Lourdes Fañanás

University of Barcelona, Barcino, Catalonia, Spain

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Publications (148)515.98 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Season of birth has been shown to influence risk for several neuropsychiatric diseases. Furthermore, it has been suggested that season of birth modifies a number of brain morphological traits. Since cortical thickness alterations have been reported across some levels of the psychosis-spectrum, this study was aimed at i) assessing the scarcely explored relationship between cortical thickness and severity of subclinical psychotic experiences (PEs) in healthy subjects, and ii) evaluating the potential impact of season of birth in the preceding thickness-PEs relationship. As both PEs and brain cortical features are heritable, the current work used monozygotic twins to separately evaluate familial and unique environmental factors. High-resolution structural MRI scans of 48 twins (24 monozygotic pairs) were analyzed to estimate cortical thickness using FreeSurfer. They were then examined in relation to PEs, accounting for the effects of birth season; putative differential relationships between PEs and cortical thickness depending on season of birth were also tested. Current results support previous findings indicative of cortical thickening in healthy individuals with high psychometrically assessed psychosis scores, probably in line with theories of compensatory aspects of brain features in non-clinical populations. Additionally, they suggest distinct patterns of cortical thickness-PEs relationships depending on birth seasonality. Familial factors underlying the presence of PEs may drive these effects.
    Journal of psychiatric research. 05/2014;
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    ABSTRACT: To test whether firstly, different parental rearing components were associated with different dimensions of psychiatric symptoms in adulthood, secondly BDNF-Val66Met polymorphism moderated this association and thirdly, this association was due to genetic confounding. Perceived parental rearing according to Parental Bonding Instrument (PBI), psychiatric symptoms evaluated with the Brief Symptom Inventory (BSI) and the BDNF-Val66Met polymorphism were analyzed in a sample of 232 adult twins from the general population. In the whole sample, paternal care was negatively associated with depression. Maternal overprotection was positively associated with paranoid ideation, obsession-compulsion and somatization. Gene-environment interaction effects were detected between the BDNF-Val66Met polymorphism and maternal care on phobic anxiety, paternal care on hostility, maternal overprotection on somatization and paternal overprotection also in somatization. In the subsample of MZ twins, intrapair differences in maternal care were associated with anxiety, paranoid ideation and somatization. Met carriers were, in general, more sensitive to the effects of parental rearing compared to Val/Val carriers in relation to anxiety and somatization. Contra-intuitively, our findings suggest that high rates of maternal care might be of risk for Met carriers regarding anxiety. Results from analyses controlling for genetic confounding were in line with this finding.
    European Psychiatry 04/2014; · 3.29 Impact Factor
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    ABSTRACT: Background Major depressive disorder (MDD) is a common disease with high morbidity and still unsatisfying treatment response. Both MDD pathogenesis and antidepressant effect are supposed to be strongly affected by genetic polymorphisms. Among promising candidate genes, distrupted in schizophrenia 1 (DISC1), translin-associated factor X (TSNAX) and D-amino acid oxidase activator (DAOA) were suggested since their regulator role in neurodevelopment, neuroplasticity and neurotransmission, and previous evidence of cross-involvement in major psychiatric diseases. Methods The present paper investigated the role of 13 SNPs within the reported genes in MDD susceptibility through a case-control (n=320 and n=150, respectively) study and in citalopram efficacy (n=157). Measures of citalopram efficacy were response (4th week) and remission (12th week). Pharmacogenetic findings were tested in the STAR⁎D genome-wide dataset (n=1892) for replication. Results Evidence of association among rs3738401 (DISC1), rs1615409 and rs766288 (TSNAX) and MDD was found (p=0.004, p=0.0019, and p=0.008, respectively). A trend of association between remission and DISC1 rs821616 and DAOA rs778294 was detected, and confirmation was found for rs778294 by repeated-measure ANOVA (p=0.0008). In the STAR⁎D a cluster of SNPs from 20 to 40 Kbp from DISC1 findings in the original sample was associated with citalopram response, as well as rs778330 (12,325 bp from rs778294). Limitations Relatively small size of the original sample and focus on only three candidate genes. Conclusions The present study supported a role of DISC1-TSNAX variants in MDD susceptibility. On the other hand, genetic regions around DAOA rs778294 and DISC1 rs6675281-rs1000731 may influence citalopram efficacy.
    Journal of Affective Disorders. 01/2014; 168:91–97.
