2021 |
Writing Committee for the Attention-Deficit/Hyperactivity Disorder, Autism Spectrum Disorder, Bipolar Disorder, Major Depressive Disorder, Obsessive-Compulsive Disorder, and Schizophrenia ENIGMA Working Groups, et al., 'Virtual Histology of Cortical Thickness and Shared Neurobiology in 6 Psychiatric Disorders.', JAMA Psychiatry, 78 47-63 (2021)
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2020 |
Hess JL, Tylee DS, Barve R, de Jong S, Ophoff RA, Kumarasinghe N, et al., 'Transcriptomic abnormalities in peripheral blood in bipolar disorder, and discrimination of the major psychoses', Schizophrenia Research, 217 124-135 (2020) [C1]
© 2019 Elsevier B.V. We performed a transcriptome-wide meta-analysis and gene co-expression network analysis to identify genes and gene networks dysregulated in the peripheral blo... [more]
© 2019 Elsevier B.V. We performed a transcriptome-wide meta-analysis and gene co-expression network analysis to identify genes and gene networks dysregulated in the peripheral blood of bipolar disorder (BD) cases relative to unaffected comparison subjects, and determined the specificity of the transcriptomic signatures of BD and schizophrenia (SZ). Nineteen genes and 4 gene modules were significantly differentially expressed in BD cases. Thirteen gene modules were shown to be differentially expressed in a combined case-group of BD and SZ subjects called ¿major psychosis¿, including genes biologically linked to apoptosis, reactive oxygen, chromatin remodeling, and immune signaling. No modules were differentially expressed between BD and SZ cases. Machine-learning classifiers trained to separate diagnostic classes based solely on gene expression profiles could distinguish BD cases from unaffected comparison subjects with an area under the curve (AUC) of 0.724, as well as BD cases from SZ cases with AUC = 0.677 in withheld test samples. We introduced a novel and straightforward method called ¿polytranscript risk scoring¿ that could distinguish BD cases from unaffected subjects (AUC = 0.672) and SZ cases (AUC = 0.607) significantly better than expected by chance. Taken together, our results highlighted gene expression alterations common to BD and SZ that involve biological processes of inflammation, oxidative stress, apoptosis, and chromatin regulation, and highlight disorder-specific changes in gene expression that discriminate the major psychoses.
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2020 |
Smith O, Bergmann J, Schall U, 'Youth mental health competencies in regional general practice', Australasian Psychiatry, (2020)
© The Royal Australian and New Zealand College of Psychiatrists 2020. Objective: General practitioners (GPs) are key health professionals for referrals to mental health specialist... [more]
© The Royal Australian and New Zealand College of Psychiatrists 2020. Objective: General practitioners (GPs) are key health professionals for referrals to mental health specialists. Youth mental health issues are particularly challenging, requiring a competent assessment and understanding of appropriate referral pathways. We surveyed local GPs about their understanding of youth mental health problems and needs to competently look after young patients. Methods: GPs working in the Hunter region were contacted via email, fax and post over a 6-month period in 2019. Results: Seventy-five GPs participated. They reported 577 of 1698 (34%) of young people seen 2 weeks prior to being surveyed presented with a mental health problem. Predominantly, referrals were to private practice psychologists and Headspace. Almost a third (31%) reported having limited understanding of ¿at-risk mental state¿ and are ¿not always comfortable¿ when facing a young person with a mental health problem. Nearly all (95%) expressed interest in attending specialised training. GPs identified treatment costs, scarce access to psychiatrists and limited patient engagement as the main obstacles to help young people. Conclusions: Effective treatment of a mental health problem relies on early identification. GPs are seeing young people on a regular basis but don¿t feel well equipped for this task and are keen to up-skill, which needs to be addressed by targeted training.
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2020 |
Holleran L, Kelly S, Alloza C, Agartz I, Andreassen OA, Arango C, et al., 'The relationship between white matter microstructure and general cognitive ability in patients with schizophrenia and healthy participants in the ENIGMA consortium', American Journal of Psychiatry, 177 537-547 (2020) [C1]
© 2020 American Psychiatric Association. All rights reserved. Objective: Schizophrenia has recently been associated with widespread white matter microstructural abnormalities, but... [more]
© 2020 American Psychiatric Association. All rights reserved. Objective: Schizophrenia has recently been associated with widespread white matter microstructural abnormalities, but the functional effects of these abnormalities remain unclear. Widespread heterogeneity of results from studies published to date preclude any definitive characterization of the relationship between white matter and cognitive performance in schizophrenia. Given the relevance of deficits in cognitive function to predicting social and functional outcomes in schizophrenia, the authors carried out a meta-analysis of available data through the ENIGMA Consortium, using a common analysis pipeline, to elucidate the relationship between white matter microstructure and a measure of general cognitive performance, IQ, in patients with schizophrenia and healthy participants. Methods: The meta-analysis included 760 patients with schizophrenia and 957 healthy participants from 11 participating ENIGMA Consortium sites. For each site, principal component analysis was used to calculate both a global fractional anisotropy component (gFA) and a fractional anisotropy component for six long association tracts (LA-gFA) previously associated with cognition. Results: Meta-analyses of regression results indicated that gFA accounted for a significant amount of variation in cognition in the full sample (effect size [Hedges¿ g]=0.27, CI=0.17¿0.36), with similar effects sizes observed for both the patient (effect size=0.20, CI=0.05¿0.35) and healthy participant groups (effect size=0.32, CI=0.18¿0.45). Comparable patterns of association were also observed between LA-gFA and cognition for the full sample (effect size=0.28, CI=0.18¿0.37), the patient group (effect size=0.23, CI=0.09¿0.38), and the healthy participant group (effect size=0.31, CI=0.18¿0.44). Conclusions: This study provides robust evidence that cognitive ability is associated with global structural connectivity, with higher fractional anisotropy associated with higher IQ. This association was independent of diagnosis; while schizophrenia patients tended to have lower fractional anisotropy and lower IQ than healthy participants, the comparable size of effect in each group suggested a more general, rather than disease-specific, pattern of association.
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2020 |
Grasby KL, Jahanshad N, Painter JN, Colodro-Conde L, Bralten J, Hibar DP, et al., 'The genetic architecture of the human cerebral cortex.', Science, 367 (2020)
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2020 |
Kamitaki N, Sekar A, Handsaker RE, de Rivera H, Tooley K, Morris DL, et al., 'Complement genes contribute sex-biased vulnerability in diverse disorders', Nature, 582 577-581 (2020) [C1]
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2020 |
Radua J, Vieta E, Shinohara R, Kochunov P, Quidé Y, Green MJ, et al., 'Increased power by harmonizing structural MRI site differences with the ComBat batch adjustment method in ENIGMA', NeuroImage, 218 (2020) [C1]
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2020 |
Rahman T, Weickert CS, Harms L, Meehan C, Schall U, Todd J, et al., 'Effect of Immune Activation during Early Gestation or Late Gestation on Inhibitory Markers in Adult Male Rats', Scientific Reports, 10 (2020) [C1]
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2020 |
Liu X, Low SK, Atkins JR, Wu JQ, Reay WR, Cairns HM, et al., 'Wnt receptor gene FZD1 was associated with schizophrenia in genome-wide SNP analysis of the Australian Schizophrenia Research Bank cohort', Australian and New Zealand Journal of Psychiatry, 54 902-908 (2020) [C1]
© The Royal Australian and New Zealand College of Psychiatrists 2019. Objectives: Large-scale genetic analysis of common variation in schizophrenia has been a powerful approach to... [more]
© The Royal Australian and New Zealand College of Psychiatrists 2019. Objectives: Large-scale genetic analysis of common variation in schizophrenia has been a powerful approach to understanding this complex but highly heritable psychotic disorder. To further investigate loci, genes and pathways associated more specifically in the well-characterized Australian Schizophrenia Research Bank cohort, we applied genome-wide single-nucleotide polymorphism analysis in these three annotation categories. Methods: We performed a case¿control genome-wide association study in 429 schizophrenia samples and 255 controls. Post-genome-wide association study analyses were then integrated with genomic annotations to explore the enrichment of variation at the gene and pathway level. We also examine candidate single-nucleotide polymorphisms with potential function within expression quantitative trait loci and investigate overall enrichment of variation within tissue-specific functional regulatory domains of the genome. Results: The strongest finding (p = 2.01 × 10-6, odds ratio = 1.82, 95% confidence interval = [1.42, 2.33]) in genome-wide association study was with rs10252923 at 7q21.13, downstream of FZD1 (frizzled class receptor 1). While this did not stand alone after correction, the involvement of FZD1 was supported by gene-based analysis, which exceeded the threshold for genome-wide significance (p = 2.78 × 10-6). Conclusion: The identification of FZD1, as an independent association signal at the gene level, supports the hypothesis that the Wnt signalling pathway is altered in the pathogenesis of schizophrenia and may be an important target for therapeutic development.
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2019 |
Lee PH, Anttila V, Won H, Feng YCA, Rosenthal J, Zhu Z, et al., 'Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders', Cell, 179 1469-1482.e11 (2019) [C1]
© 2019 Elsevier Inc. Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and m... [more]
© 2019 Elsevier Inc. Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.
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2019 |
Hess JL, Tylee DS, Mattheisen M, Adolfsson R, Agartz I, Agerbo E, et al., 'A polygenic resilience score moderates the genetic risk for schizophrenia', Molecular Psychiatry, (2019)
© 2019, The Author(s). 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 disea... [more]
© 2019, The Author(s). 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 individuals 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 samples. This work establishes a generalizable framework for finding resilience variants for any complex, heritable disorder.
