ORCID Profile
0000-0003-0496-7262
Current Organisations
Centre for Addiction and Mental Health
,
University of Toronto
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Publisher: Elsevier BV
Date: 10-2008
DOI: 10.1016/J.SCHRES.2008.08.015
Abstract: The Schizophrenia International Research Society held its first scientific conference in Venice, Italy, June 21 to 25th, 2008. A wide range of controversial topics were presented in overlapping and plenary oral sessions. These included new genetic studies, controversies about early detection of schizophrenia and the prodrome, treatment issues, clinical characteristics, cognition, neuropathology and neurophysiology, other etiological considerations, substance abuse co-morbidity, and animal models for investigating disease etiology and for use as targets in drug studies. Young investigators in the field were awarded travel grants to participate in the congress and one of their roles was to summarize the oral sessions and subsequent discussions. The reports that follow are the culmination of this work produced by 30 young investigators who attended the congress. It is hoped that these summaries will be useful synopses of what actually occurred at the congress for those who did not attend each session or were unable to be present. The abstracts of all presentations, as submitted by the authors a few months prior, were previously published as supplement 2 to volume 102/1-3, June 2008.
Publisher: Springer Science and Business Media LLC
Date: 11-05-2020
Publisher: Springer Science and Business Media LLC
Date: 21-11-2016
DOI: 10.1038/NG.3725
Publisher: Springer Science and Business Media LLC
Date: 02-2016
DOI: 10.1038/NN.4228
Publisher: Elsevier BV
Date: 02-2022
Publisher: American Psychiatric Association Publishing
Date: 08-2019
Publisher: Public Library of Science (PLoS)
Date: 28-10-2016
Publisher: Elsevier BV
Date: 12-2019
Publisher: Elsevier BV
Date: 06-2018
Publisher: Elsevier BV
Date: 06-2018
Publisher: Elsevier BV
Date: 02-2009
Publisher: Springer Science and Business Media LLC
Date: 02-02-2015
DOI: 10.1038/NG.3211
Publisher: Springer Science and Business Media LLC
Date: 07-2014
DOI: 10.1038/NATURE13595
Publisher: Royal College of Psychiatrists
Date: 25-08-2021
DOI: 10.1192/BJP.2021.102
Abstract: Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools. To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics. Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO ( n = 12 977) and PAO ( n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication s le ( n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts. Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO. AAO and PAO are associated with indicators of bipolar disorder severity. In iduals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.
Publisher: Wiley
Date: 16-12-2012
DOI: 10.1002/AJMG.B.32017
Publisher: Frontiers Media SA
Date: 03-12-2021
DOI: 10.3389/FPSYT.2021.734077
Abstract: Background: The prevalence of insomnia and hypersomnia in depressed in iduals is substantially higher than that found in the general population. Unfortunately, these concurrent sleep problems can have profound effects on the disease course. Although the full biology of sleep remains to be elucidated, a recent genome-wide association (GWAS) of insomnia, and other sleep traits in over 1 million in iduals was recently published and provides many promising hits for genetics of insomnia in a population-based s le. Methods: Using data from the largest available GWAS of insomnia and other sleep traits, we sought to test if sleep variable PRS scores derived from population-based studies predicted sleep variables in s les of depressed cases [Psychiatric Genomics Consortium - Major Depressive Disorder subjects (PGC MDD)]. A leave-one-out analysis was performed to determine the effects that each in idual study had on our results. Results: The only significant finding was for insomnia, where p -value threshold, p = 0.05 was associated with insomnia in our PGC MDD s le ( R 2 = 1.75 −3 , p = 0.006). Conclusion: Our results reveal that & % of variance is explained by the variants that cover the two significant p -value thresholds, which is in line with the fact that depression and insomnia are both polygenic disorders. To the best of our knowledge, this is the first study to investigate genetic overlap between the general population and a depression s le for insomnia, which has important treatment implications, such as leading to novel drug targets in future research efforts.