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    ABSTRACT: Purpose To test whether firstly, different parental rearing components were associated with different dimensions of psychiatric symptoms in adulthood, secondly BDNF-Val66Met polymorphism moderated this association and thirdly, this association was due to genetic confounding. Method Perceived parental rearing according to Parental Bonding Instrument (PBI), psychiatric symptoms evaluated with the Brief Symptom Inventory (BSI) and the BDNF-Val66Met polymorphism were analyzed in a sample of 232 adult twins from the general population. Results In the whole sample, paternal care was negatively associated with depression. Maternal overprotection was positively associated with paranoid ideation, obsession-compulsion and somatization. Gene-environment interaction effects were detected between the BDNF-Val66Met polymorphism and maternal care on phobic anxiety, paternal care on hostility, maternal overprotection on somatization and paternal overprotection also in somatization. In the subsample of MZ twins, intrapair differences in maternal care were associated with anxiety, paranoid ideation and somatization. Conclusions Met carriers were, in general, more sensitive to the effects of parental rearing compared to Val/Val carriers in relation to anxiety and somatization. Contra-intuitively, our findings suggest that high rates of maternal care might be of risk for Met carriers regarding anxiety. Results from analyses controlling for genetic confounding were in line with this finding.
    European Psychiatry. 01/2014;
  • Psychological Medicine 11/2013; · 5.59 Impact Factor
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    ABSTRACT: INTRODUCTION: The structural brain anomalies, present in a high percentage of psychotic patients, might have a progressive course in psychotic patients. The present study aimed to explore possible effects of BDNF Val66Met polymorphism variations on progressive structural brain changes after 3years from a first episode of psychosis. METHOD: Patients were part of a large epidemiological and longitudinal intervention program of first-episode psychosis, carried out at the University Hospital Marqués de Valdecilla, Cantabria, Spain. Eighty first-episode patients and 54 healthy controls were included in the final analyses. Brain magnetic resonance imaging (baseline and 3-year follow-up) and BDNF genotype, and clinical and functional outcome were investigated. RESULTS: We did not detect significant association between brain changes and BDNF Val66Met polymorphism variations in patients and controls (all p›0.060). At baseline, there were no significant associations between brain anomalies and BDNF genotype. Functional deficits were similar in Met-carrier and Val homozygote patients after 3-year follow-up (X(2)=0.66; p=0.564); there was no relationship between significant volume change across time and functional outcome. Otherwise, Met-carrier controls had significant high rates of alcohol-consumption (p=0.019) compared to Val homozygote controls. CONCLUSION: Our findings do not support the notion that BDNF genotype variations may mediate brain macroscopic morphological changes across time.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 06/2013; · 3.55 Impact Factor
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    ABSTRACT: While evidence is accumulating to support specific neurocognitive deficits as putative endophenotypes for schizophrenia, the heritability of these deficits in healthy subjects and whether they share common genetic influences, is not well established. In the present study, 529 healthy adult twins from two centers within the European Twin Study Network on Schizophrenia (EUTwinsS) were assessed on two domains that are consistently found to be particularly compromised in schizophrenia. Specifically, Intellectual Quotient Score (IQ) and the Letter-Number Sequencing Test (LNS), a measure of working memory, were measured in all twins. Latent variable components were explored through structural equation modeling, and common genetic underpinnings were examined using bivariate analyses. Results showed that the phenotypic correlation between IQ and working memory was almost entirely attributed to shared genetic variance (95.5%). We discuss the potential use of a combined measure of IQ and working memory to improve the power of molecular studies in detecting the genetic mechanisms underlying schizophrenia. © 2013 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 05/2013; · 3.23 Impact Factor
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    ABSTRACT: Little is known about how genetic and environmental factors contribute to the association between parental negativity and behavior problems from early childhood to adolescence. The current study fitted a cross-lagged model in a sample consisting of 4,075 twin pairs to explore (a) the role of genetic and environmental factors in the relationship between parental negativity and behavior problems from age 4 to age 12, (b) whether parent-driven and child-driven processes independently explain the association, and (c) whether there are sex differences in this relationship. Both phenotypes showed substantial genetic influence at both ages. The concurrent overlap between them was mainly accounted for by genetic factors. Causal pathways representing stability of the phenotypes and parent-driven and child-driven effects significantly and independently account for the association. Significant but slight differences were found between males and females for parent-driven effects. These results were highly similar when general cognitive ability was added as a covariate. In summary, the longitudinal association between parental negativity and behavior problems seems to be bidirectional and mainly accounted for by genetic factors. Furthermore, child-driven effects were mainly genetically mediated, and parent-driven effects were a function of both genetic and shared-environmental factors.
