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Sökning: WFRF:(Menchon JM)

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1.
  • Patel, Yash, et al. (författare)
  • Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders.
  • 2020
  • Ingår i: JAMA psychiatry. - 2168-6238.
  • Tidskriftsartikel (refereegranskat)abstract
    • Large-scale neuroimaging studies have revealed group differences in cortical thickness across many psychiatric disorders. The underlying neurobiology behind these differences is not well understood.To determine neurobiologic correlates of group differences in cortical thickness between cases and controls in 6 disorders: attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), bipolar disorder (BD), major depressive disorder (MDD), obsessive-compulsive disorder (OCD), and schizophrenia.Profiles of group differences in cortical thickness between cases and controls were generated using T1-weighted magnetic resonance images. Similarity between interregional profiles of cell-specific gene expression and those in the group differences in cortical thickness were investigated in each disorder. Next, principal component analysis was used to reveal a shared profile of group difference in thickness across the disorders. Analysis for gene coexpression, clustering, and enrichment for genes associated with these disorders were conducted. Data analysis was conducted between June and December 2019. The analysis included 145 cohorts across 6 psychiatric disorders drawn from the ENIGMA consortium. The numbers of cases and controls in each of the 6 disorders were as follows: ADHD: 1814 and 1602; ASD: 1748 and 1770; BD: 1547 and 3405; MDD: 2658 and 3572; OCD: 2266 and 2007; and schizophrenia: 2688 and 3244.Interregional profiles of group difference in cortical thickness between cases and controls.A total of 12 721 cases and 15 600 controls, ranging from ages 2 to 89 years, were included in this study. Interregional profiles of group differences in cortical thickness for each of the 6 psychiatric disorders were associated with profiles of gene expression specific to pyramidal (CA1) cells, astrocytes (except for BD), and microglia (except for OCD); collectively, gene-expression profiles of the 3 cell types explain between 25% and 54% of variance in interregional profiles of group differences in cortical thickness. Principal component analysis revealed a shared profile of difference in cortical thickness across the 6 disorders (48% variance explained); interregional profile of this principal component 1 was associated with that of the pyramidal-cell gene expression (explaining 56% of interregional variation). Coexpression analyses of these genes revealed 2 clusters: (1) a prenatal cluster enriched with genes involved in neurodevelopmental (axon guidance) processes and (2) a postnatal cluster enriched with genes involved in synaptic activity and plasticity-related processes. These clusters were enriched with genes associated with all 6 psychiatric disorders.In this study, shared neurobiologic processes were associated with differences in cortical thickness across multiple psychiatric disorders. These processes implicate a common role of prenatal development and postnatal functioning of the cerebral cortex in these disorders.
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2.
  • Frangou, Sophia, et al. (författare)
  • Cortical thickness across the lifespan: Data from 17,075 healthy individuals aged 3–90 years
  • 2021
  • Ingår i: Human Brain Mapping. - : John Wiley & Sons. - 1065-9471 .- 1097-0193.
  • Tidskriftsartikel (refereegranskat)abstract
    • Delineating the association of age and cortical thickness in healthy individuals is critical given the association of cortical thickness with cognition and behavior. Previous research has shown that robust estimates of the association between age and brain morphometry require large-scale studies. In response, we used cross-sectional data from 17,075 individuals aged 3–90 years from the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Consortium to infer age-related changes in cortical thickness. We used fractional polynomial (FP) regression to quantify the association between age and cortical thickness, and we computed normalized growth centiles using the parametric Lambda, Mu, and Sigma method. Interindividual variability was estimated using meta-analysis and one-way analysis of variance. For most regions, their highest cortical thickness value was observed in childhood. Age and cortical thickness showed a negative association; the slope was steeper up to the third decade of life and more gradual thereafter; notable exceptions to this general pattern were entorhinal, temporopolar, and anterior cingulate cortices. Interindividual variability was largest in temporal and frontal regions across the lifespan. Age and its FP combinations explained up to 59% variance in cortical thickness. These results may form the basis of further investigation on normative deviation in cortical thickness and its significance for behavioral and cognitive outcomes.