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2019 |
Rammos A, Gonzalez LAN, Weinberger DR, Mitchell KJ, Nicodemus KK, 'The role of polygenic risk score gene-set analysis in the context of the omnigenic model of schizophrenia', NEUROPSYCHOPHARMACOLOGY, 44 1562-1569 (2019) [C1]
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2019 |
Huckins LM, Dobbyn A, Ruderfer DM, Hoffman G, Wang W, Pardiñas AF, et al., 'Gene expression imputation across multiple brain regions provides insights into schizophrenia risk', Nature Genetics, 51 659-674 (2019) [C1]
© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. Transcriptomic imputation approaches combine eQTL reference panels with large-scale genotype data i... [more]
© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. Transcriptomic imputation approaches combine eQTL reference panels with large-scale genotype data in order to test associations between disease and gene expression. These genic associations could elucidate signals in complex genome-wide association study (GWAS) loci and may disentangle the role of different tissues in disease development. We used the largest eQTL reference panel for the dorso-lateral prefrontal cortex (DLPFC) to create a set of gene expression predictors and demonstrate their utility. We applied DLPFC and 12 GTEx-brain predictors to 40,299 schizophrenia cases and 65,264 matched controls for a large transcriptomic imputation study of schizophrenia. We identified 413 genic associations across 13 brain regions. Stepwise conditioning identified 67 non-MHC genes, of which 14 did not fall within previous GWAS loci. We identified 36 significantly enriched pathways, including hexosaminidase-A deficiency, and multiple porphyric disorder pathways. We investigated developmental expression patterns among the 67 non-MHC genes and identified specific groups of pre- and postnatal expression.
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2019 |
van den Heuvel MP, Scholtens LH, van der Burgh HK, Agosta F, Alloza C, Arango C, et al., '10Kin1day: A Bottom-Up Neuroimaging Initiative', FRONTIERS IN NEUROLOGY, 10 (2019) [C1]
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2019 |
Pouget JG, Schizophrenia Working Group of the Psychiatric Genomics Consortium, Han B, Wu Y, Mignot E, Ollila HM, et al., 'Cross-disorder analysis of schizophrenia and 19 immune-mediated diseases identifies shared genetic risk.', Human molecular genetics, 28 3498-3513 (2019) [C1]
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2019 |
Mallett X, Schall U, 'The psychological and physiological sequel of child maltreatment: A forensic perspective', Neurology Psychiatry and Brain Research, 34 9-12 (2019) [C1]
© 2019 Background: It has long been recognized that sustained or repeated child maltreatment has lasting psychological and emotional effects on the victims. This has helped to inf... [more]
© 2019 Background: It has long been recognized that sustained or repeated child maltreatment has lasting psychological and emotional effects on the victims. This has helped to inform the criminal and civil justice systems how best to deal with perpetrators of abuse, as well social and health services when treating the victims. However, what is generally less well recognized is that physical and emotional abuse has a lasting and potentially non-reversible effect on brain function. Methods: We conducted a literature review on the forensic, mental, psychological, and pathophysiological impact of child maltreatment and discuss the implications of child maltreatment as a potential mitigating factor in criminal court in cases where victims of abuse become perpetrators themselves. Findings: Repeated exposure to traumatic experiences changes the responsiveness in the hypothalamus-pituitary-adrenal axis with lasting consequences in the developing brain for structures, such as the hippocampus and amygdala. These physiological changes are thought to cause a range of mental disorders, which are associated with poor affect regulation, anxiety, depression, and substance abuse. Conclusions: The importance of developing our understanding of the long-term effects of child abuse and neglect cannot be overestimated as the result of child maltreatment will perpetrate criminal acts since offenders have higher rates of mental illness than the general community.
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2019 |
Harold D, Connolly S, Riley BP, Kendler KS, McCarthy SE, McCombie WR, et al., 'Population-based identity-by-descent mapping combined with exome sequencing to detect rare risk variants for schizophrenia', American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics, 180 223-231 (2019) [C1]
© 2019 Wiley Periodicals, Inc. Genome-wide association studies (GWASs) are highly effective at identifying common risk variants for schizophrenia. Rare risk variants are also impo... [more]
© 2019 Wiley Periodicals, Inc. Genome-wide association studies (GWASs) are highly effective at identifying common risk variants for schizophrenia. Rare risk variants are also important contributors to schizophrenia etiology but, with the exception of large copy number variants, are difficult to detect with GWAS. Exome and genome sequencing, which have accelerated the study of rare variants, are expensive so alternative methods are needed to aid detection of rare variants. Here we re-analyze an Irish schizophrenia GWAS dataset (n = 3,473) by performing identity-by-descent (IBD) mapping followed by exome sequencing of individuals identified as sharing risk haplotypes to search for rare risk variants in coding regions. We identified 45 rare haplotypes (>1 cM) that were significantly more common in cases than controls. By exome sequencing 105 haplotype carriers, we investigated these haplotypes for functional coding variants that could be tested for association in independent GWAS samples. We identified one rare missense variant in PCNT but did not find statistical support for an association with schizophrenia in a replication analysis. However, IBD mapping can prioritize both individual samples and genomic regions for follow-up analysis but genome rather than exome sequencing may be more effective at detecting risk variants on rare haplotypes.
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2019 |
Huckins LM, Dobbyn A, Ruderfer DM, Hoffman G, Wang W, Pardiñas AF, et al., 'Publisher Correction: Gene expression imputation across multiple brain regions provides insights into schizophrenia risk (Nature Genetics, (2019), 51, 4, (659-674), 10.1038/s41588-019-0364-4)', Nature Genetics, 51 1068 (2019)
© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. In the HTML version of the article originally published, the author group ¿The Schizophrenia Workin... [more]
© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. In the HTML version of the article originally published, the author group ¿The Schizophrenia Working Group of the Psychiatric Genomics Consortium¿ was displayed incorrectly. The error has been corrected in the HTML version of the article.
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2019 |
van Erp TGM, Walton E, Hibar DP, Schmaal L, Jiang W, Glahn DC, et al., 'Reply to: New Meta- and Mega-analyses of Magnetic Resonance Imaging Findings in Schizophrenia: Do They Really Increase Our Knowledge About the Nature of the Disease Process?', BIOLOGICAL PSYCHIATRY, 85 E35-E39 (2019)
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2019 |
Lam M, Chen CY, Li Z, Martin AR, Bryois J, Ma X, et al., 'Comparative genetic architectures of schizophrenia in East Asian and European populations', Nature Genetics, 51 1670-1678 (2019) [C1]
© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. Schizophrenia is a debilitating psychiatric disorder with approximately 1% lifetime risk globally. ... [more]
© 2019, The Author(s), under exclusive licence to Springer Nature America, Inc. Schizophrenia is a debilitating psychiatric disorder with approximately 1% lifetime risk globally. Large-scale schizophrenia genetic studies have reported primarily on European ancestry samples, potentially missing important biological insights. Here, we report the largest study to date of East Asian participants (22,778 schizophrenia cases and 35,362 controls), identifying 21 genome-wide-significant associations in 19 genetic loci. Common genetic variants that confer risk for schizophrenia have highly similar effects between East Asian and European ancestries (genetic correlation = 0.98 ± 0.03), indicating that the genetic basis of schizophrenia and its biology are broadly shared across populations. A fixed-effect meta-analysis including individuals from East Asian and European ancestries identified 208 significant associations in 176 genetic loci (53 novel). Trans-ancestry fine-mapping reduced the sets of candidate causal variants in 44 loci. Polygenic risk scores had reduced performance when transferred across ancestries, highlighting the importance of including sufficient samples of major ancestral groups to ensure their generalizability across populations.
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2018 |
LeBlanc M, Zuber V, Thompson WK, Andreassen OA, Frigessi A, Andreassen BK, 'A correction for sample overlap in genome-wide association studies in a polygenic pleiotropy-informed framework', BMC GENOMICS, 19 (2018)
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2018 |
Ni G, Gratten J, Wray NR, Lee SH, Ripke S, Neale BM, et al., 'Age at first birth in women is genetically associated with increased risk of schizophrenia', Scientific Reports, 8 (2018) [C1]
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2018 |
Kelly S, Jahanshad N, Zalesky A, Kochunov P, Agartz I, Alloza C, et al., 'Widespread white matter microstructural differences in schizophrenia across 4322 individuals: results from the ENIGMA Schizophrenia DTI Working Group.', Molecular psychiatry, 23 1261-1269 (2018) [C1]
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2018 |
Harms L, Fulham WR, Todd J, Meehan C, Schall U, Hodgson DM, Michie PT, 'Late deviance detection in rats is reduced, while early deviance detection is augmented by the NMDA receptor antagonist MK-801', Schizophrenia Research, 191 43-50 (2018) [C1]
© 2017 Elsevier B.V. One of the most robust electrophysiological features of schizophrenia is reduced mismatch negativity, a component of the event related potential (ERP) induced... [more]
© 2017 Elsevier B.V. One of the most robust electrophysiological features of schizophrenia is reduced mismatch negativity, a component of the event related potential (ERP) induced by rare and unexpected stimuli in an otherwise regular pattern. Emerging evidence suggests that mismatch negativity (MMN) is not the only ERP index of deviance detection in the mammalian brain and that sensitivity to deviant sounds in a regular background can be observed at earlier latencies in both the human and rodent brain. Pharmacological studies in humans and rodents have previously found that MMN reductions similar to those seen in schizophrenia can be elicited by N-methyl-D-aspartate (NMDA) receptor antagonism, an observation in agreement with the hypothesised role of NMDA receptor hypofunction in schizophrenia pathogenesis. However, it is not known how NMDA receptor antagonism affects early deviance detection responses. Here, we show that NMDA antagonism impacts both early and late deviance detection responses. By recording EEG in awake, freely-moving rats in a drug-free condition and after varying doses of NMDA receptor antagonist MK-801, we found the hypothesised reduction of deviance detection for a late, negative potential (N55). However, the amplitude of an early component, P13, as well as deviance detection evident in the same component, were increased by NMDA receptor antagonism. These findings indicate that late deviance detection in rats is similar to human MMN, but the surprising effect of MK-801 in increasing ERP amplitudes as well as deviance detection at earlier latencies suggests that future studies in humans should examine ERPs over early latencies in schizophrenia and after NMDA antagonism.