    Development and Psychopathology 05/2013; 25(2):487-500. · 4.40 Impact Factor
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    ABSTRACT: BACKGROUND: To evaluate, in patients affected by an acute major depressive episode, what predictive value certain baseline psychopathological characteristics have with regard to expected therapeutic remission following biological antidepressant treatment (pharmacological/electroconvulsive; non-psychological). METHODS: Six predefined psychopathological characteristics in acute major depressive episode were evaluated using a logistic regression model through a protocolised antidepressant treatment to assess their predictive value with regard to expected remission rate. RESULTS: The final study sample consisted of 129 subjects affected by an acute major depressive episode. From the baseline evaluation of the anguish/restlessness, reduced emotional reactivity, reduced attention, reduced motor response, feeling of worthlessness, and mood characteristics items, it was possible to correctly classify 88.1% of the sample as remitter/non-remitter with sensitivity of 0.77 and specificity of 0.96. Addition of the 17-item HRSD baseline variable to the regression model increased the capacity for correct classification of the baseline sample by only 0.09%. LIMITATIONS: Protocolised antidepressant treatment was used. The results of this study may not be generalisable to pharmacological treatments not included in this protocol. CONCLUSIONS: The results of this study suggest that certain baseline psychopathological characteristics (and perhaps other clinical variables too) of the acute major depressive episode may be of great use in establishing patient subgroups according to expected clinical remission to the administration of biological antidepressant treatment. This could have considerable consequences for individualised therapeutic decision-making and for future researches (clinical trials included).
    Journal of affective disorders 04/2013; · 3.76 Impact Factor
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    ABSTRACT: The relationship between cannabis and cognitive performance is controversial. While both acute administration and long-term cannabis use impair cognitive performance in healthy subjects, several studies have shown improved cognitive outcomes in patients with schizophrenia spectrum disorders who use cannabis. The aim of this study was to determine the relationship between lifetime cannabis use, as assessed longitudinally over 10 years of follow-up in a sample of 42 patients and 35 of their unaffected siblings, and current cognitive performance. Forty-two healthy control subjects were assessed at follow-up with the same instruments. Stepwise linear regression revealed a negative effect of longitudinal cannabis use on performance in a social cognition task in the patient group. In the sibling group, lifetime cannabis use had a negative effect on processing speed and declarative memory performance. In the control group, cannabis use per se did not predict cognitive performance; however, when adding lifetime tobacco use to the model, we found a negative association between lifetime cannabis and tobacco use and processing speed and social cognition performance. Moreover, a lower IQ associated with current cannabis use predicted worse attentional performance in the control group. The differential pattern of associations between cannabis use and cognitive performance in patients compared with siblings and controls can be explained by the negative impact of illness on cognition.
    European Archives of Psychiatry and Clinical Neuroscience 04/2013; · 2.75 Impact Factor
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    ABSTRACT: The functional variant Val(158)Met in the coding sequence of COMT gene is involved in the modulation of dopamine availability in the prefrontal cortex in both clinical and general population samples. It has been suggested that the interplay between this genotype and early environmental factors could be used to predict the observed variation in cognitive flexibility. However, other genetic variants and environmental factors may confound the association and produce the inconsistent results commonly found in the literature. In the present study we aimed at testing putative interaction mechanisms between childhood maltreatment and COMT genotypic variability that might explain a proportion of the observed variability of cognitive flexibility in the population. Our design was based on a sample of adult monozygotic twins, which allowed us to test these effects free from potential genetic and shared-environmental confounding factors. Results showed that unique environmental effects of childhood maltreatment significantly impacted cognitive performance among Met/Met subjects. Interestingly, the direction of the association indicated that exposure to early stressful experiences was associated with enhanced cognitive flexibility in this genotype group. These results suggest that COMT may operate as a plasticity gene that provides differential cognitive capacity to respond to environmental stressors.
    Journal of psychiatric research 03/2013; · 3.72 Impact Factor
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    ABSTRACT: OBJECTIVE: To test whether the association between childhood abuse, cannabis use and psychotic experiences (PEs) was moderated by the COMT (catechol-O-methyltransferase) gene. METHOD: Psychotic experiences (PEs), childhood abuse, cannabis use and COMT Val158Met genotypes were assessed in 533 individuals from the general population. Data were analysed hierarchically by means of multiple linear regression models. RESULTS: Childhood abuse showed a significant main effect on both positive (β = 0.09; SE = 0.04; P = 0.047) and negative PEs (β = 0.11; SE = 0.05; P = 0.038). A significant three-way interaction effect was found among childhood abuse, cannabis use and the COMT gene on positive PEs (β = -0.30; SE = 0.11; P = 0.006). This result suggests that COMT genotypes and cannabis use only influenced PE scores among individuals exposed to childhood abuse. Furthermore, exposure to childhood abuse and cannabis use increased PE scores in Val carriers. However, in individuals exposed to childhood abuse but who did not use cannabis, PEs increased as a function of the Met allele copies of the COMT gene. CONCLUSION: Cannabis use after exposure to childhood abuse may have opposite effects on the risk of PEs, depending on the COMT genotypes providing evidence for a qualitative interaction. Val carriers exposed to childhood abuse are vulnerable to the psychosis-inducing effects of cannabis.
    Acta Psychiatrica Scandinavica 02/2013; · 4.86 Impact Factor
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    ABSTRACT: BACKGROUND: The influence of genetic and/or environmental factors on the volumetric brain changes observed in subjects affected by anxiety and depression disorders remains unclear. The current study aimed to investigate whether genetic and environmental liabilities make different contributions to abnormalities in gray matter volume (GMV) in anxiety and depression using a concordant and discordant MZ twin pairs design. METHODS: Fifty-three magnetic resonance imaging (3T) brain scans were obtained from monozygotic (MZ) twins concordant (6 pairs) and discordant (10 pairs) for lifetime anxiety and depression disorders and from healthy twins (21 subjects). We applied voxel-based morphometry to analyse GMV differences. Concordant affected twins were compared to healthy twins and within-pairs comparisons were performed in the discordant group. RESULTS: GMV reductions in bilateral fusiform gyrus and amygdala were observed in concordant affected twins for anxiety and depression compared to healthy twins. No intrapair differences were found in GMV between discordant affected twins and their healthy co-twins. LIMITATIONS: The sample size was modest. This might explain why no intrapair differences were found in the discordant MZ twin group. CONCLUSIONS: As concordant affected MZ twins are believed to have a particularly high genetic liability for the disorder, our findings suggest that fusiform gyrus and amygdala gray matter reductions are related to a genetic risk for anxiety and depression. Discrepancies in regard to brain abnormalities in anxiety and depression may be related to the admixture of patients with GMV abnormalities mainly accounted for by genetic factors with patients presenting GMV mainly accounted for by environmental factors.
    Journal of affective disorders 02/2013; · 3.76 Impact Factor
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    ABSTRACT: RATIONALE: The endocannabinoid system has been implicated in the pathogenesis of major depression (MD) as well as in the mediation of antidepressant drug effects. OBJECTIVES: To analyze CNR1 gene variants in MD and clinical response to citalopram (selective serotonin re-uptake inhibitors [SSRI]). METHODS: The role of CNR1 gene (rs806368, rs1049353, rs806371, rs806377 and rs1535255) was investigated in 319 outpatients with MD and 150 healthy individuals. A subsample of 155 depressive patients were treated with citalopram and evaluated for response (fourth week) and remission (12th week) by the 21-item Hamilton Depression Rating Scale (HDRS). RESULTS: We observed a higher frequency of rs806371 G carriers in MD patients with both presence of melancholia (p = 0.018) and psychotic symptoms (p = 0.007) than in controls. Haplotype frequency distributions between MD sample and controls showed a significant difference for Block 1 (rs806368-rs1049353-rs806371) (p = 0.008). This haplotype finding was consistent when we compared controls with MD subsample stratified by melancholia (p = 0.0009) and psychotic symptoms (p = 0.014). The TT homozygous of the rs806368 and rs806371 presented more risk of no Remission than the C carriers (p = 0.008 and 0.012, respectively). Haplotype frequency distributions according to Remission status showed a significant difference for Block 1 (p = 0.032). Also, we observed significant effect of time-sex-genotype interaction for the rs806368, showing that the C carrier men presented a better response to antidepressant treatment throughout the follow-up than TT homozygous men and women group (p = 0.026). CONCLUSIONS: These results suggest an effect of CNR1 gene in the etiology of MD and clinical response to citalopram.
