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Articles by A Mechelli
Total Records ( 5 ) for A Mechelli
  Z Jia , X Huang , Q Wu , T Zhang , S Lui , J Zhang , N Amatya , W Kuang , R. C. K Chan , G. J Kemp , A Mechelli and Q. Gong

Suicide is a major social and public health problem, but its neurobiology in major depressive disorder is poorly understood. The purpose of this study was to use magnetic resonance diffusion tensor imaging to characterize abnormalities of white matter integrity in major depressive disorder patients with and without a history of suicide attempts.


Participants were 52 patients with major depressive disorder, with (N=16) and without (N=36) a history of suicide attempts, and 52 healthy comparison subjects matched for age, gender, education, and ethnicity. Diffusion tensor imaging in a 3.0 Tesla magnetic resonance scanner was performed. Whole-brain voxel-based analysis was used to compare fractional anisotropy across the three groups and analyze the correlation with symptom severity. A region-of-interest analysis was applied to the bilateral hippocampus, thalamus, and lentiform nucleus


Fractional anisotropy was decreased in the left anterior limb of the internal capsule in suicide attempters relative to both nonattempters and healthy comparison subjects, in the right frontal lobe relative to comparison subjects only, and in the right lentiform nucleus relative to nonattempters only. There was no significant correlation with symptom severity.


Decreased fractional anisotropy in the left anterior limb of the internal capsule appears to characterize patients with major depressive disorder who have a history of attempting suicide. Longitudinal studies are required to validate this as a potential marker that may inform the development of strategies for reducing suicide.

  D. P Prata , A Mechelli , M. M Picchioni , C. H. Y Fu , T Toulopoulou , E Bramon , M Walshe , R. M Murray , D. A Collier and P. McGuire

Context  The dopamine transporter plays a key role in the regulation of central dopaminergic transmission, which modulates cognitive processing. Disrupted dopamine function and impaired executive processing are robust features of schizophrenia.

Objective  To examine the effect of a polymorphism in the dopamine transporter gene (the variable number of tandem repeats in the 3' untranslated region) on brain function during executive processing in healthy volunteers and patients with schizophrenia. We hypothesized that this variation would have a different effect on prefrontal and striatal activation in schizophrenia, reflecting altered dopamine function.

Design  Case-control study.

Setting  Psychiatric research center.

Participants  Eighty-five subjects, comprising 44 healthy volunteers (18 who were 9-repeat carriers and 26 who were 10-repeat homozygotes) and 41 patients with DSM-IV schizophrenia (18 who were 9-repeat carriers and 23 who were 10-repeat homozygotes).

Main Outcome Measures  Regional brain activation during word generation relative to repetition in an overt verbal fluency task measured by functional magnetic resonance imaging. Main effects of genotype and diagnosis on activation and their interaction were estimated with analysis of variance in SPM5.

Results  Irrespective of diagnosis, the 10-repeat allele was associated with greater activation than the 9-repeat allele in the left anterior insula and right caudate nucleus. Trends for the same effect in the right insula and for greater deactivation in the rostral anterior cingulate cortex were also detected. There were diagnosis x genotype interactions in the left middle frontal gyrus and left nucleus accumbens, where the 9-repeat allele was associated with greater activation than the 10-repeat allele in patients but not controls.

Conclusions  Insular, cingulate, and striatal function during an executive task is normally modulated by variation in the dopamine transporter gene. Its effect on activation in the dorsolateral prefrontal cortex and ventral striatum is altered in patients with schizophrenia. This may reflect altered dopamine function in these regions in schizophrenia.

  F. V Rijsdijsk , E Viding , S De Brito , M Forgiarini , A Mechelli , A. P Jones and E. McCrory

Context  Genetic vulnerability to psychopathic traits is likely to also manifest at the neural level. We have recently reported increased gray matter concentration in several brain areas in boys with psychopathic traits.

Objective  To explore whether these gray matter concentration differences can be regarded as endophenotypes for psychopathic traits by (1) assessing their heritability and (2) examining the etiology of the co-occurrence of psychopathic traits and increased gray matter concentration.

Design  Community twin sample.

Setting  On-campus neuroimaging facility.

Patients or Other Participants  One hundred twenty-three male twins (56 monozygotic and 67 dizygotic individuals; mean age 11.55 years; range, 10-13 years).

Main Outcome Measures  We analyzed structural magnetic resonance imaging scans. Voxel-based morphometry analyses were used to obtain gray matter concentration values that were analyzed in a biometrical genetic twin model.

Results  Left posterior cingulate and right dorsal anterior cingulate gray matter concentrations were found to be the strongest endophenotype markers, with heritability estimates of 46% and 37%, respectively, and common genes explaining the phenotypic relationship between these regions and psychopathic traits. No significant heritabilities were found for several regions, including the right orbitofrontal cortex and insula.

Conclusions  These findings suggest that structural endophenotypes, in the form of variations in gray matter concentration, reflect genetic vulnerability for psychopathic traits. Specifically, gray matter concentration in the left posterior cingulate and right dorsal anterior cingulate, brain areas implicated in empathy, moral processing, and introspection, are potential candidate endophenotypes for psychopathic traits.

  S Benetti , A Mechelli , M Picchioni , M Broome , S Williams and P. McGuire

Recent neuroimaging studies have reported deficits in functional integration between prefrontal cortex and the hippocampal formation in schizophrenia. It is unclear whether these alterations are a consequence of chronic illness or its treatment, and whether they are also evident in non-psychotic subjects at increased risk of the disorder. We addressed these issues by investigating prefrontal–hippocampal interactions in patients with first episode schizophrenia and subjects with an At Risk Mental State (ARMS). Using functional Magnetic Resonance Imaging, we measured brain responses from 16 individuals with an ARMS, 10 patients with first episode schizophrenia and 14 healthy controls during a delayed matching to sample task. Dynamic causal modelling was used to estimate the effective connectivity between prefrontal cortex and anterior and posterior hippocampal regions. The normal pattern of effective connectivity from the right posterior hippocampus to the right inferior frontal gyrus was significantly decreased in both first episode patients and subjects with an ARMS (ANOVA; F = 8.16, P = 0.01). Interactions between the inferior frontal gyrus and the anterior part of the hippocampus did not differ across the three groups. Perturbed hippocampal–prefrontal interactions are evident in individuals at high risk of developing psychosis and in patients who have just developed schizophrenia. This suggests that it may be a correlate of increased vulnerability to psychosis and that it is not attributable to an effect of chronic illness or its treatment.

  S. A De Brito , S Hodgins , E. J.P Mccrory , A Mechelli , M Wilke , A. P Jones and E. Viding

A series of neuroimaging studies have reported structural differences in several subcortical and frontal systems in individuals with stable antisocial behavior (sASB). Specifically, differences have been observed in the prefrontal and temporal cortices (e.g., amygdala and hippocampus). However, the sASB population is typically characterized by co-occurring hyperactivity— inattention symptoms and low cognitive ability. These nuisance variables are likely to complicate the interpretation of findings regarding structural differences associated with sASB. The way in which each study deals with these variables influences the conclusions that can be drawn about the brain structure and function of children and adults with sASB. This article briefly reviews the extant literature in this field before considering two approaches that may be used to deal with comorbidities conceptualized as nuisance variables--namely, the analysis of covariance (ANCOVA) and the matched-group design. Then, the authors illustrate, with their own data, checks that may be performed to ensure the validity of results using ANCOVA.

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