Publisher: Wiley
Date: 23-02-2019
DOI: 10.1002/AJMG.B.32716
Publisher: Springer Science and Business Media LLC
Date: 05-07-2018
DOI: 10.1038/S41598-018-28160-Z
Abstract: Previous studies have shown an increased risk for mental health problems in children born to both younger and older parents compared to children of average-aged parents. We previously used a novel design to reveal a latent mechanism of genetic association between schizophrenia and age at first birth in women (AFB). Here, we use independent data from the UK Biobank (N = 38,892) to replicate the finding of an association between predicted genetic risk of schizophrenia and AFB in women, and to estimate the genetic correlation between schizophrenia and AFB in women stratified into younger and older groups. We find evidence for an association between predicted genetic risk of schizophrenia and AFB in women (P-value = 1.12E-05), and we show genetic heterogeneity between younger and older AFB groups (P-value = 3.45E-03). The genetic correlation between schizophrenia and AFB in the younger AFB group is −0.16 (SE = 0.04) while that between schizophrenia and AFB in the older AFB group is 0.14 (SE = 0.08). Our results suggest that early, and perhaps also late, age at first birth in women is associated with increased genetic risk for schizophrenia in the UK Biobank s le. These findings contribute new insights into factors contributing to the complex bio-social risk architecture underpinning the association between parental age and offspring mental health.
Publisher: Springer Science and Business Media LLC
Date: 25-03-2019
Publisher: Springer Science and Business Media LLC
Date: 08-06-2021
DOI: 10.1038/S41398-021-01471-Y
Abstract: Tar e dyskinesia (TD) is a severe condition characterized by repetitive involuntary movement of orofacial regions and extremities. Patients treated with antipsychotics typically present with TD symptomatology. Here, we conducted the largest GWAS of TD to date, by meta-analyzing s les of East-Asian, European, and African American ancestry, followed by analyses of biological pathways and polygenic risk with related phenotypes. We identified a novel locus and three suggestive loci, implicating immune-related pathways. Through integrating trans -ethnic fine mapping, we identified putative credible causal variants for three of the loci. Post-hoc analysis revealed that SNPs harbored in TNFRSF1B and CALCOCO1 independently conferred three-fold increase in TD risk, beyond clinical risk factors like Age of onset and Duration of illness to schizophrenia. Further work is necessary to replicate loci that are reported in the study and evaluate the polygenic architecture underlying TD.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-2011
Publisher: Springer Science and Business Media LLC
Date: 21-03-2017
DOI: 10.1038/NCOMMS14774
Abstract: We have previously shown higher-than-expected rates of schizophrenia in relatives of patients with amyotrophic lateral sclerosis (ALS), suggesting an aetiological relationship between the diseases. Here, we investigate the genetic relationship between ALS and schizophrenia using genome-wide association study data from over 100,000 unique in iduals. Using linkage disequilibrium score regression, we estimate the genetic correlation between ALS and schizophrenia to be 14.3% (7.05–21.6 P =1 × 10 −4 ) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS ( P =8.4 × 10 −7 ). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08–1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.
Publisher: Springer Science and Business Media LLC
Date: 08-04-2022
Publisher: Springer Science and Business Media LLC
Date: 06-09-2019
DOI: 10.1038/S41380-019-0463-8
Abstract: Based on the discovery by the Resilience Project (Chen R. et al. Nat Biotechnol 34:531–538, 2016) of rare variants that confer resistance to Mendelian disease, and protective alleles for some complex diseases, we posited the existence of genetic variants that promote resilience to highly heritable polygenic disorders1,0 such as schizophrenia. Resilience has been traditionally viewed as a psychological construct, although our use of the term resilience refers to a different construct that directly relates to the Resilience Project, namely: heritable variation that promotes resistance to disease by reducing the penetrance of risk loci, wherein resilience and risk loci operate orthogonal to one another. In this study, we established a procedure to identify unaffected in iduals with relatively high polygenic risk for schizophrenia, and contrasted them with risk-matched schizophrenia cases to generate the first known “polygenic resilience score” that represents the additive contributions to SZ resistance by variants that are distinct from risk loci. The resilience score was derived from data compiled by the Psychiatric Genomics Consortium, and replicated in three independent s les. This work establishes a generalizable framework for finding resilience variants for any complex, heritable disorder.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 12-2016
No related grants have been discovered for Clement C Zai.