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2018 |
van Erp TGM, Walton E, Hibar DP, Schmaal L, Jiang W, Glahn DC, et al., 'Cortical Brain Abnormalities in 4474 Individuals With Schizophrenia and 5098 Control Subjects via the Enhancing Neuro Imaging Genetics Through Meta Analysis (ENIGMA) Consortium', Biological Psychiatry, 84 644-654 (2018) [C1]
© 2018 Society of Biological Psychiatry Background: The profile of cortical neuroanatomical abnormalities in schizophrenia is not fully understood, despite hundreds of published s... [more]
© 2018 Society of Biological Psychiatry Background: The profile of cortical neuroanatomical abnormalities in schizophrenia is not fully understood, despite hundreds of published structural brain imaging studies. This study presents the first meta-analysis of cortical thickness and surface area abnormalities in schizophrenia conducted by the ENIGMA (Enhancing Neuro Imaging Genetics through Meta Analysis) Schizophrenia Working Group. Methods: The study included data from 4474 individuals with schizophrenia (mean age, 32.3 years; range, 11¿78 years; 66% male) and 5098 healthy volunteers (mean age, 32.8 years; range, 10¿87 years; 53% male) assessed with standardized methods at 39 centers worldwide. Results: Compared with healthy volunteers, individuals with schizophrenia have widespread thinner cortex (left/right hemisphere: Cohen's d = -0.530/-0.516) and smaller surface area (left/right hemisphere: Cohen's d = -0.251/-0.254), with the largest effect sizes for both in frontal and temporal lobe regions. Regional group differences in cortical thickness remained significant when statistically controlling for global cortical thickness, suggesting regional specificity. In contrast, effects for cortical surface area appear global. Case-control, negative, cortical thickness effect sizes were two to three times larger in individuals receiving antipsychotic medication relative to unmedicated individuals. Negative correlations between age and bilateral temporal pole thickness were stronger in individuals with schizophrenia than in healthy volunteers. Regional cortical thickness showed significant negative correlations with normalized medication dose, symptom severity, and duration of illness and positive correlations with age at onset. Conclusions: The findings indicate that the ENIGMA meta-analysis approach can achieve robust findings in clinical neuroscience studies; also, medication effects should be taken into account in future genetic association studies of cortical thickness in schizophrenia.
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2018 |
Anttila V, Bulik-Sullivan B, Finucane HK, Walters RK, Bras J, Duncan L, et al., 'Analysis of shared heritability in common disorders of the brain', Science, 360 (2018) [C1]
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2018 |
Ruderfer DM, Ripke S, McQuillin A, Boocock J, Stahl EA, Pavlides JMW, et al., 'Genomic Dissection of Bipolar Disorder and Schizophrenia, Including 28 Subphenotypes', Cell, 173 1705-1715.e16 (2018) [C1]
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2018 |
Stain H, Halpin S, Baker A, Startup M, Carr V, Schall U, et al., 'The impact of rurality and substance use on young people at ultra-high risk for psychosis', Early Intervention in Psychiatry, 12 1173-1180 (2018) [C1]
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2018 |
Ni G, Moser G, Ripke S, Neale BM, Corvin A, Walters JTR, et al., 'Estimation of Genetic Correlation via Linkage Disequilibrium Score Regression and Genomic Restricted Maximum Likelihood', American Journal of Human Genetics, 102 1185-1194 (2018) [C1]
© 2018 American Society of Human Genetics Genetic correlation is a key population parameter that describes the shared genetic architecture of complex traits and diseases. It can b... [more]
© 2018 American Society of Human Genetics Genetic correlation is a key population parameter that describes the shared genetic architecture of complex traits and diseases. It can be estimated by current state-of-art methods, i.e., linkage disequilibrium score regression (LDSC) and genomic restricted maximum likelihood (GREML). The massively reduced computing burden of LDSC compared to GREML makes it an attractive tool, although the accuracy (i.e., magnitude of standard errors) of LDSC estimates has not been thoroughly studied. In simulation, we show that the accuracy of GREML is generally higher than that of LDSC. When there is genetic heterogeneity between the actual sample and reference data from which LD scores are estimated, the accuracy of LDSC decreases further. In real data analyses estimating the genetic correlation between schizophrenia (SCZ) and body mass index, we show that GREML estimates based on ~150,000 individuals give a higher accuracy than LDSC estimates based on ~400,000 individuals (from combined meta-data). A GREML genomic partitioning analysis reveals that the genetic correlation between SCZ and height is significantly negative for regulatory regions, which whole genome or LDSC approach has less power to detect. We conclude that LDSC estimates should be carefully interpreted as there can be uncertainty about homogeneity among combined meta-datasets. We suggest that any interesting findings from massive LDSC analysis for a large number of complex traits should be followed up, where possible, with more detailed analyses with GREML methods, even if sample sizes are lesser.
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2017 |
Le Hellard S, Wang Y, Witoelar A, Zuber V, Bettella F, Hugdahl K, et al., 'Identification of Gene Loci That Overlap Between Schizophrenia and Educational Attainment', Schizophrenia Bulletin, 43 654-664 (2017) [C1]
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2017 |
Meehan C, Harms L, Frost JD, Barreto R, Todd J, Schall U, et al., 'Effects of immune activation during early or late gestation on schizophrenia-related behaviour in adult rat offspring', Brain, Behavior, and Immunity, 63 8-20 (2017) [C1]
© 2016 Maternal exposure to infectious agents during gestation has been identified as a significant risk factor for schizophrenia. Using a mouse model, past work has demonstrated ... [more]
© 2016 Maternal exposure to infectious agents during gestation has been identified as a significant risk factor for schizophrenia. Using a mouse model, past work has demonstrated that the gestational timing of the immune-activating event can impact the behavioural phenotype and expression of dopaminergic and glutamatergic neurotransmission markers in the offspring. In order to determine the inter-species generality of this effect to rats, another commonly used model species, the current study investigated the impact of a viral mimetic Poly (I:C) at either an early (gestational day 10) or late (gestational day 19) time-point on schizophrenia-related behaviour and neurotransmitter receptor expression in rat offspring. Exposure to Poly (I:C) in late, but not early, gestation resulted in transient impairments in working memory. In addition, male rats exposed to maternal immune activation (MIA) in either early or late gestation exhibited sensorimotor gating deficits. Conversely, neither early nor late MIA exposure altered locomotor responses to MK-801 or amphetamine. In addition, increased dopamine 1 receptor mRNA levels were found in the nucleus accumbens of male rats exposed to early gestational MIA. The findings from this study diverge somewhat from previous findings in mice with MIA exposure, which were often found to exhibit a more comprehensive spectrum of schizophrenia-like phenotypes in both males and females, indicating potential differences in the neurodevelopmental vulnerability to MIA exposure in the rat with regards to schizophrenia related changes.
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2017 |
Atkinson RJ, Fulham WR, Michie PT, Ward PB, Todd J, Stain H, et al., 'Electrophysiological, cognitive and clinical profiles of at-risk mental state: The longitudinal Minds in Transition (MinT) study', PLOS ONE, 12 (2017) [C1]
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2017 |
Conrad AM, Lewin TJ, Sly KA, Schall U, Halpin SA, Hunter M, Carr VJ, 'Utility of risk-status for predicting psychosis and related outcomes: evaluation of a 10-year cohort of presenters to a specialised early psychosis community mental health service', Psychiatry Research, 247 336-344 (2017) [C1]
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2017 |
Rahman T, Zavitsanou K, Purves-Tyson T, Harms LR, Meehan C, Schall U, et al., 'Effects of Immune Activation during Early or Late Gestation on N-Methyl-D-Aspartate Receptor Measures in Adult Rat Offspring', FRONTIERS IN PSYCHIATRY, 8 (2017) [C1]
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2017 |
Klauser P, Baker ST, Cropley VL, Bousman C, Fornito A, Cocchi L, et al., 'White Matter Disruptions in Schizophrenia Are Spatially Widespread and Topologically Converge on Brain Network Hubs', Schizophrenia bulletin, 43 425-435 (2017) [C1]
© The Author 2016. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permiss... [more]
© The Author 2016. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com. White matter abnormalities associated with schizophrenia have been widely reported, although the consistency of findings across studies is moderate. In this study, neuroimaging was used to investigate white matter pathology and its impact on whole-brain white matter connectivity in one of the largest samples of patients with schizophrenia. Fractional anisotropy (FA) and mean diffusivity (MD) were compared between patients with schizophrenia or schizoaffective disorder (n = 326) and age-matched healthy controls (n = 197). Between-group differences in FA and MD were assessed using voxel-based analysis and permutation testing. Automated whole-brain white matter fiber tracking and the network-based statistic were used to characterize the impact of white matter pathology on the connectome and its rich club. Significant reductions in FA associated with schizophrenia were widespread, encompassing more than 40% (234ml) of cerebral white matter by volume and involving all cerebral lobes. Significant increases in MD were also widespread and distributed similarly. The corpus callosum, cingulum, and thalamic radiations exhibited the most extensive pathology according to effect size. More than 50% of cortico-cortical and cortico-subcortical white matter fiber bundles comprising the connectome were disrupted in schizophrenia. Connections between hub regions comprising the rich club were disproportionately affected. Pathology did not differ between patients with schizophrenia and schizoaffective disorder and was not mediated by medication. In conclusion, although connectivity between cerebral hubs is most extensively disturbed in schizophrenia, white matter pathology is widespread, affecting all cerebral lobes and the cerebellum, leading to disruptions in the majority of the brain's fiber bundles.
