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631 results on '"Zammit S."'

101. Wake-up call for British psychiatry Reply

Author

Craddock, N, Antebi, D, Attenburrow, M-J, Bailey, T, Carson, A, Cowen, P, Ebmeier, K, Farmer, A, Fazel, S, Ferrier, N, Geddes, J, Goodwin, G, Harrison, P, Hawton, K, Hunter, S, Jacoby, R, Jones, I, Keedwell, P, Kerr, M, Mackin, P, McGuffin, P, McIntyre, D, McConville, P, Mountain, D, O'Donovan, MC, Owen, MJ, Oyebode, F, Phillips, M, Price, J, Shah, P, Smith, DJ, Walters, J, Woodruff, P, Young, A, and Zammit, S

Published
2008

102. Assessing causality in associations between cannabis use and schizophrenia risk: a two-sample Mendelian randomization study.

Author

Gage, S. H., Jones, H. J., Burgess, S., Bowden, J., Davey Smith, G., Zammit, S., and Munafò, M. R.

Subjects
SCHIZOPHRENIA risk factors, CANNABIS (Genus), CONFIDENCE intervals, GENETIC polymorphisms, SUBSTANCE abuse, ODDS ratio
Abstract

BackgroundObservational associations between cannabis and schizophrenia are well documented, but ascertaining causation is more challenging. We used Mendelian randomization (MR), utilizing publicly available data as a method for ascertaining causation from observational data.MethodWe performed bi-directional two-sample MR using summary-level genome-wide data from the International Cannabis Consortium (ICC) and the Psychiatric Genomics Consortium (PGC2). Single nucleotide polymorphisms (SNPs) associated with cannabis initiation (p < 10−5) and schizophrenia (p < 5 × 10−8) were combined using an inverse-variance-weighted fixed-effects approach. We also used height and education genome-wide association study data, representing negative and positive control analyses.ResultsThere was some evidence consistent with a causal effect of cannabis initiation on risk of schizophrenia [odds ratio (OR) 1.04 per doubling odds of cannabis initiation, 95% confidence interval (CI) 1.01–1.07, p = 0.019]. There was strong evidence consistent with a causal effect of schizophrenia risk on likelihood of cannabis initiation (OR 1.10 per doubling of the odds of schizophrenia, 95% CI 1.05–1.14, p = 2.64 × 10−5). Findings were as predicted for the negative control (height: OR 1.00, 95% CI 0.99–1.01, p = 0.90) but weaker than predicted for the positive control (years in education: OR 0.99, 95% CI 0.97–1.00, p = 0.066) analyses.ConclusionsOur results provide some that cannabis initiation increases the risk of schizophrenia, although the size of the causal estimate is small. We find stronger evidence that schizophrenia risk predicts cannabis initiation, possibly as genetic instruments for schizophrenia are stronger than for cannabis initiation. [ABSTRACT FROM PUBLISHER]

Published
2017
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105. ASD and schizophrenia show distinct developmental profiles in common genetic overlap with population-based social communication difficulties

Author

St Pourcain, B, Robinson, E B, Anttila, V, Sullivan, B B, Maller, J, Golding, J, Skuse, D, Ring, S, Evans, D M, Zammit, S, Fisher, S E, Neale, B M, Anney, R J L, Ripke, S, Hollegaard, M V, Werge, T, Ronald, A, Grove, J, Hougaard, D M, Børglum, A D, Mortensen, P B, Daly, M J, and Davey Smith, G

Abstract

Difficulties in social communication are part of the phenotypic overlap between autism spectrum disorders (ASD) and schizophrenia. Both conditions follow, however, distinct developmental patterns. Symptoms of ASD typically occur during early childhood, whereas most symptoms characteristic of schizophrenia do not appear before early adulthood. We investigated whether overlap in common genetic influences between these clinical conditions and impairments in social communication depends on the developmental stage of the assessed trait. Social communication difficulties were measured in typically-developing youth (Avon Longitudinal Study of Parents and Children, N⩽5553, longitudinal assessments at 8, 11, 14 and 17 years) using the Social Communication Disorder Checklist. Data on clinical ASD (PGC-ASD: 5305 cases, 5305 pseudo-controls; iPSYCH-ASD: 7783 cases, 11 359 controls) and schizophrenia (PGC-SCZ2: 34 241 cases, 45 604 controls, 1235 trios) were either obtained through the Psychiatric Genomics Consortium (PGC) or the Danish iPSYCH project. Overlap in genetic influences between ASD and social communication difficulties during development decreased with age, both in the PGC-ASD and the iPSYCH-ASD sample. Genetic overlap between schizophrenia and social communication difficulties, by contrast, persisted across age, as observed within two independent PGC-SCZ2 subsamples, and showed an increase in magnitude for traits assessed during later adolescence. ASD- and schizophrenia-related polygenic effects were unrelated to each other and changes in trait-disorder links reflect the heterogeneity of genetic factors influencing social communication difficulties during childhood versus later adolescence. Thus, both clinical ASD and schizophrenia share some genetic influences with impairments in social communication, but reveal distinct developmental profiles in their genetic links, consistent with the onset of clinical symptoms.

