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Articles by D. A Collier
Total Records ( 3 ) for D. A Collier
  A. C Iervolino , N Perroud , M. A Fullana , M Guipponi , L Cherkas , D. A Collier and D. Mataix Cols

OBJECTIVE: Compulsive hoarding is a serious health problem for the sufferers, their families, and the community at large. It appears to be highly prevalent and to run in families. However, this familiality could be due to genetic or environmental factors. This study examined the prevalence and heritability of compulsive hoarding in a large sample of twins. METHOD: A total of 5,022 twins completed a validated measure of compulsive hoarding. The prevalence of severe hoarding was determined using empirically derived cutoffs. Genetic and environmental influences on compulsive hoarding were estimated using liability threshold models, and maximum-likelihood univariate model-fitting analyses were employed to decompose the variance in the liability to compulsive hoarding into additive genetic and shared and nonshared environmental factors (female twins only; N=4,355). RESULTS: A total of 2.3% of twins met criteria for caseness, with significantly higher rates observed for male (4.1%) than for female (2.1%) twins. Model-fitting analyses in female twins showed that genetic factors accounted for approximately 50% of the variance in compulsive hoarding, with nonshared environmental factors and measurement error accounting for the other half. CONCLUSIONS: Compulsive hoarding is highly prevalent and heritable, at least in women, with nonshared environmental factors also likely to play an important role.

  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.

  M. L Hamshere , E. K Green , I. R Jones , L Jones , V Moskvina , G Kirov , D Grozeva , I Nikolov , D Vukcevic , S Caesar , K Gordon Smith , C Fraser , E Russell , G Breen , D St Clair , D. A Collier , A. H Young , I. N Ferrier , A Farmer , P McGuffin , Holmans Wellcome Trust Case Control Consortium , M. J Owen , M. C O'Donovan and N. Craddock


Psychiatric phenotypes are currently defined according to sets of descriptive criteria. Although many of these phenotypes are heritable, it would be useful to know whether any of the various diagnostic categories in current use identify cases that are particularly helpful for biological–genetic research.


To use genome-wide genetic association data to explore the relative genetic utility of seven different descriptive operational diagnostic categories relevant to bipolar illness within a large UK case–control bipolar disorder sample.


We analysed our previously published Wellcome Trust Case Control Consortium (WTCCC) bipolar disorder genome-wide association data-set, comprising 1868 individuals with bipolar disorder and 2938 controls genotyped for 276 122 single nucleotide polymorphisms (SNPs) that met stringent criteria for genotype quality. For each SNP we performed a test of association (bipolar disorder group v. control group) and used the number of associated independent SNPs statistically significant at P<0.00001 as a metric for the overall genetic signal in the sample. We next compared this metric with that obtained using each of seven diagnostic subsets of the group with bipolar disorder: Research Diagnostic Criteria (RDC): bipolar I disorder; manic disorder; bipolar II disorder; schizoaffective disorder, bipolar type; DSM–IV: bipolar I disorder; bipolar II disorder; schizoaffective disorder, bipolar type.


The RDC schizoaffective disorder, bipolar type (v. controls) stood out from the other diagnostic subsets as having a significant excess of independent association signals (P<0.003) compared with that expected in samples of the same size selected randomly from the total bipolar disorder group data-set. The strongest association in this subset of participants with bipolar disorder was at rs4818065 (P = 2.42x10–7). Biological systems implicated included gamma amniobutyric acid (GABA)A receptors. Genes having at least one associated polymorphism at P<10–4 included B3GALTS, A2BP1, GABRB1, AUTS2, BSN, PTPRG, GIRK2 and CDH12.


Our findings show that individuals with broadly defined bipolar schizoaffective features have either a particularly strong genetic contribution or that, as a group, are genetically more homogeneous than the other phenotypes tested. The results point to the importance of using diagnostic approaches that recognise this group of individuals. Our approach can be applied to similar data-sets for other psychiatric and non-psychiatric phenotypes.

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