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2017 |
Marshall CR, Howrigan DP, Merico D, Thiruvahindrapuram B, Wu W, Greer DS, et al., 'Contribution of copy number variants to schizophrenia from a genome-wide study of 41,321 subjects', Nature Genetics, 49 27-35 (2017) [C1]
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2017 |
McLaughlin RL, Schijven D, Van Rheenen W, Van Eijk KR, O'Brien M, Kahn RS, et al., 'Genetic correlation between amyotrophic lateral sclerosis and schizophrenia', Nature Communications, 8 (2017) [C1]
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2016 |
McCabe KL, Marlin S, Cooper G, Morris R, Schall U, Murphy DG, et al., 'Visual perception and processing in children with 22q11.2 deletion syndrome: associations with social cognition measures of face identity and emotion recognition', JOURNAL OF NEURODEVELOPMENTAL DISORDERS, 8 (2016) [C1]
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2016 |
Hess JL, Tylee DS, Barve R, de Jong S, Ophoff RA, Kumarasinghe N, et al., 'Transcriptome-wide mega-analyses reveal joint dysregulation of immunologic genes and transcription regulators in brain and blood in schizophrenia', Schizophrenia Research, 176 114-124 (2016) [C1]
© 2016 The application of microarray technology in schizophrenia research was heralded as paradigm-shifting, as it allowed for high-throughput assessment of cell and tissue functi... [more]
© 2016 The application of microarray technology in schizophrenia research was heralded as paradigm-shifting, as it allowed for high-throughput assessment of cell and tissue function. This technology was widely adopted, initially in studies of postmortem brain tissue, and later in studies of peripheral blood. The collective body of schizophrenia microarray literature contains apparent inconsistencies between studies, with failures to replicate top hits, in part due to small sample sizes, cohort-specific effects, differences in array types, and other confounders. In an attempt to summarize existing studies of schizophrenia cases and non-related comparison subjects, we performed two mega-analyses of a combined set of microarray data from postmortem prefrontal cortices (n = 315) and from ex-vivo blood tissues (n = 578). We adjusted regression models per gene to remove non-significant covariates, providing best-estimates of transcripts dysregulated in schizophrenia. We also examined dysregulation of functionally related gene sets and gene co-expression modules, and assessed enrichment of cell types and genetic risk factors. The identities of the most significantly dysregulated genes were largely distinct for each tissue, but the findings indicated common emergent biological functions (e.g. immunity) and regulatory factors (e.g., predicted targets of transcription factors and miRNA species across tissues). Our network-based analyses converged upon similar patterns of heightened innate immune gene expression in both brain and blood in schizophrenia. We also constructed generalizable machine-learning classifiers using the blood-based microarray data. Our study provides an informative atlas for future pathophysiologic and biomarker studies of schizophrenia.
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2016 |
Hauberg ME, Roussos P, Grove J, Børglum AD, Mattheisen M, 'Analyzing the Role of MicroRNAs in Schizophrenia in the Context of Common Genetic Risk Variants', JAMA Psychiatry, 73 369-369 (2016) [C1]
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2016 |
Franke B, Stein JL, Ripke S, Anttila V, Hibar DP, van Hulzen KJE, et al., 'Genetic influences on schizophrenia and subcortical brain volumes: large-scale proof of concept', Nature Neuroscience, 19 420-431 (2016) [C1]
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2016 |
Stain HJ, Bucci S, Baker AL, Carr V, Emsley R, Halpin S, et al., 'A randomised controlled trial of cognitive behaviour therapy versus non-directive reflective listening for young people at ultra high risk of developing psychosis: The detection and evaluation of psychological therapy (DEPTh) trial', Schizophrenia Research, 176 212-219 (2016) [C1]
© 2016 Elsevier B.V. Background Intervention trials for young people at ultra high risk (UHR) for psychosis have shown cognitive behaviour therapy (CBT) to have promising effects ... [more]
© 2016 Elsevier B.V. Background Intervention trials for young people at ultra high risk (UHR) for psychosis have shown cognitive behaviour therapy (CBT) to have promising effects on treating psychotic symptoms but have not focused on functional outcomes. We hypothesized that compared to an active control, CBT would: (i) reduce the likelihood of, and/or delay, transition to psychosis; (ii) reduce symptom severity while improving social functioning and quality of life, whether or not transition occurred. Method This was a single-blind randomised controlled trial for young people at UHR for psychosis comparing CBT to an active control condition, Non Directive Reflective Listening (NDRL), both in addition to standard care, with a 6 month treatment phase and 12 months of follow-up. Statistical analysis is based on intention-to-treat and used random effect models to estimate treatment effects common to all time-points. Results Fifty-seven young people (mean age = 16.5 years) were randomised to CBT (n = 30) or NDRL (n = 27). Rate of transition to psychosis was 5%; the 3 transitions occurred in the CBT condition (baseline, 2 months, 5 months respectively). The NDRL condition resulted in a significantly greater reduction in distress associated with psychotic symptoms compared to CBT (treatment effect = 36.71, standard error = 16.84, p = 0.029). There were no significant treatment effects on frequency and intensity of psychotic symptoms, global, social or role functioning. Conclusion Our sample was higher functioning, younger and experiencing lower levels of psychotic like experiences than other trials. The significantly better treatment effect of NDRL on distress associated with psychotic symptoms supports the recommendations for a stepped-care model of service delivery. This treatment approach would accommodate the younger UHR population and facilitate timely intervention. Trial registration: ANZCTR 12606000101583
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2016 |
Sekar A, Bialas AR, de Rivera H, Davis A, Hammond TR, Kamitaki N, et al., 'Schizophrenia risk from complex variation of complement component 4', Nature, 530 177-183 (2016) [C1]
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2016 |
Bigdeli TB, Ripke S, Bacanu S-A, Lee SH, Wray NR, Gejman PV, et al., 'Genome-wide association study reveals greater polygenic loading for schizophrenia in cases with a family history of illness', American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 171 276-289 (2016) [C1]
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2016 |
Schall U, 'Is it time to move mismatch negativity into the clinic?', Biological Psychology, 116 41-46 (2016) [C1]
© 2015 Elsevier B.V. Since its inception in the 1970s, the mismatch negativity (MMN) event-related potential has improved our understanding of pre-attentive detection of rule viol... [more]
© 2015 Elsevier B.V. Since its inception in the 1970s, the mismatch negativity (MMN) event-related potential has improved our understanding of pre-attentive detection of rule violations, which is a fundamental cognitive process considered by some a form of "primitive intelligence". The body of research to date ranges from animal studies (i.e. when investigating the neural mechanisms and pharmacological properties of MMN generation) to researching the psychophysiological nature of human consciousness. MMN therefore offers the possibility to detect abnormal functioning in the neural system involved in MMN generation, such as it occurs in some neurodevelopmental disorders or patients in vegetative state. While the clinical research data holds considerable promise for translation into clinical practice, standardization and normative data of an optimized (i.e. disorder-specific) MMN recording algorithm is needed in order for MMN to become a valuable clinical investigation tool.
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2016 |
Srinivasan S, Bettella F, Mattingsdal M, Wang Y, Witoelar A, Schork AJ, et al., 'Genetic Markers of Human Evolution Are Enriched in Schizophrenia', Biological Psychiatry, 80 284-292 (2016) [C1]
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2016 |
Mehta D, Tropf FC, Gratten J, Bakshi A, Zhu Z, Bacanu S-A, et al., 'Evidence for Genetic Overlap Between Schizophrenia and Age at First Birth in Women.', JAMA psychiatry, 73 497-505 (2016) [C1]
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2016 |
Näätänen R, Todd J, Schall U, 'Mismatch negativity (MMN) as biomarker predicting psychosis in clinically at-risk individuals', Biological Psychology, 116 36-40 (2016) [C1]
© 2015 Elsevier B.V. The early detection of young people at-risk of developing a severe mental illness like schizophrenia offers the opportunity of introducing treatment earlier t... [more]
© 2015 Elsevier B.V. The early detection of young people at-risk of developing a severe mental illness like schizophrenia offers the opportunity of introducing treatment earlier than currently possible. There is some evidence that early intervention improves prognosis and functional outcome, or even prevents the full clinical manifestation of the condition in some individuals. A key prerequisite to facilitate early intervention would be a biomarker that can reliably predict a transition to schizophrenia. A smaller event-related mismatch negativity (MMN) potential has emerged as one of the most robust psychophysiological finding in schizophrenia akin of a biomarker of the condition. More recent research further demonstrates that MMN, but also P3a amplitudes, are already reduced in the prodromal phase of illness. Several lines of pre-clinical and clinical research support this notion and are reviewed in this article together with current obstacles, which are still limiting the translation of MMN as a biomarker into clinical practice.
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2015 |
Campbell LE, McCabe KL, Melville JL, Strutt PA, Schall U, 'Social cognition dysfunction in adolescents with 22q11.2 deletion syndrome (velo-cardio-facial syndrome): Relationship with executive functioning and social competence/functioning', Journal of Intellectual Disability Research, 59 845-859 (2015) [C1]
© 2015 John Wiley & Sons, Ltd. Background: Social difficulties are often noted among people with intellectual disabilities. Children and adults with 22q.11.2 deletion syndro... [more]
© 2015 John Wiley & Sons, Ltd. Background: Social difficulties are often noted among people with intellectual disabilities. Children and adults with 22q.11.2 deletion syndrome (22q11DS) often have poorer social competence as well as poorer performance on measures of executive and social-cognitive skills compared with typically developing young people. However, the relationship between social functioning and more basic processes of social cognition and executive functioning are not well understood in 22q11DS. The present study examined the relationship between social-cognitive measures of emotion attribution and theory of mind with executive functioning and their contribution to social competence in 22q11DS. Method: The present cross-sectional study measured social cognition and executive performance of 24 adolescents with 22q11DS compared with 27 age-matched typically developing controls. Social cognition was tested using the emotion attribution task (EAT) and a picture sequencing task (PST), which tested mentalising (false-belief), sequencing, cause and effect, and inhibition. Executive functioning was assessed using computerised versions of the Tower of London task and working memory measures of spatial and non-spatial ability. Social competence was also assessed using the parent-reported Strengths and Difficulties Questionnaire. Results: Adolescents with 22q11DS showed impaired false-belief, emotion attribution and executive functioning compared with typically developing control participants. Poorer performance was reported on all story types in the PST, although, patterns of errors and response times across story types were similar in both groups. General sequencing ability was the strongest predictor of false-belief, and performance on the false-belief task predicted emotion attribution accuracy. Intellectual functioning, rather than theory of mind or executive functioning, predicted social competence in 22q11DS. Conclusions: Performance on social-cognitive tasks of theory of mind indicate evidence of a general underlying dysfunction in 22q11DS that includes executive ability to understand cause and effect, to logically reason about social scenarios and also to inhibit responses to salient, but misleading cues. However, general intellectual ability is closely related to actual social competence suggesting that a generalised intellectual deficit coupled with more specific executive impairments may best explain poor social cognition in 22q11DS.
