 years (OR=1.12, 95%CI:1.03-1.21). In the whole new dataset for adults (n=481, mean age=22.8 years) no association was detected in either an unadjusted model or adjusting for gender and age. Overall, our results indicate that the association between winter SOB and increased subclinical psychosis may hold in children, but does not in the broad general adult population. Nevertheless, the epidemiological and clinicopathological significance of winter SOB as a risk factor for subclinical psychosis would probably be slight due to the small effect sizes indicated by the reports available to date. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.
    Psychiatry Research 12/2014; 225(3). DOI:10.1016/j.psychres.2014.11.072 · 2.68 Impact Factor
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    ABSTRACT: In aetiologically complex illnesses such as schizophrenia, there is no direct link between genotype and phenotype. Intermediate phenotypes could help clarify the underlying biology and assist in the hunt for genetic vulnerability variants. We have previously shown that cognition shares substantial genetic variance with schizophrenia; however, it is unknown if this reflects pleiotropic effects, direct causality or some shared third factor that links both, for example, brain volume (BV) changes. We quantified the degree of net genetic overlap and tested the direction of causation between schizophrenia liability, brain structure and cognition in a pan-European schizophrenia twin cohort consisting of 1243 members from 626 pairs. Cognitive deficits lie upstream of the liability for schizophrenia with about a quarter of the variance in liability to schizophrenia explained by variation in cognitive function. BV changes lay downstream of schizophrenia liability, with 4% of BV variation explained directly by variation in liability. However, our power to determine the nature of the relationship between BV deviation and schizophrenia liability was more limited. Thus, while there was strong evidence that cognitive impairment is causal to schizophrenia liability, we are not in a position to make a similar statement about the relationship between liability and BV. This is the first study to demonstrate that schizophrenia liability is expressed partially through cognitive deficits. One prediction of the finding that BV changes lie downstream of the disease liability is that the risk loci that influence schizophrenia liability will thereafter influence BV and to a lesser extent. By way of contrast, cognitive function lies upstream of schizophrenia, thus the relevant loci will actually have a larger effect size on cognitive function than on schizophrenia. These are testable predictions.Molecular Psychiatry advance online publication, 2 December 2014; doi:10.1038/mp.2014.152.
    Molecular Psychiatry 12/2014; DOI:10.1038/mp.2014.152 · 15.15 Impact Factor
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    ABSTRACT: Background Histone deacetylases (HDACs) are key enzymes of histone acetylation, and abnormalities in histone modifications and in the level of HDAC proteins have been reported in schizophrenia. The objective of the present study was to systematically test the HDAC genes for its association with schizophrenia. Methods A family-based genetic association study (951 Caucasian subjects in 313 nuclear families) using 601 tag-single nucleotide polymorphisms in HDAC genes was conducted followed by a replication study of top-ranked markers in a sample of 1427 Caucasian subjects from 241 multiplex families and 176 trios. Epistasis interaction was tested by using the pedigree-based generalized multifactor dimensionality reduction (GMDR). Furthermore, we analyzed exome sequencing data of 1134 subjects for detection of rare mutations in HDAC genomic regions. Results In the exploratory study, ten markers were in significant association with schizophrenia (P < 0.01). One maker rs14251 (HDAC3) was replicated (P = 0.04) and remained significant in the whole sample (P = 0.004). GMDR identified that a significant three-locus interaction model was detected involving rs17265596 (HDAC9), rs7290710 (HDAC10) and rs7634112 (HDAC11) with a good testing accuracy (0.58). No rare mutations were found associated with schizophrenia. Conclusion This first exploratory systematic study of the HDAC genes provides consistent support for the involvement of the HDAC3 gene in the etiology of schizophrenia. A statistical epistatic interaction between HDAC9, HDAC10, and HDAC11 was detected and seems biologically plausible.
    Schizophrenia Research 12/2014; 160(1-3). DOI:10.1016/j.schres.2014.09.029 · 4.43 Impact Factor
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    ABSTRACT: The post-central gyrus (PoCG) has received little attention in brain imaging literature. However, some magnetic resonance imaging (MRI) studies have detected the presence of PoCG abnormalities in patients with schizophrenia. Fifty-six first-episode schizophrenia patients, selected through the PAFIP Program and carefully assessed for dimensional psychopathology and cognitive functioning, and 56 matched healthy controls were scanned twice over 1-year follow-up. PoCG gray matter volumes were measured at both time-points and compared between the groups. Differences in volume change over time and the relationship between PoCG volume and clinical and cognitive variables were also investigated. The right PoCG volume was significantly smaller in patients than in controls at the 1-year follow-up; furthermore, it was significantly smaller in male patients compared with male controls, with no differences in female. Although there was no significant time by group interaction in the overall sample, a trend-level interaction was found for the right PoCG in males. This is the first study, as per our knowledge, to focus on PoCG in first-episode schizophrenia patients. The presence of PoCG abnormalities in the first year of schizophrenia suggests a possible contribution to the pathophysiology of the illness, probably as part of a more extensive network of abnormalities.
    Psychiatry Research: Neuroimaging 11/2014; 231(1). DOI:10.1016/j.pscychresns.2014.10.023 · 2.83 Impact Factor
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    ABSTRACT: Goal The present study aimed to examine the prevalence of child abuse across the continuum of psychosis. Patients and methods The sample consisted of 198 individuals divided in three groups: (1) 48 FEP patients, (2) 77 individuals scoring high in Community Assessment of Psychic Experiences (CAPE), classified as “High CAPE” group and (3) 73 individuals scoring low, classified as “Low CAPE” group. Childhood abuse was assessed using self-report instruments. Chi2 tests and logistic regression models controlling by sex, age and cannabis were used to perform three comparisons: (i) FEP vs. Low CAPE; (ii) FEP vs. High CAPE and (iii) High CAPE vs. Low CAPE. Results The frequency of individuals exposed to childhood abuse for FEP, High CAPE and Low CAPE groups were 52.1%, 41.6% and 11%, respectively. FEP and High CAPE group presented significantly higher rates of childhood abuse compared to Low CAPE group, however, no significant differences were found between FEP and High CAPE groups regarding the frequency of childhood abuse. Conclusion There is an increasing frequency of childhood abuse from low subclinical psychosis to FEP patients. However, childhood abuse is equally common in FEP and at risk individuals.
    European Psychiatry 10/2014; 30(1). DOI:10.1016/j.eurpsy.2014.08.005 · 3.44 Impact Factor

Publication Stats

3k Citations
802.58 Total Impact Points

Institutions

  • 2011–2015
    • Centro de Investigación Biomedica En Red del Área de Salud Mental
      Madrid, Madrid, Spain
  • 2008–2015
    • Instituto de Salud Carlos III
      • CIBER of Mental Health (CIBERSAM)
      Madrid, Madrid, Spain
    • Utrecht University
      Utrecht, Utrecht, Netherlands
  • 1990–2015
    • University of Barcelona
      • • Department of Animal Biology
      • • Department of Psychiatry and Clinical Psychobiology
      Barcino, Catalonia, Spain
  • 2012
    • Catholic University of Louvain
      Лувен-ла-Нев, Walloon, Belgium
  • 2010–2012
    • Complejo Hospitalario de Navarra
      Iruña, Navarre, Spain
  • 2000–2007
    • Maastricht University
      • Psychiatrie en Neuropsychologie
      Maastricht, Provincie Limburg, Netherlands
  • 2003
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain