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      Functional magnetic resonance imaging in schizophrenia Translated title: Imágenes de resonancia magnética funcional en la esquizofrenia Translated title: L'imagerie par résonance magnétique fonctionnelle dans la schizophrénie

      research-article
      , MD, PhD * , Phd
      Dialogues in Clinical Neuroscience
      Les Laboratoires Servier
      fMRI, BOLD, event-related, functional connectivity

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          Abstract

          The integration of functional magnetic resonance imaging (fMRI) with cognitive and affective neuroscience paradigms enables examination of the brain systems underlying the behavioral deficits manifested in schizophrenia; there have been a remarkable increase in the number of studies that apply fMRI in neurobiological studies of this disease. This article summarizes features of fMRI methodology and highlights its application in neurobehavioral studies in schizophrenia. Such work has helped elucidate potential neural substrates of deficits in cognition and affect by providing measures of activation to neurobehavioral probes and connectivity among brain regions. Studies have demonstrated abnormalities at early stages of sensory processing that may influence downstream abnormalities in more complex evaluative processing. The methodology can help bridge integration with neuropharmacologic and genomic investigations.

          Translated abstract

          L'intégration de l'IRMf (imagerie par résonance magnétique fonctionnelle) aux paradigmes de neuroscience cognitifs et affectifs permet d'examiner des circuits cérébraux qui sous-tendent les déficits comportementaux observés dans la schizophrénie ; les études neurobiologiques utilisant l'IRMf dans cette maladie sont de plus en plus nombreuses. Cet article résume les caractéristiques de la méthodologie de l'IRMf et présente ses applications dans les études neurocomportementales sur la schizophrénie. Cette technique a permis de trouver des substrats neuraux potentiels des déficits cognitifs et affectifs en fournissant des mesures d'activation aux sondes neurocomportementales et en objectivant la connectivité dans les régions cérébrales. Des études ont montré des anomalies au stade précoce du traitement de l'information sensorielle pouvant induire en aval des anomalies dans certains processus de traitement plus complexes. Cette méthodologie peut permettre de relier les résultats des investigations neuropharmacologiques et génomiques.

          Translated abstract

          La integración de las imágenes de resonancia magnética funcional (IRMf) con paradigmas cognitivos y afectivos de las neurociencias permite el examen de los sistemas cerebrales que están a la base de los déficit conductuales que aparecen en la esquizofrenia. Se ha producido un notable aumento en el número de estudios que aplican las IRMf en los estudios neurobiológicos de esta enfermedad. Este artículo resume las características de la metodología de las IRMf y destaca su aplicación en los estudios neuroconductuales en la esquizofrenia. Dicho trabajo ha ayudado a dilucidar los potenciales sustratos neurales en déficit cognitivos y afectivos al proporcionar mediciones de activación para las exploraciones neuroconductuales y de conectividad entre regiones cerebrales. Los estudios han demostrado anormalidades en las etapas iniciales del procesamiento sensorial que pueden influir en una cascada de anormalidades en procesamientos de evaluatión más complejos. La metodología puede ayudar a generar puentes de integración con investigaciones neurofarmacológicas y genómicas.

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          Most cited references28

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          Effect of COMT Val108/158 Met genotype on frontal lobe function and risk for schizophrenia.

          Abnormalities of prefrontal cortical function are prominent features of schizophrenia and have been associated with genetic risk, suggesting that susceptibility genes for schizophrenia may impact on the molecular mechanisms of prefrontal function. A potential susceptibility mechanism involves regulation of prefrontal dopamine, which modulates the response of prefrontal neurons during working memory. We examined the relationship of a common functional polymorphism (Val(108/158) Met) in the catechol-O-methyltransferase (COMT) gene, which accounts for a 4-fold variation in enzyme activity and dopamine catabolism, with both prefrontally mediated cognition and prefrontal cortical physiology. In 175 patients with schizophrenia, 219 unaffected siblings, and 55 controls, COMT genotype was related in allele dosage fashion to performance on the Wisconsin Card Sorting Test of executive cognition and explained 4% of variance (P = 0.001) in frequency of perseverative errors. Consistent with other evidence that dopamine enhances prefrontal neuronal function, the load of the low-activity Met allele predicted enhanced cognitive performance. We then examined the effect of COMT genotype on prefrontal physiology during a working memory task in three separate subgroups (n = 11-16) assayed with functional MRI. Met allele load consistently predicted a more efficient physiological response in prefrontal cortex. Finally, in a family-based association analysis of 104 trios, we found a significant increase in transmission of the Val allele to the schizophrenic offspring. These data suggest that the COMT Val allele, because it increases prefrontal dopamine catabolism, impairs prefrontal cognition and physiology, and by this mechanism slightly increases risk for schizophrenia.
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            When doors of perception close: bottom-up models of disrupted cognition in schizophrenia.