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2015 |
Weismüller B, Thienel R, Youlden AM, Fulham R, Koch M, Schall U, 'Psychophysiological Correlates of Developmental Changes in Healthy and Autistic Boys', Journal of Autism and Developmental Disorders, 45 2168-2175 (2015) [C1]
© 2015, Springer Science+Business Media New York. This study investigated neurodevelopmental changes in sound processing by recording mismatch negativity (MMN) in response to vari... [more]
© 2015, Springer Science+Business Media New York. This study investigated neurodevelopmental changes in sound processing by recording mismatch negativity (MMN) in response to various degrees of sound complexity in 18 mildly to moderately autistic versus 15 healthy boys aged between 6 and 15¿years. Autistic boys presented with lower IQ and poor performance on a range of executive and social function measures when compared to their healthy counterparts. We found that MMN in response to duration deviants was less lateralized in the clinical group whereas larger amplitudes correlated with advanced age, thus capturing neurodevelopmental changes. Larger MMN in response to speech-like sound deviants was associated with better verbal fluency and executive function performance, respectively, but did not reliably discriminate the two groups.
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2015 |
Cohen M, Johnston P, Ehlkes T, Fulham R, Ward P, Thienel R, et al., 'Functional magnetic resonance brain imaging of executive cognitive performance in young first-episode schizophrenia patients and age-matched long-term cannabis users', Neurology Psychiatry and Brain Research, 21 51-63 (2015) [C1]
© 2014 Elsevier GmbH. All rights reserved. Converging evidence from epidemiological, clinical and neuropsychological research suggests a link between cannabis use and increased ri... [more]
© 2014 Elsevier GmbH. All rights reserved. Converging evidence from epidemiological, clinical and neuropsychological research suggests a link between cannabis use and increased risk of psychosis. Long-term cannabis use has also been related to deficit-like "negative" symptoms and cognitive impairment that resemble some of the clinical and cognitive features of schizophrenia. The current functional brain imaging study investigated the impact of a history of heavy cannabis use on impaired executive function in first-episode schizophrenia patients. Whilst performing the Tower of London task in a magnetic resonance imaging scanner, event-related blood oxygenation level-dependent (BOLD) brain activation was compared between four age and gender-matched groups: 12 first-episode schizophrenia patients; 17 long-term cannabis users; seven cannabis using first-episode schizophrenia patients; and 17 healthy control subjects. BOLD activation was assessed as a function of increasing task difficulty within and between groups as well as the main effects of cannabis use and the diagnosis of schizophrenia. Cannabis users and non-drug using first-episode schizophrenia patients exhibited equivalently reduced dorsolateral prefrontal activation in response to task difficulty. A trend towards additional prefrontal and left superior parietal cortical activation deficits was observed in cannabis-using first-episode schizophrenia patients while a history of cannabis use accounted for increased activation in the visual cortex. Cannabis users and schizophrenia patients fail to adequately activate the dorsolateral prefrontal cortex, thus pointing to a common working memory impairment which is particularly evident in cannabis-using first-episode schizophrenia patients. A history of heavy cannabis use, on the other hand, accounted for increased primary visual processing, suggesting compensatory imagery processing of the task.
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2015 |
Bulik-Sullivan B, Loh PR, Finucane HK, Ripke S, Yang J, Patterson N, et al., 'LD score regression distinguishes confounding from polygenicity in genome-wide association studies', Nature Genetics, 47 291-295 (2015) [C1]
Both polygenicity (many small genetic effects) and confounding biases, such as cryptic relatedness and population stratification, can yield an inflated distribution of test statis... [more]
Both polygenicity (many small genetic effects) and confounding biases, such as cryptic relatedness and population stratification, can yield an inflated distribution of test statistics in genome-wide association studies (GWAS). However, current methods cannot distinguish between inflation from a true polygenic signal and bias. We have developed an approach, LD Score regression, that quantifies the contribution of each by examining the relationship between test statistics and linkage disequilibrium (LD). The LD Score regression intercept can be used to estimate a more powerful and accurate correction factor than genomic control. We find strong evidence that polygenicity accounts for the majority of the inflation in test statistics in many GWAS of large sample size.
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2015 |
Bergon A, Belzeaux R, Comte M, Pelletier F, Hervé M, Gardiner EJ, et al., 'CX3CR1 is dysregulated in blood and brain from schizophrenia patients', Schizophrenia Research, 168 434-443 (2015) [C1]
© 2015 Elsevier B.V. The molecular mechanisms underlying schizophrenia remain largely unknown. Although schizophrenia is a mental disorder, there is increasing evidence to indicat... [more]
© 2015 Elsevier B.V. The molecular mechanisms underlying schizophrenia remain largely unknown. Although schizophrenia is a mental disorder, there is increasing evidence to indicate that inflammatory processes driven by diverse environmental factors play a significant role in its development. With gene expression studies having been conducted across a variety of sample types, e.g., blood and postmortem brain, it is possible to investigate convergent signatures that may reveal interactions between the immune and nervous systems in schizophrenia pathophysiology. We conducted two meta-analyses of schizophrenia microarray gene expression data (N= 474) and non-psychiatric control (N= 485) data from postmortem brain and blood. Then, we assessed whether significantly dysregulated genes in schizophrenia could be shared between blood and brain. To validate our findings, we selected a top gene candidate and analyzed its expression by RT-qPCR in a cohort of schizophrenia subjects stabilized by atypical antipsychotic monotherapy (N= 29) and matched controls (N= 31). Meta-analyses highlighted inflammation as the major biological process associated with schizophrenia and that the chemokine receptor CX3CR1 was significantly down-regulated in schizophrenia. This differential expression was also confirmed in our validation cohort. Given both the recent data demonstrating selective CX3CR1 expression in subsets of neuroimmune cells, as well as behavioral and neuropathological observations of CX3CR1 deficiency in mouse models, our results of reduced CX3CR1 expression adds further support for a role played by monocyte/microglia in the neurodevelopment of schizophrenia.
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2015 |
Andreassen OA, Harbo HF, Wang Y, Thompson WK, Schork AJ, Mattingsdal M, et al., 'Genetic pleiotropy between multiple sclerosis and schizophrenia but not bipolar disorder: differential involvement of immune-related gene loci', Molecular Psychiatry, 20 207-214 (2015) [C1]
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2015 |
Garrison JR, Fernyhough C, McCarthy-Jones S, Haggard M, Carr V, Schall U, et al., 'Paracingulate sulcus morphology is associated with hallucinations in the human brain', Nature Communications, 6 (2015) [C1]
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2015 |
Vilhjálmsson BJ, Yang J, Finucane HK, Gusev A, Lindström S, Ripke S, et al., 'Modeling Linkage Disequilibrium Increases Accuracy of Polygenic Risk Scores', American Journal of Human Genetics, 97 576-592 (2015) [C1]
© 2015 The American Society of Human Genetics. All rights reserved. Polygenic risk scores have shown great promise in predicting complex disease risk and will become more accurate... [more]
© 2015 The American Society of Human Genetics. All rights reserved. Polygenic risk scores have shown great promise in predicting complex disease risk and will become more accurate as training sample sizes increase. The standard approach for calculating risk scores involves linkage disequilibrium (LD)-based marker pruning and applying a p value threshold to association statistics, but this discards information and can reduce predictive accuracy. We introduce LDpred, a method that infers the posterior mean effect size of each marker by using a prior on effect sizes and LD information from an external reference panel. Theory and simulations show that LDpred outperforms the approach of pruning followed by thresholding, particularly at large sample sizes. Accordingly, predicted R2 increased from 20.1% to 25.3% in a large schizophrenia dataset and from 9.8% to 12.0% in a large multiple sclerosis dataset. A similar relative improvement in accuracy was observed for three additional large disease datasets and for non-European schizophrenia samples. The advantage of LDpred over existing methods will grow as sample sizes increase.
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2015 |
Schall U, Müller BW, Kärgel C, Güntürkün O, 'Electrophysiological mismatch response recorded in awake pigeons from the avian functional equivalent of the primary auditory cortex', NeuroReport, (2015) [C1]
The neural response to occasional variations in acoustic stimuli in a regular sequence of sounds generates an N-methyl-D-aspartate receptor-modulated event-related potential in pr... [more]
The neural response to occasional variations in acoustic stimuli in a regular sequence of sounds generates an N-methyl-D-aspartate receptor-modulated event-related potential in primates and rodents in the primary auditory cortex known as mismatch negativity (MMN). The current study investigated MMN in pigeons (Columba livia L) through intracranial recordings from Field L of the caudomedial nidopallium, the avian functional equivalent of the mammalian primary auditory cortex. Auditory evoked field potentials were recorded from awake birds using a low-frequency (800 Hz) and high-frequency (1400 Hz) deviant auditory oddball procedure with deviant-as-standard (flip-flop design) and multiple-standard control conditions. An MMN-like field potential was recorded and blocked with systemic 5 mg/kg ketamine administration. Our results are similar to human and rodent findings of an MMN-like event-related potential in birds suggestive of similar auditory sensory memory mechanisms in birds and mammals that are homologue from a common ancestor 300 million years ago or resulted from convergent evolution.