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3.
  • Dima, Danai, et al. (författare)
  • Subcortical volumes across the lifespan : Data from 18,605 healthy individuals aged 3-90 years.
  • 2021
  • Ingår i: Human Brain Mapping. - 1065-9471 .- 1097-0193.
  • Tidskriftsartikel (refereegranskat)abstract
    • Age has a major effect on brain volume. However, the normative studies available are constrained by small sample sizes, restricted age coverage and significant methodological variability. These limitations introduce inconsistencies and may obscure or distort the lifespan trajectories of brain morphometry. In response, we capitalized on the resources of the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Consortium to examine age-related trajectories inferred from cross-sectional measures of the ventricles, the basal ganglia (caudate, putamen, pallidum, and nucleus accumbens), the thalamus, hippocampus and amygdala using magnetic resonance imaging data obtained from 18,605 individuals aged 3-90 years. All subcortical structure volumes were at their maximum value early in life. The volume of the basal ganglia showed a monotonic negative association with age thereafter; there was no significant association between age and the volumes of the thalamus, amygdala and the hippocampus (with some degree of decline in thalamus) until the sixth decade of life after which they also showed a steep negative association with age. The lateral ventricles showed continuous enlargement throughout the lifespan. Age was positively associated with inter-individual variability in the hippocampus and amygdala and the lateral ventricles. These results were robust to potential confounders and could be used to examine the functional significance of deviations from typical age-related morphometric patterns.
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7.
  • Granero, Roser, et al. (författare)
  • Is pathological gambling moderated by age?
  • 2014
  • Ingår i: Journal of Gambling Studies. - : Springer-Verlag New York. - 1050-5350 .- 1573-3602. ; 30:2, s. 475-92
  • Tidskriftsartikel (refereegranskat)abstract
    • The age of a patient is a strong moderator of both the course and the evolution of disorders/diseases. However, the effects of current age in pathological gambling (PG) have rarely been examined. The aim of this study is to explore the moderating effects of the patients' current age in relation to personality traits and clinical outcomes of PG. A total sample of 2,309 treatment-seeking patients for PG, diagnosed according to DSM-IV criteria, participated in this study and were assessed with the Diagnostic Questionnaire for Pathological Gambling according to DSM-IV criteria, the South Oaks Gambling Screen, the Symptom Checklist, the Temperament and Character Inventory-R, and other clinical and psychopathological measures. Orthogonal polynomial contrasts showed linear trends in the relationship between age and PG: the older the patient, the more comorbid health problems were visible. The presence of additional quadratic trends also suggests that age plays a significant role in moderating the possibility of existing PG problems and general psychopathology. No interaction term was found between age and sex, but it was present for age and some personality traits: self-transcendence and reward dependence (these two traits were only relevant to the level of impairment due to PG at specific ages). This study suggests that the patients' age influences psychopathological and clinical aspects associated to PG. Intervention in the earliest manifestations of this complex problem is essential in order to better address the need of successful treatment planning.
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8.
  • Jiménez-Murcia, Susana, et al. (författare)
  • Typologies of young pathological gamblers based on sociodemographic and clinical characteristics.
  • 2013
  • Ingår i: Comprehensive Psychiatry. - : Elsevier. - 0010-440X .- 1532-8384. ; 54:8, s. 1153-60
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: The aim of this study is to explore empirical clusters within the population of young Spanish individuals attending outpatient pathological gambling treatment.METHOD: The South Oaks Gambling Screen (SOGS), the Symptom Checklist (SCL-90-R), the Temperament and Character Inventory-R (TCI-R) and other clinical and psychopathological measures were administered to 154 patients (between 17 and 25 years old). The two-step cluster analysis explored the presence of empirical heterogeneous groups based on clinical and socio-demographic characteristics.RESULTS: Three clusters of young pathological gambling patients emerged. Type I showed less psychopathology and more functional personality traits. Type II showed a profile characterized by major emotional distress, shame, immaturity, hostility and negative feelings. Type III showed the most severe psychopathological profile and most psychopathological disturbances and schizotypal traits.CONCLUSIONS: These results suggest that three distinct endophenotypes exist, and that environmental factors have a stronger influence in the first, while in the second and third, individual factors related to deficits of emotional regulation stand out.