    Psychopharmacology 02/2013; · 4.06 Impact Factor
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    ABSTRACT: Executive dysfunction represents a core deficit that is associated with schizophrenia spectrum disorders (SSDs). However, the longitudinal course of executive deficits in SSDs is still controversial. The aim of this study was to examine the executive performance of 34 SSD patients in relation to 34 of their unaffected siblings over a period of 10years. Both groups completed psychopathological and executive assessments. Thirteen healthy controls were assessed using the same instruments. At baseline, the SSD patients differed significantly from siblings and controls in their performance on the Trail Making Test-B (TMT-B) and the number of categories in which they succeeded in the Wisconsin Card Sorting Test (WCST). They also differed significantly from the controls in the total number of errors in the WCST. The siblings did not differ in executive functioning from the controls over the follow-up. Longitudinally, the patients demonstrated significant improvement only for the TMT-B. However, only 14.71% of the patients showed reliable and clinically significant improvements for the TMT-B, and 8.82% made more errors on the WCST at the follow-up evaluation. Less than 3% of the patients showed either improved or worse results on the remaining measures of the WCST. A stabilisation pattern for the WCST was observed in the three groups. The patients performed worse than their siblings and controls on both executive tests. Some patients exhibited significant improvements in the TMT-B over time, but this improvement was reliable and clinically significant for less than 15% of the sample. Thus, we conclude that the patients exhibited stable impairments over time in the executive functions assessed.
    Schizophrenia Research 12/2012; · 4.59 Impact Factor
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    ABSTRACT: Background: Serotonergic genes have been widely investigated regarding antidepressant response in major depressive disorder (MDD) but results are still not univocal. Methods: 159 MDD patients treated with citalopram were genotyped and evaluated by the 21-item Hamilton Depression Rating Scale at the beginning and every 4 weeks during the 12-week follow-up. Four serotonin-related genetic variants were tested for association with treatment outcome: tryptophane hydroxylase 1 (TPH1) rs1800532, monoamine oxidase A µVNTR, serotonin 2A receptor rs6311 and serotonin 2C receptor rs6318. The effect of these polymorphisms was tested both in the whole sample and in depressive subtypes with usually higher clinical severity: psychotic and melancholic MDD. Results: No effect on response, remission and symptom improvement was found for the four polymorphisms. However, rs1800532 was found to affect the outcome depending on the MDD subtype: the A allele predicted worse response both in MDD with psychotic (F((6, 378)) = 2.90; p = 0.009) and melancholic (F((6, 381)) = 2.86; p = 0.0097) features. Conclusions: The A allele at TPH1 rs1800532 may be associated with citalopram efficacy only in melancholic and psychotic MDD. These results suggest the usefulness of investigating the effect of genetic variants in conjunction with specific clinical features.
    Neuropsychobiology 12/2012; 67(1):41-47. · 2.37 Impact Factor
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    ABSTRACT: Childhood maltreatment and low socioeconomic status (SES) are considered stressful environmental events with lasting detrimental effects on adult mental health and associated cognitive performance, such as memory. However, the association between childhood maltreatment and low SES remains unclear, probably due to design limitations and putative confounding factors. Particular concerns have been raised on genetic influences, as genetic background may modulate the effects of environmental stressors. The aim of the present study was to examine the effect of childhood maltreatment on adult memory in low- and high-SES subjects, free of confounding due to other environmental and genetic influences. A monozygotic twin design based on 188 healthy adult subjects (94 twin pairs) from the general population was conducted. This design based on genetically identical individuals allowed disentangling the unique environmental effects of childhood maltreatment on memory, which was explored in low and high SES. Results showed that the unique environmental effects of childhood maltreatment were only evident in the high-SES group (β = -0.22; SE = 0.08; p < 0.01; 95 % CI = -0.375 to -0.066). By contrast, no evidence for this effect could be detected in the more stressful low-SES group. These results suggest that enriched environments may provide a more stable context where early stressful experiences can influence cognitive processes. This study provides preliminary support for the inclusion of environmental enrichment in studies addressing the impact of childhood maltreatment on adult cognition and psychiatric disorders.