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2015 |
Finucane HK, Bulik-Sullivan B, Gusev A, Trynka G, Reshef Y, Loh P-R, et al., 'Partitioning heritability by functional annotation using genome-wide association summary statistics', Nature Genetics, 47 1228-1235 (2015) [C1]
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2015 |
Loh P-R, Bhatia G, Gusev A, Finucane HK, Bulik-Sullivan BK, Pollack SJ, et al., 'Contrasting genetic architectures of schizophrenia and other complex diseases using fast variance-components analysis', Nature Genetics, 47 1385-1392 (2015) [C1]
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2015 |
Ingason A, Giegling I, Hartmann AM, Genius J, Konte B, Friedl M, et al., 'Expression analysis in a rat psychosis model identifies novel candidate genes validated in a large case control sample of schizophrenia', Translational Psychiatry, 5 e656-e656 (2015) [C1]
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2014 |
Fulham WR, Michie PT, Ward PB, Rasser PE, Todd J, Johnston PJ, et al., 'Mismatch negativity in recent-onset and chronic schizophrenia: a current source density analysis.', PLoS One, 9 e100221 (2014) [C1]
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2014 |
Gusev A, Lee SH, Trynka G, Finucane H, Vilhjálmsson BJ, Xu H, et al., 'Partitioning Heritability of Regulatory and Cell-Type-Specific Variants across 11 Common Diseases', The American Journal of Human Genetics, 95 535-552 (2014) [C1]
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2014 |
Nicodemus KK, Hargreaves A, Morris D, Anney R, Gill M, Corvin A, Donohoe G, 'Variability in Working Memory Performance Explained by Epistasis vs Polygenic Scores in theZNF804APathway', JAMA Psychiatry, 71 778-778 (2014) [C1]
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2014 |
Harms L, Fulham WR, Todd J, Budd TW, Hunter M, Meehan C, et al., 'Mismatch negativity (MMN) in freely-moving rats with several experimental controls', PLoS ONE, 9 (2014) [C1]
© 2014 Harms et al. Mismatch negativity (MMN) is a scalp-recorded electrical potential that occurs in humans in response to an auditory stimulus that defies previously established... [more]
© 2014 Harms et al. Mismatch negativity (MMN) is a scalp-recorded electrical potential that occurs in humans in response to an auditory stimulus that defies previously established patterns of regularity. MMN amplitude is reduced in people with schizophrenia. In this study, we aimed to develop a robust and replicable rat model of MMN, as a platform for a more thorough understanding of the neurobiology underlying MMN. One of the major concerns for animal models of MMN is whether the rodent brain is capable of producing a human-like MMN, which is not a consequence of neural adaptation to repetitive stimuli. We therefore tested several methods that have been used to control for adaptation and differential exogenous responses to stimuli within the oddball paradigm. Epidural electroencephalographic electrodes were surgically implanted over different cortical locations in adult rats. Encephalographic data were recorded using wireless telemetry while the freely-moving rats were presented with auditory oddball stimuli to assess mismatch responses. Three control sequences were utilized: the flip-flop control was used to control for differential responses to the physical characteristics of standards and deviants; the many standards control was used to control for differential adaptation, as was the cascade control. Both adaptation and adaptation-independent deviance detection were observed for high frequency (pitch), but not low frequency deviants. In addition, the many standards control method was found to be the optimal method for observing both adaptation effects and adaptation-independent mismatch responses in rats. Inconclusive results arose from the cascade control design as it is not yet clear whether rats can encode the complex pattern present in the control sequence. These data contribute to a growing body of evidence supporting the hypothesis that rat brain is indeed capable of exhibiting human-like MMN, and that the rat model is a viable platform for the further investigation of the MMN and its associated neurobiology.
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2014 |
Ripke S, Neale BM, Corvin A, Walters JTR, Farh KH, Holmans PA, et al., 'Biological insights from 108 schizophrenia-associated genetic loci', Nature, 511 421-427 (2014) [C1]
Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wid... [more]
Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain, providing biological plausibility for the findings. Many findings have the potential to provide entirely new insights into aetiology, but associations at DRD2 and several genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that have important roles in immunity, providing support for the speculated link between the immune system and schizophrenia. © 2014 Macmillan Publishers Limited. All rights reserved.
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2014 |
Todd J, Whitson L, Smith E, Michie PT, Schall U, Ward PB, 'What's intact and what's not within the mismatch negativity system in schizophrenia', Psychophysiology, 51 337-347 (2014) [C1]
Repetitive patterning facilitates inferences about likely properties of sound to follow. Mismatch negativity (MMN) occurs when sound fails to match an inference. Smaller MMN in sc... [more]
Repetitive patterning facilitates inferences about likely properties of sound to follow. Mismatch negativity (MMN) occurs when sound fails to match an inference. Smaller MMN in schizophrenia indexes deficient gain control (difference in utilizing a limited dynamic range). Although it is clear that this group has a lower limit to MMN size, this study addressed whether smaller MMN indicates impaired perceptual inference. MMN was elicited to four deviants in two sequences: one in which occurrence was random and one in which it was paired. Despite smaller MMN, persons with schizophrenia are equally able to reduce MMN size evoked by a deviant when its occurrence is cued. Results also expose alterations in the evoked response to repeated sounds that appear to be exacerbations of age-related amplitude decline. Since these anomalies impact the computed MMN, they highlight the need to identify all contributions to limits in gain control in schizophrenia. © 2014 Society for Psychophysiological Research.
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2014 |
Knechtel L, Schall U, Cooper G, Ramadan S, Stanwell P, Jolly T, Thienel R, 'Transcranial direct current stimulation of prefrontal cortex: An auditory event-related potential and proton magnetic resonance spectroscopy study', Neurology Psychiatry and Brain Research, (2014) [C1]
Transcranial direct current stimulation (tDCS) is a non-invasive intervention altering neural plasticity by modulating neuronal excitability of pre- and postsynaptic neuron popula... [more]
Transcranial direct current stimulation (tDCS) is a non-invasive intervention altering neural plasticity by modulating neuronal excitability of pre- and postsynaptic neuron populations, which has been shown to improve depression symptoms and cognition. We investigated the effects of a single session of 20 min of 2 mA left-prefrontal anodal versus sham stimulation on auditory event-related potentials (ERPs) in 11 male and 5 female healthy subjects (mean age of 28.6 [SD 6.2] years) by employing a randomized single-blind crossover design. Stimulation effects on cortical glutamate (Glu) and glutamine (Glx) levels were subsequently measured in 12 of the 16 healthy subjects in a 3 T proton magnetic resonance spectroscopy scan. tDCS was associated with a significant increase of N1 amplitudes while smaller P3b amplitudes correlated with higher cortical Glu and Glx levels in the stimulated brain area when performing an auditory go/no-go discrimination task. tDCS did not change mismatch negativity, nor task performance or cortical Glu/Glx levels which, together with N1 amplitudes, depended on stimulation order ("sham" versus "active"). Increased N1 amplitudes are consistent with higher levels of cortical excitability following prefrontal anodal tDCS. The failure to replicate Glu/Glx changes with tDCS may have been masked by between-session carry-over effects while ceiling effects may have masked tDCS effects on task performance. © 2014 Elsevier GmbH. All rights reserved.
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2014 |
Kumarasinghe N, Rasser PE, Mendis J, Bergmann J, Knechtel L, Oxley S, et al., 'Age effects on cerebral grey matter and their associations with psychopathology, cognition and treatment response in previously untreated schizophrenia patients', Neurology Psychiatry and Brain Research, 20 29-36 (2014) [C1]
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2014 |
Conrad AM, Lewin TJ, Sly KA, Schall U, Halpin SA, Hunter M, Carr VJ, 'Ten-year audit of clients presenting to a specialised service for young people experiencing or at increased risk for psychosis', BMC PSYCHIATRY, 14 (2014) [C1]
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2014 |
McCabe KL, Atkinson RJ, Cooper G, Melville JL, Harris J, Schall U, et al., 'Pre-pulse inhibition and antisaccade performance indicate impaired attention modulation of cognitive inhibition in 22q11.2 deletion syndrome (22q11DS)', Journal of Neurodevelopmental Disorders, 6 (2014) [C1]
© 2014 McCabe et al.; licensee BioMed Central Ltd. Background: 22q11.2 deletion syndrome (22q11DS) is associated with a number of physical anomalies and neuropsychological deficit... [more]
© 2014 McCabe et al.; licensee BioMed Central Ltd. Background: 22q11.2 deletion syndrome (22q11DS) is associated with a number of physical anomalies and neuropsychological deficits including impairments in executive and sensorimotor function. It is estimated that 25% of children with 22q11DS will develop schizophrenia and other psychotic disorders later in life. Evidence of genetic transmission of information processing deficits in schizophrenia suggests performance in 22q11DS individuals will enhance understanding of the neurobiological and genetic substrates associated with information processing. In this report, we examine information processing in 22q11DS using measures of startle eyeblink modification and antisaccade inhibition to explore similarities with schizophrenia and associations with neurocognitive performance. Methods: Startle modification (passive and active tasks; 120- and 480-ms pre-pulse intervals) and antisaccade inhibition were measured in 25 individuals with genetically confirmed 22q11DS and 30 healthy control subjects. Results: Individuals with 22q1 1DS exhibited increased antisaccade error as well as some evidence (trend-level effect) of impaired sensorimotor gating during the active condition, suggesting a dysfunction in controlled attentional processing, rather than a pre-attentive dysfunction using this paradigm. Conclusions: The findings from the present study show similarities with previous studies in clinical populations associated with 22q11DS such as schizophrenia that may indicate shared dysfunction of inhibition pathways in these groups.
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2014 |
Knechtel L, Thienel R, Cooper G, Case V, Schall U, 'Transcranial direct current stimulation of prefrontal cortex: An auditory event-related potential study in schizophrenia', Neurology Psychiatry and Brain Research, 20 102-106 (2014) [C1]
© 2014 Elsevier GmbH. All rights reserved. Cognitive impairment is one of the most significant factors determining the long-term rehabilitation prospects of schizophrenia patients... [more]
© 2014 Elsevier GmbH. All rights reserved. Cognitive impairment is one of the most significant factors determining the long-term rehabilitation prospects of schizophrenia patients. Cognitive training has been shown to be beneficial; however, effect sizes of cognitive remediation remain relatively low. Anodal transcranial direct current stimulation (tDCS) increases cortical excitability along with larger N1 auditory event-related potentials (ERPs), thus providing a non-invasive physiological mechanism that is potentially capable of facilitating cognitive training of schizophrenia patients. The current study investigated the effects of left-prefrontal anodal tDCS on auditory discrimination performance and N1, Mismatch Negativity (MMN), and P3b ERPs, which have been linked to cognitive and global function deficits in schizophrenia. We compared 20 min of 2 mA tDCS versus sham stimulation in 14 schizophrenia patients by employing a randomised crossover design. Patients performed equally well in a go/no-go auditory discrimination task when compared to healthy subjects but presented with significantly smaller N1, MMN and P3b amplitudes, which did not change with tDCS. Auditory discrimination performance and reaction times also remained unaffected by tDCS. Our findings suggest that a single application of tDCS has no acute effects on ERPs and associated auditory information processing in schizophrenia patients.