            Schizophrenia is a major mental disorder that affects approximately 1% of the population worldwide. Cognitive deficits are a key feature of schizophrenia and a primary cause of long-term disability. Current neurophysiological models of schizophrenia focus on distributed brain dysfunction with bottom-up as well as top-down components. Bottom-up deficits in cognitive processing are driven by impairments in basic perceptual processes that localize to primary sensory brain regions. Within the auditory system, deficits are apparent in elemental sensory processing, such as tone matching following brief delay. Such deficits lead to impairments in higher-order processes such as phonological processing and auditory emotion recognition. Within the visual system, deficits are apparent in functioning of the magnocellular visual pathway, leading to higher-order deficits in processes such as perceptual closure, object recognition, and reading. In both auditory and visual systems, patterns of deficit are consistent with underlying impairment of brain N-methyl-d-aspartate receptor systems.
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              Variation in GRM3 affects cognition, prefrontal glutamate, and risk for schizophrenia.

              GRM3, a metabotropic glutamate receptor-modulating synaptic glutamate, is a promising schizophrenia candidate gene. In a family-based association study, a common GRM3 haplotype was strongly associated with schizophrenia (P = 0.0001). Within this haplotype, the A allele of single-nucleotide polymorphism (SNP) 4 (hCV11245618) in intron 2 was slightly overtransmitted to probands (P = 0.02). We studied the effects of this SNP on neurobiological traits related to risk for schizophrenia and glutamate neurotransmission. The SNP4 A allele was associated with poorer performance on several cognitive tests of prefrontal and hippocampal function. The physiological basis of this effect was assessed with functional MRI, which showed relatively deleterious activation patterns in both cortical regions in control subjects homozygous for the SNP4 A allele. We next looked at SNP4's effects on two indirect measures of prefrontal glutamate neurotransmission. Prefrontal N-acetylaspartate, an in vivo MRI measure related to synaptic activity and closely correlated with tissue glutamate, was lower in SNP4 AA homozygotes. In postmortem human prefrontal cortex, AA homozygotes had lower mRNA levels of the glial glutamate transporter EAAT2, a protein regulated by GRM3 that critically modulates synaptic glutamate. Effects of SNP4 on prefrontal GRM3 mRNA and protein levels were marginal. Resequencing revealed no missense or splice-site SNPs, suggesting that the intronic SNP4 or related haplotypes may exert subtle regulatory effects on GRM3 transcription. These convergent data point to a specific molecular pathway by which GRM3 genotype alters glutamate neurotransmission, prefrontal and hippocampal physiology and cognition, and thereby increased risk for schizophrenia.
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                Author and article information

                Contributors
                Departments of Psychiatry, Neurology and Radiology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA
                Departments of Psychiatry, Neurology and Radiology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA
                Journal
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues in Clinical Neuroscience
                Les Laboratoires Servier (France )
                1294-8322
                1958-5969
                September 2010
                : 12
                : 3
                : 333-343
                Affiliations
                Departments of Psychiatry, Neurology and Radiology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA
                Departments of Psychiatry, Neurology and Radiology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania, USA
                Author notes
                [* ] To whom correspondence should be addressed. E-mail: raquel@ 123456upenn.edu
                Article
                10.31887/DCNS.2010.12.3/rgur
                3181978
                20954429
                34887612-7140-4a9e-b5ea-dd446913b9a9
                Copyright: © 2010 LLS

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Translational Research

                Neurosciences
                fmri,bold,event-related,functional connectivity
                Neurosciences
                fmri, bold, event-related, functional connectivity

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