Published
2018
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119. Psychology, Measurement and Management of Pain [319-321]: 319. Hospital Anxiety and Depression (Had) Scores in Rheumatoid Arthritis: Associations with Function, Disease Duration and Employment Status

Author

Mo, N., primary, Oakley, J., additional, O'Sullivan, M., additional, Shaikh, M. F., additional, Soory, D., additional, Parker, R. A., additional, Shenker, N. G., additional, Farrugia, C., additional, Chetcuti Zammit, S., additional, Lauri, J., additional, and Borg, A. A., additional

Published
2010
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126. Authors' reply

Author

Zammit, S., primary, Allebeck, P., additional, Dalman, C., additional, Lundberg, I., additional, Hemmingson, T., additional, Owen, M. J., additional, and Lewis, G., additional

Published
2004
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127. Identification in 2 Independent Samples of a Novel Schizophrenia RiskHaplotype of the Dystrobrevin Binding Protein Gene (DTNBP1)

Author

Williams, N. M., primary, Preece, A, additional, Morris, D. W., additional, Spurlock, G., additional, Bray, N. J., additional, Stephens, M., additional, Norton, N., additional, Williams, H., additional, Clement, M., additional, Dwyer, S., additional, Curran, C., additional, Wilkinson, J., additional, Moskvina, V., additional, Waddington, J. L., additional, Gill, M., additional, Corvin, A. P., additional, Zammit, S., additional, Kirov, G., additional, Owen, M. J., additional, and O'Donovan, M. C., additional

Published
2004
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136. If cannabis caused schizophrenia--how many cannabis users may need to be prevented in order to prevent one case of schizophrenia? England and Wales calculations.

Author

Hickman M, Vickerman P, Macleod J, Lewis G, Zammit S, Kirkbride J, and Jones P

Abstract

Background We consider how many cannabis users may need to be prevented in order to prevent one case of schizophrenia or psychosis [defined as number needed to prevent (NNP)]. Method Calculation for England and Wales using best available estimates of: incidence of schizophrenia; rates of heavy and light cannabis use; and risk that cannabis causes schizophrenia. Results In men the annual mean NNP for heavy cannabis and schizophrenia ranged from 2800 [90% confidence interval (CI) 2018-4530] in those aged 20-24 years to 4700 (90% CI 3114-8416) in those aged 35-39. In women, mean NNP for heavy cannabis use and schizophrenia ranged from 5470 (90% CI 3640-9839) in those aged 25-29 to 10 870 (90% CI 6786-22 732) in 35-39-year-olds. Equivalent mean NNP for heavy cannabis use and psychosis were lower, from 1360 (90% CI 1007-2124) in men aged 20-24 and 2480 (90% CI 1408-3518) in women aged 16-19. The mean and median number of light cannabis users that would need to be prevented in order to prevent one case of schizophrenia or psychosis per year are four to five times greater than among heavy users. Conclusions The number of young people who need to be exposed to an intervention to generate NNP and prevent one case of schizophrenia will be even larger. The public health importance of preventing cannabis to reduce schizophrenia or psychosis remains uncertain. More attention should be given to testing the hypothesis that cannabis is related causally to psychotic outcomes, and to considering what strategies will be the most effective in reducing heavy cannabis use among young people. [ABSTRACT FROM AUTHOR]

Published
2009
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138. Characterisation, mutation detection, and association analysis of alternative promoters and 5' UTRs of the human dopamine D3 receptor gene in schizophrenia.

Author

Anney, R.J., Rees, M.I., Bryan, E., Spurlock, G., Williams, N., Norton, N., Williams, H., Cardno, A., Zammit, S., Jones, S., Jones, G., Hoogendoorn, B., Smith, K., Hamshere, M.L., Coleman, S., Guy, C., O'Donovan, M.C., Owen, M.J., and Buckland, P.R.

Subjects
GENETICS of schizophrenia, DOPAMINE receptors
Abstract

The dopamine D[sub 3] receptor gene (DRD3) is a candidate for a number of psychiatric conditions including schizophrenia, bipolar disorder and alcohol and drug abuse. Previous studies have reported associations between polymorphisms in DRD3 and these disorders, but these findings may have reflected linkage disequilibrium with pathogenic variants that are further upstream. We have isolated and sequenced approximately 9 kb of genomic sequence upstream of the human DRD3 translational start site. Using 5' RACE, we have identified within this region three additional exons and two putative promoter regions which show promoter activity in three different cell lines. A 5' UTR identified only in lymphoblasts is spread over three exons and is 353 bp long. A second 5' UTR, found in adult and fetal brain, lymphocytes, kidney and placenta is spread over two exons and is 516 bp long. A 260-bp sequence within this 9 kb corresponds to a previously reported EST, but corresponding mRNA could not be found in the tissues above. The EST, 5' UTRs and putative promoter regions have been analysed for polymorphisms, revealing 10 single nucleotide polymorphisms, seven of which were tested for association in a large sample of unrelated patients with schizophrenia and matched controls. No associations were observed with schizophrenia. In addition we failed to replicate previous findings of association with homozygosity of the Ser9Gly variant. The results from this study imply that neither the coding nor the regulatory region of DRD3 plays a major role in predisposition to schizophrenia. [ABSTRACT FROM AUTHOR]

Published
2002
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139. IGF1, growth pathway polymorphisms and schizophrenia: A pooling studyPlease cite this article as follows: Gunnell D, Lewis S, Wilkinson J, Georgieva L, Davey Smith G, Day INM, Holly JMP, O'Donovan MC, Owen MJ, Kirov G, Zammit S. 2007. IGF1, Growth Pathway Polymorphisms and Schizophrenia: A Pooling Study. Am J Med Genet Part B 144B:117–120.

Author

Gunnell, D., Lewis, S., Wilkinson, J., Georgieva, L., Davey, G. Smith, Day, I.N.M., Holly, J.M.P., O'Donovan, M.C., Owen, M.J., Kirov, G., and Zammit, S.

Abstract

It has been hypothesized that insulin‐like growth factors (IGFs) and components of the growth‐hormone (GH)‐IGF axis may underlie reported associations of poor fetal and childhood growth with schizophrenia. We have investigated the association of schizophrenia with 16 SNPs spanning the IGF1 gene with an inter‐marker distance of approximately 2–3 kb. We also examined associations with four common functional polymorphisms of genes involved in aspects of the GH‐IGF system—the IGF1 receptor (IGF1R), insulin receptor substrate (IRS1), growth hormone (GH1), and IGF binding protein‐3 (IGFBP3). The study was based on an analysis of pooled DNA samples from 648 UK and Irish cases of schizophrenia and 712 blood donor controls and of 297 Bulgarian parent offspring trios. In replicated pool analyses, none of the 16 SNPs in IGF1 nor the 4 key SNPs in the other growth pathway genes were associated with schizophrenia. SNP coverage of IGF1 was extensive, so our findings do not support a major role for IGF‐I in the aetiology of schizophrenia. © 2006 Wiley‐Liss, Inc.

Published
2007
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140. Mutation screening of the <TOGGLE>Homer</TOGGLE> gene family and association analysis in schizophrenia<FNR HREF="fn1"></FNR><FN ID="fn1">N. Norton and H.J. Williams contributed equally to this work.</FN>

Author

Norton, N., Williams, H.J., Williams, N.M., Spurlock, G., Zammit, S., Jones, G., Jones, S., Owen, R., O'Donovan, M.C., and Owen, M.J.

Abstract

Homer proteins are a group of proteins that regulate group 1 metabotropic glutamate receptor function. As altered glutamate function has been implicated in many neuro psychiatric disorders, particularly schizophrenia, we have screened all three known Homer genes for sequence variation for use under the candidate gene association paradigm. We found seven SNPs, including three in exons. Of these, none was non-synonymous. Allele frequencies of all the detected SNPs were estimated in DNA pools of 368 schizophrenics and 368 controls. Only one (Homer 1 IVS4 + 18A > G) was associated with schizophrenia in this sample, a finding confirmed by individual genotyping (P = 0.01). However, in our extended sample of 680 cases and 671 controls, the evidence for association diminished (P = 0.05). Our results suggest it is unlikely that sequence variants in the Homer genes contribute to the aetiology of schizophrenia, but the variants we identified are plausible candidates for other neuropsychiatric phenotypes. © 2003 Wiley-Liss, Inc.