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2013 |
Todd J, Harms L, Schall U, Michie PT, 'Mismatch negativity: Translating the potential', Frontiers in Psychiatry, 4 1-22 (2013) [C1]
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2013 |
Terwisscha van Scheltinga AF, Bakker SC, van Haren NEM, Derks EM, Buizer-Voskamp JE, Boos HBM, et al., 'Genetic Schizophrenia Risk Variants Jointly Modulate Total Brain and White Matter Volume', Biological Psychiatry, 73 525-531 (2013) [C1]
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2013 |
Budd TW, Nakamura T, Fulham WR, Todd J, Schall U, Hunter M, et al., 'Repetition suppression of the rat auditory evoked potential at brief stimulus intervals', BRAIN RESEARCH, 1498 59-68 (2013) [C1]
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2013 |
Sharip S, Michie P, Schall U, Drysdale K, Case V, Sankaranarayanan A, et al., 'Generalization of cognitive training in an Australian sample of schizophrenia patients', Comprehensive Psychiatry, 54 865-872 (2013) [C1]
Objective The present study was undertaken to evaluate the effect of cognitive training in improving trained and untrained cognitive processes in schizophrenia. Methods A simple p... [more]
Objective The present study was undertaken to evaluate the effect of cognitive training in improving trained and untrained cognitive processes in schizophrenia. Methods A simple pre- and post experimental study with a three month follow-up was conducted to determine the efficacy of cognitive training in speed of processing and executive functions improving cognition in 22 schizophrenia patients. Results Significant improvement was found in those cognitive domains specifically targeted in the training protocol, but also to a limited extent on verbal memory and social cognition. There was also evidence of improvements in symptoms and social functioning. The training effects failed to transfer to community functioning skills however. Except for social cognition, these improvements were maintained at 3 month follow-up. Conclusion The study highlights the importance of understanding the mechanisms that contribute to the transfer of skills as well as the maintenance of cognitive changes in individuals with schizophrenia. © 2013 Elsevier Inc. All rights reserved.
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2013 |
Ripke S, O'Dushlaine C, Chambert K, Moran JL, Kähler AK, Akterin S, et al., 'Genome-wide association analysis identifies 13 new risk loci for schizophrenia', Nature Genetics, 45 1150-1159 (2013)
Schizophrenia is an idiopathic mental disorder with a heritable component and a substantial public health impact. We conducted a multi-stage genome-wide association study (GWAS) f... [more]
Schizophrenia is an idiopathic mental disorder with a heritable component and a substantial public health impact. We conducted a multi-stage genome-wide association study (GWAS) for schizophrenia beginning with a Swedish national sample (5,001 cases and 6,243 controls) followed by meta-Analysis with previous schizophrenia GWAS (8,832 cases and 12,067 controls) and finally by replication of SNPs in 168 genomic regions in independent samples (7,413 cases, 19,762 controls and 581 parent-offspring trios). We identified 22 loci associated at genome-wide significance; 13 of these are new, and 1 was previously implicated in bipolar disorder. Examination of candidate genes at these loci suggests the involvement of neuronal calcium signaling. We estimate that 8,300 independent, mostly common SNPs (95% credible interval of 6,300-10,200 SNPs) contribute to risk for schizophrenia and that these collectively account for at least 32% of the variance in liability. Common genetic variation has an important role in the etiology of schizophrenia, and larger studies will allow more detailed understanding of this disorder. © 2013 Nature America, Inc. All rights reserved.
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2013 |
Van Scheltinga AFT, Bakker SC, Van Haren NEM, Derks EM, Buizer-Voskamp JE, Cahn W, et al., 'Schizophrenia genetic variants are not associated with intelligence', Psychological Medicine, 43 2563-2570 (2013) [C1]
Background Schizophrenia is associated with lower pre-morbid intelligence (IQ) in addition to (pre-morbid) cognitive decline. Both schizophrenia and IQ are highly heritable traits... [more]
Background Schizophrenia is associated with lower pre-morbid intelligence (IQ) in addition to (pre-morbid) cognitive decline. Both schizophrenia and IQ are highly heritable traits. Therefore, we hypothesized that genetic variants associated with schizophrenia, including copy number variants (CNVs) and a polygenic schizophrenia (risk) score (PSS), may influence intelligence. Method IQ was estimated with the Wechsler Adult Intelligence Scale (WAIS). CNVs were determined from single nucleotide polymorphism (SNP) data using the QuantiSNP and PennCNV algorithms. For the PSS, odds ratios for genome-wide SNP data were calculated in a sample collected by the Psychiatric Genome-Wide Association Study (GWAS) Consortium (8690 schizophrenia patients and 11 831 controls). These were used to calculate individual PSSs in our independent sample of 350 schizophrenia patients and 322 healthy controls. Results Although significantly more genes were disrupted by deletions in schizophrenia patients compared to controls (p = 0.009), there was no effect of CNV measures on IQ. The PSS was associated with disease status (R 2 = 0.055, p = 2.1 × 10 -7) and with IQ in the entire sample (R 2 = 0.018, p = 0.0008) but the effect on IQ disappeared after correction for disease status. Conclusions Our data suggest that rare and common schizophrenia-associated variants do not explain the variation in IQ in healthy subjects or in schizophrenia patients. Thus, reductions in IQ in schizophrenia patients may be secondary to other processes related to schizophrenia risk. © Cambridge University Press 2013.
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2013 |
McCabe KL, Melville JL, Rich D, Strutt PA, Cooper G, Loughland CM, et al., 'Divergent Patterns of Social Cognition Performance in Autism and 22q11.2 Deletion Syndrome (22q11DS)', JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS, 43 1926-1934 (2013) [C1]
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2013 |
Sinderberry B, Brown SD, Hammond P, Stevens AF, Schall UA, Murphy DGM, et al., 'Subtypes in 22q11.2 deletion syndrome associated with behaviour and neurofacial morphology', Research in Developmental Disabilities, 34 116-125 (2013) [C1]
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2013 |
Kumarasinghe N, Beveridge NJ, Gardiner E, Scott RJ, Yasawardene S, Perera A, et al., 'Gene expression profiling in treatment-naive schizophrenia patients identifies abnormalities in biological pathways involving AKT1 that are corrected by antipsychotic medication', INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY, 16 1483-1503 (2013) [C1]
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2013 |
Schork AJ, Thompson WK, Pham P, Torkamani A, Roddey JC, Sullivan PF, et al., 'All SNPs Are Not Created Equal: Genome-Wide Association Studies Reveal a Consistent Pattern of Enrichment among Functionally Annotated SNPs', PLOS GENETICS, 9 (2013) [C1]
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2013 |
Knechtel L, Thienel R, Schall U, 'Transcranial direct current stimulation: neurophysiology and clinical applications', NEUROPSYCHIATRY, 3 89-96 (2013) [C1]
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2012 |
Kumarasinghe KMN, Tooney PA, Schall UA, 'Finding the needle in the haystack: A review of microarray gene expression research into schizophrenia', Australian and New Zealand Journal of Psychiatry, 46 598-610 (2012) [C1]
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2012 |
Atkinson RJ, Michie PT, Schall UA, 'Duration mismatch negativity and P3a in first-episode psychosis and individuals at ultra-high risk of psychosis', Biological Psychiatry, 71 98-104 (2012) [C1]
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2012 |
Todd J, Michie PT, Schall UA, Ward PB, Catts SV, 'Mismatch negativity (MMN) reduction in schizophrenia-Impaired prediction-error generation, estimation or salience?', International Journal of Psychophysiology, 83 222-231 (2012) [C1]
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2012 |
Cohen M, Rasser PE, Peck G, Carr VJ, Ward PB, Thompson PM, et al., 'Cerebellar grey-matter deficits, cannabis use and first-episode schizophrenia in adolescents and young adults', International Journal of Neuropsychopharmacology, 15 297-307 (2012) [C1]
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2012 |
Levinson DF, Shi J, Wang K, Oh S, Riley B, Pulver AE, et al., 'Genome-wide association study of multiplex schizophrenia pedigrees', American Journal of Psychiatry, 169 963-973 (2012)
Objective: The authors used a genome-wide association study (GWAS) of multiply affected families to investigate the association of schizophrenia to common single-nucleotide polymo... [more]
Objective: The authors used a genome-wide association study (GWAS) of multiply affected families to investigate the association of schizophrenia to common single-nucleotide polymorphisms (SNPs) and rare copy number variants (CNVs). Method: The family sample included 2,461 individuals from 631 pedigrees (581 in the primary European-ancestry analyses). Association was tested for single SNPs and genetic pathways. Polygenic scores based on family study results were used to predict case-control status in the Schizophrenia Psychiatric GWAS Consortium (PGC) data set, and consistency of direction of effect with the family study was determined for top SNPs in the PGC GWAS analysis. Withinfamily segregation was examined for schizophrenia-associated rare CNVs. Results: No genome-wide significant associations were observed for single SNPs or for pathways. PGC case and control subjects had significantly different genome-wide polygenic scores (computed by weighting their genotypes by log-odds ratios from the family study) (best p=10<sup>-17</sup>, explaining 0.4% of the variance). Family study and PGC analyses had consistent directions for 37 of the 58 independent best PGC SNPs (p=0.024). The overall frequency of CNVs in regions with reported associations with schizophrenia (chromosomes 1q21.1, 15q13.3, 16p11.2, and 22q11.2 and the neurexin-1 gene [NRXN1]) was similar to previous case-control studies. NRXN1 deletions and 16p11.2 duplications (both of which were transmitted from parents) and 22q11.2 deletions (de novo in four cases) did not segregate with schizophrenia in families. Conclusions: Many common SNPs are likely to contribute to schizophrenia risk, with substantial overlap in genetic risk factors between multiply affected families and cases in large case-control studies. Our findings are consistent with a role for specific CNVs in disease pathogenesis, but the partial segregation of some CNVs with schizophrenia suggests that researchers should exercise caution in using them for predictive genetic testing until their effects in diverse populations have been fully studied.