    European Archives of Psychiatry and Clinical Neuroscience 11/2012; · 2.75 Impact Factor
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    ABSTRACT: PURPOSE: To test whether the association between childhood adversity and positive and negative psychotic experiences is due to genetic confounding. METHOD: Childhood adversity and psychotic experiences were assessed in an ongoing sample of 226 twins from the general population. A monozygotic (MZ) twin differences approach was used to assess possible genetic confounding. RESULTS: In the whole sample, childhood adversity was significantly associated with positive (β=45; SE=0.16; P=0.008) and negative psychotic experiences (β=0.77; SE=0.18; P<0.01). Within-pair MZ twin differences in exposure to childhood adversity were significantly associated with differences in positive (β=71; SE=0.29; P=0.016) and negative psychotic experiences (β=98; SE=0.38; P=0.014) in a subsample of 85 MZ twin pairs. CONCLUSIONS: Individuals exposed to childhood adversity are more likely to report psychotic experiences. Furthermore, our findings indicate that this association is not due to genetic confounding.
    European Psychiatry 08/2012; · 3.29 Impact Factor
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    ABSTRACT: First line treatment of major depression is based on selective serotonin re-uptake inhibitors (SSRIs) that enhance serotonergic neurotransmission by blocking the serotonin transporter. However, clinical response is a complex phenomenon in which other systems such as the endocannabinoid system could be involved. Given the evidence for the role of the endocannabinoid system in the pathogenesis of depression as well as in the mediation of antidepressant drug effects, the aim of this study was to analyze genetic variability in the endocannabinoid system genes (CNR1, CNR2 and FAAH genes) and their role in clinical response (at week 4) and remission (at week 12) in SSRI (citalopram) treatment in a sample of 154 depressive outpatients, all of Spanish origin. All patients were treated with citalopram and followed over 12 weeks. Severity of depressive symptomatology was evaluated by means of the 21-item Hamilton Depression Rating Score (HDRS). No differences were found in any of the genotype distributions according to response or remission. The longitudinal study showed that (i) the CNR1 rs1049353-GG genotype conferred a better response to citalopram treatment in the subgroup of male patients and (ii) G allele carriers (CNR2 rs2501431) presented higher HDRS scores in the follow-up than AA homozygous allele carriers. Our results seem to suggest the involvement of CNR1 and CNR2 genes in clinical responses to citalopram treatment.
    Journal of Psychopharmacology 07/2012; 26(10):1391-8. · 3.37 Impact Factor
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    ABSTRACT: Genetic studies have found that the interleukin-1β gene (IL1B, 2q13) influences the risk for schizophrenia, but the underlying biological mechanisms of the association are still unclear. Investigation of the effects of genetic variability in this gene on brain function could provide more information about its role in the disorder. The present study examined the effects of a functional polymorphism at IL1B gene promoter (-511C/T; rs16944) on brain correlates of working memory performance in schizophrenia. Forty-eight schizophrenia patients and 46 control subjects underwent functional magnetic resonance imaging while performing the n-back task. In the pooled sample, genetic variability at this locus was associated with differential brain activation in a bilateral frontal region including the dorsolateral prefrontal cortex. There was also a significant diagnosis × genotype interaction effect in an overlapping frontal region: the IL1B polymorphism did not affect activation in the control subjects in this area, but the schizophrenia patients who were T carriers showed significantly higher activation than the CC homozygotes. The findings support a role for IL1B variability in the dorsolateral prefrontal cortex dysfunction classically associated with schizophrenia.
    Biological psychiatry 07/2012; 72(9):758-65. · 8.93 Impact Factor

Publication Stats

2k Citations
515.98 Total Impact Points

Institutions

  • 1990–2014
    • University of Barcelona
      • Department of Animal Biology
      Barcino, Catalonia, Spain
  • 2008–2013
    • Instituto de Salud Carlos III
      Madrid, Madrid, Spain
  • 2009–2012
    • Centro de Investigación Biomedica En Red del Área de Salud Mental
      Madrid, Madrid, Spain
  • 2011
    • Universidad de Salamanca
      • Departamento de Psiquiatría, Psicología, Medicina Legal e Historia de la Medicina
      Salamanca, Castile and Leon, Spain
  • 2010
    • Complejo Hospitalario de Navarra
      Iruña, Navarre, Spain
  • 2007
    • University of Granada
      Granata, Andalusia, Spain
    • Autonomous University of Barcelona
      • Departamento de Biología Animal, de Biología Vegetal y de Ecología
      Cerdanyola del Vallès, Catalonia, Spain
  • 2000–2007
    • University Pompeu Fabra
      • Department of Experimental and Health Sciences
      Barcino, Catalonia, Spain
  • 2001
    • Fundació Clínic per a la Recerca Biomèdica
      Barcino, Catalonia, Spain
  • 1997
    • Maastricht University
      • Department of Psychiatry & Neuropsychology
      Maestricht, Limburg, Netherlands