Published
2003
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141. Total Synthesis of (−)-Reveromycin B

Author

Cuzzupe, A. N., Hutton, C. A., Lilly, M. J., Mann, R. K., Rizzacasa, M. A., and Zammit, S. C.

Abstract

The total synthesis of the epidermal growth factor inhibitor reveromycin B (2) is described. A novel, convergent, and stereoselective reaction sequence was utilized to construct the 5,6-spiroketal system 10 which was converted into the natural product 2 by a 16-step sequence.

Published
2000

143. Investigating causality in associations between smoking initiation and schizophrenia using Mendelian randomization

Author

Gage, SH, Jones, HJ, Taylor, AE, Burgess, S, Zammit, S, and Munafò, MR

Subjects
Male, Smoking, Genetic Variation, Mendelian Randomization Analysis, Risk Assessment, 3. Good health, Phenotype, Risk Factors, Odds Ratio, Schizophrenia, Humans, Female, Disease Susceptibility, Genome-Wide Association Study
Abstract

Smoking is strongly associated with schizophrenia. Although it has been widely assumed that this reflects self-medication, recent studies suggest that smoking may be a risk factor for schizophrenia. We performed two-sample bi-directional Mendelian randomization using summary level genomewide association data from the Tobacco And Genetics Consortium and Psychiatric Genomics Consortium. Variants associated with smoking initiation and schizophrenia were combined using an inverse-variance weighted fixed-effects approach. We found evidence consistent with a causal effect of smoking initiation on schizophrenia risk (OR 1.73, 95% CI 1.30-2.25, p < 0.001). However, after relaxing the p-value threshold to include variants from more than one gene and minimize the potential impact of pleiotropy, the association was attenuated (OR 1.03, 95% CI 0.97-1.09, p = 0.32). There was little evidence in support of a causal effect of schizophrenia on smoking initiation (OR 1.01, 95% CI 0.98-1.04, p = 0.32). MR Egger regression sensitivity analysis indicated no evidence for pleiotropy in the effect of schizophrenia on smoking initiation (intercept OR 1.01, 95% CI 0.99-1.02, p = 0.49). Our findings provide little evidence of a causal association between smoking initiation and schizophrenia, in either direction. However, we cannot rule out a causal effect of smoking on schizophrenia related to heavier, lifetime exposure, rather than initiation.

145. Association analysis of TBX1 and schizophrenia

Author

Williams, H. J., Khazanehdari, K., Sutherland, H., Murphy, K. C., Jones, S., Mccarthy, G. S., Jones, G., Zammit, S., Cardno, A., Owen, R., Scambler, P., Michael O'Donovan, and Owen, M. J.

148. Association between serum C-reactive protein and DSM-IV generalized anxiety disorder in adolescence: Findings from the ALSPAC cohort

Author

Khandaker, GM, Zammit, S, Lewis, G, and Jones, PB

Subjects
birth cohort study, systemic inflammation, generalized anxiety disorder, biological markers, 3. Good health, C-reactive protein
Abstract

$\textit{$Background:}$ Animal studies suggest a role of inflammation in the pathophysiology of anxiety, but human studies of inflammatory markers and anxiety disorders are scarce. We report a study of serum C-reactive protein (CRP) and generalised anxiety disorder (GAD) from the general population-based ALSPAC birth cohort. $\textit{Methods:}$ DSM-IV diagnosis of GAD was obtained from 5365 cohort members during face-to-face clinical assessment at age 16 years, of which 3392 also provided data on serum high sensitivity CRP levels. Logistic regression calculated odds ratio (OR) for GAD among individuals in top and middle thirds of CRP distribution compared with the bottom third. Effect of comorbid depression was assessed. Age, sex, body mass, ethnicity, social class, maternal education, maternal age at delivery, and family history of inflammatory conditions were included as potential confounders. $\textit{Results:}$ Forty participants met DSM-IV criteria for GAD (0.74%). CRP levels were higher in GAD cases compared with the rest of the cohort (P = 0.005). After adjusting for potential confounders, participants in the top third of CRP values compared with the bottom third were more likely to have GAD; adjusted OR 5.06 (95% CI, 1.31-19.59). The association between CRP and GAD was consistent with a linear dose-response relationship. The pattern of association between CRP and GAD remained unchanged after excluding cases with co-morbid depression. $\textit{Conclusions:}$ The findings are consistent with a role of inflammation in anxiety disorders. Longitudinal studies of inflammatory markers, subsequent anxiety taking into account current and past psychological stress are required to understand this association further.

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