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9.
  • Moragas, Laura, et al. (författare)
  • Comparative analysis of distinct phenotypes in gambling disorder based on gambling preferences.
  • 2015
  • Ingår i: BMC Psychiatry. - : BioMed Central. - 1471-244X .- 1471-244X. ; 15
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Studies examining gambling preferences have identified the importance of the type of gambling practiced on distinct individual profiles. The objectives were to compare clinical, psychopathological and personality variables between two different groups of individuals with a gambling disorder (strategic and non-strategic gamblers) and to evaluate the statistical prediction capacity of these preferences with respect to the severity of the disorder.METHOD: A total sample of 2010 treatment-seeking patients with a gambling disorder participated in this stand-alone study. All were recruited from a single Pathological Gambling Unit in Spain (1709 strategic and 301 non-strategic gamblers). The design of the study was cross-sectional and data were collected at the start of treatment. Data was analysed using logistic regression for binary outcomes and analysis of variance (ANOVA) for quantitative responses.RESULTS: There were significant differences in several socio-demographic and clinical variables, as well as in personality traits (novelty seeking and cooperativeness). Multiple regression analysis showed harm avoidance and self-directedness were the main predictors of gambling severity and psychopathology, while age at assessment and age of onset of gambling behaviour were predictive of gambling severity. Strategic gambling (as opposed to non-strategic) was significantly associated with clinical outcomes, but the effect size of the relationships was small.CONCLUSIONS: It is possible to identify distinct phenotypes depending on the preference of gambling. While these phenotypes differ in relation to the severity of the gambling disorder, psychopathology and personality traits, they can be useful from a clinical and therapeutic perspective in enabling risk factors to be identified and prevention programs targeting specific individual profiles to be developed.
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10.
  • Valle-Leon, Marta, et al. (författare)
  • Decreased striatal adenosine A2A-dopamine D2 receptor heteromerization in schizophrenia
  • 2021
  • Ingår i: Neuropsychopharmacology. - : Springer Nature. - 0893-133X .- 1740-634X. ; 46, s. 665-672
  • Tidskriftsartikel (refereegranskat)abstract
    • According to the adenosine hypothesis of schizophrenia, the classically associated hyperdopaminergic state may be secondary to a loss of function of the adenosinergic system. Such a hypoadenosinergic state might either be due to a reduction of the extracellular levels of adenosine or alterations in the density of adenosine A(2A)receptors (A(2A)Rs) or their degree of functional heteromerization with dopamine D(2)receptors (D2R). In the present study, we provide preclinical and clinical evidences for this latter mechanism. Two animal models for the study of schizophrenia endophenotypes, namely the phencyclidine (PCP) mouse model and the A(2A)R knockout mice, were used to establish correlations between behavioural and molecular studies. In addition, a new AlphaLISA-based method was implemented to detect native A(2A)R-D2R heteromers in mouse and human brain. First, we observed a reduction of prepulse inhibition in A(2A)R knockout mice, similar to that observed in the PCP animal model of sensory gating impairment of schizophrenia, as well as a significant upregulation of striatal D2R without changes in A(2A)R expression in PCP-treated animals. In addition, PCP-treated animals showed a significant reduction of striatal A(2A)R-D2R heteromers, as demonstrated by the AlphaLISA-based method. A significant and pronounced reduction of A(2A)R-D2R heteromers was next demonstrated in postmortem caudate nucleus from schizophrenic subjects, even though both D2R and A(2A)R were upregulated. Finally, in PCP-treated animals, sub-chronic administration of haloperidol or clozapine counteracted the reduction of striatal A(2A)R-D2R heteromers. The degree of A(2A)R-D2R heteromer formation in schizophrenia might constitute a hallmark of the illness, which indeed should be further studied to establish possible correlations with chronic antipsychotic treatments.
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