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2012 |
Ehlkes T, Michie PT, Schall UA, 'Brain imaging correlates of emerging schizophrenia', Neuropsychiatry, 2 147-154 (2012) [C1]
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2011 |
Nakamura T, Michie PT, Fulham WR, Todd J, Budd TW, Schall UA, et al., 'Epidural auditory event-related potentials in the rat to frequency and duration deviants: evidence of mismatch negativity?', Frontiers in Psychology, 2 367 (2011) [C1]
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2011 |
Todd J, Finch B, Smith E, Budd TW, Schall UA, 'Temporal processing ability is related to ear-asymmetry for detecting time cues in sound: A mismatch negativity (MMN) study', Neuropsychologia, 49 69-82 (2011) [C1]
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2011 |
McCabe KL, Rich D, Loughland CM, Schall UA, Campbell LE, 'Visual scanpath abnormalities in 22q11.2 deletion syndrome: Is this a face specific deficit?', Psychiatry Research, 189 292-298 (2011) [C1]
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2011 |
Case VS, Soyland A, Tooney PA, Thompson PM, Rasser PE, Schall UA, et al., 'Gray matter deficits, mismatch negativity, and outcomes in schizophrenia', Schizophrenia Bulletin, 37 131-140 (2011) [C1]
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2011 |
Gwas Consortium, Henskens FA, Loughland CM, Michie PT, Schall UA, Scott R, 'Genome-wide association study identifies five new schizophrenia loci', Nature Genetics, 43 969-U77 (2011) [C1]
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2010 |
Stain HJ, Clark SC, O'Donnell M, Schall UA, 'Young rural people at risk for schizophrenia: Time for mental health services to translate research evidence into best practice of care', Australian and New Zealand Journal of Psychiatry, 44 872-882 (2010) [C1]
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2010 |
Loughland CM, Draganic D, McCabe KL, Richards JM, Nasir MA, Allen J, et al., 'Australian Schizophrenia Research Bank: A database of comprehensive clinical, endophenotypic and genetic data for aetiological studies of schizophrenia', Australian and New Zealand Journal of Psychiatry, 44 1029-1035 (2010) [C1]
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2010 |
Campbell LE, McCabe KL, Leadbeater KE, Schall UA, Loughland CM, Rich D, 'Visual scanning of faces in 22q11.2 deletion syndrome: Attention to the mouth or the eyes?', Psychiatry Research, 177 211-215 (2010) [C1]
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2010 |
Kadota Y, Cooper GJ, Burton AR, Lemon J, Schall UA, Lloyd A, Vollmer-Conna U, 'Autonomic hyper-vigilance in post-infective fatigue syndrome', Biological Psychology, 85 97-103 (2010) [C1]
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2010 |
Rasser PE, Schall UA, Peck G, Cohen M, Johnston P, Khoo K, et al., 'Cerebellar grey matter deficits in first-episode schizophrenia mapped using cortical pattern matching', NeuroImage, 53 1175-1180 (2010) [C1]
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2009 |
Schall UA, 'Consciousness and hallucinations in schizophrenia: Secondary aspects of generalized neuropil pathology?', Australian and New Zealand Journal of Psychiatry, 43 393-394 (2009) [C3]
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2009 |
Thienel RA, Kellermann T, Schall UA, Voss B, Reske M, Halfter S, et al., 'Muscarinic antagonist effects on executive control of attention', International Journal of Neuropsychopharmacology, 12 1307-1317 (2009) [C1]
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2009 |
Thienel RA, Voss B, Kellermann T, Reske M, Halfter S, Sheldrick AJ, et al., 'Nicotinic antagonist effects on functional attention networks', International Journal of Neuropsychopharmacology, 12 1295-1305 (2009) [C1]
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2009 |
Hanlon M-C, Karayanidis F, Schall UA, 'Intact sensorimotor gating in adult attention deficit hyperactivity disorder', International Journal of Neuropsychopharmacology, 12 701-707 (2009) [C1]
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2008 |
Michie PT, Budd TW, Fulham WR, Hughes ME, Jamadar S, Johnston P, et al., 'The potential for new understandings of normal and abnormal cognition by integration of neuroimaging and behavioral data: Not an exercise in carrying coals to Newcastle', Brain Imaging and Behavior, 2 1-9 (2008) [C1]
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2008 |
Schall UA, 'Dual constraints on synapse formation and regression in schizophrenia: More evidence required', Australian and New Zealand Journal of Psychiatry, 42 1071-1072 (2008) [C3]
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2008 |
Todd J, Michie PT, Schall UA, Karayanidis F, Yabe H, Naatanen R, 'Deviant matters: Duration, frequency, and intensity deviants reveal different patterns of mismatch negativity reduction in early and late schizophrenia', Biological Psychiatry, 63 58-64 (2008) [C1]
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2007 |
Campbell LE, Hughes ME, Budd TW, Cooper GJ, Fulham WR, Karayanidis F, et al., 'Primary and secondary neural networks of auditory prepulse inhibition: a functional magnetic resonance imaging study of sensorimotor gating of the human acoustic startle response', European Journal of Neuroscience, 26 2327-2333 (2007) [C1]
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2006 |
Silverstein S, Uhlhaas PJ, Essex B, Halpin SA, Schall UA, Carr VJ, 'Perceptual organization in first episode schizophrenia and ultra-high-risk states', Schizophrenia Research, 83 41-52 (2006) [C1]
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2006 |
Bowden NA, Weidenhofer JC, Scott R, Schall U, Todd J, Michie PT, Tooney PA, 'Preliminary investigation of gene expression profiles in peripheral blood lymphocytes in schizophrenia', Schizophrenia Research, 82 175-183 (2006) [C1]
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2006 |
Karayanidis F, Nicholson RA, Schall UA, Meem LC, Fulham WR, Michie PT, 'Switching between univalent task-sets in schizophrenia: ERP evidence of an anticipatory task-set reconfiguration deficit', Clinical Neurophysiology, 117 2172-2190 (2006) [C1]
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2006 |
Bender S, Dittmann-Balcar A, Schall UA, Wolstein J, Klimke A, Riedel M, et al., 'Influence of atypical neuroleptics on executive funtioning inpatients with schizophrenia: a randomized, double-blind comparison of Olanzapine vs. clozapine', International Journal of Neuropsychopharmacology, 9 135-145 (2006) [C1]
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2006 |
Schall UA, Dittmann-Balcar A, Bender S, 'Does atypical antipsychotic medication improve executive function in schizophrenia?', International Journal of Neuropsychopharmacology, 9 631-632 (2006) [C3] |
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2006 |
Cohen M, Carr V, Ward PB, Ehlkes T, Johnston P, Thienel R, Schall U, '01-03 fMRI in schizophrenia and cannabis users.', Acta Neuropsychiatr, 18 314 (2006)
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2006 |
Fulham R, Michie P, Ward P, Hughes M, Schall U, 'Multimodal imaging of the mismatch negativity deficit in schizophrenia.', Acta Neuropsychiatr, 18 250-251 (2006)
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2005 |
Johnston PJ, Stojanov WM, Devir H, Schall UA, 'Functional MRI of facial emotion recognition deficits in schizophrenia and their electrophysiological correlates', European Journal of Neuroscience, 22 1221-1232 (2005) [C1]
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2005 |
Rasser PE, Johnston PJ, Lagopoulos J, Ward PB, Schall UA, Thienel R, et al., 'Functional MRI BOLD response to Tower of London performance of first-episode schizophrenia patients using cortical pattern matching', Neuroimage, 26 941-951 (2005) [C1]
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2005 |
Bullock GL, Schall UA, 'Dyssomnia in children diagnosed with attention deficit hyperactivity disorder: a critical review', Australian and New Zealand Journal of Psychiatry, 39 373-377 (2005) [C1]
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2004 |
Startup MJ, Mason O, Halpin S, Schall UA, Conrad A, Carr VJ, 'State and trait predictors of transition to first episode psychosis among individuals at ultra-high risk', Schizophrenia Research, 70 44 (2004) [C3]
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2004 |
Mason O, Startup MJ, Halpin SA, Schall UA, Conrad A, Carr VJ, 'Risk factors for transition to first episode psychosis among individuals with 'at-risk mental states'', Schizophrenia Research, 71 227-237 (2004) [C1]
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2004 |
Budd TW, Case V, Cooper G, Michie PT, Schall UA, 'A psychoacoustic and fMRI investigation of auditory temporal processing in schizophrenia', NeuroImage, 22 S39 (2004) [C3]
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2004 |
Bender S, Linka T, Wolstein J, Gehendges S, Paulus H-J, Schall UA, Gastper M, 'Safety and efficacy of combined clozapine-lithium pharmacotherap', International Journal of Neuropsychopharmacology, 7 59-63 (2004) [C1]
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2003 |
Johnston PJ, McCabe KL, Schall UA, 'Differential susceptibility to performance degradation across categories of facial emotion - a model confirmation', Biological Psychology, 45-58 (2003) [C1]
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2003 |
Schall UA, Johnston PJ, Lagopoulos J, Juptner M, Jentzen W, Thienel R, et al., 'Functional brain maps of Tower of London performance: a positron emission tomography and functional magnetic resonance imaging study', NeuroImage, 1154-1161 (2003) [C1]
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2003 |
Schall UA, Johnston PJ, Todd J, Ward P, Michie PT, 'Functional neuroanatomy of auditory mismatch processing: an event-related fMRI study of duration-deviant oddballs', NeuroImage, 729-736 (2003) [C1]
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2002 |
Bender S, Dittmann-Balcar A, Schall U, Klimke A, Riedel M, Vorbach U, et al., 'Effects of olanzapine versus clozapine on executive functions in schizophrenia', SCHIZOPHRENIA RESEARCH, 53 194-194 (2002)
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2002 |
Muller B, Achenbach C, Oades R, Bender S, Schall UA, 'Modulation of mismatch negativity by stimulus deviance and modality of attention', NeuroReport, 13 1317-1320 (2002) [C3]
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2002 |
Schall U, 'Psychiatric drugs explained, 3rd edn', DRUG AND ALCOHOL REVIEW, 21 408-409 (2002) |
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2002 |
Schall UA, 'Psychotropic Drugs, 3rd Edn', Drug and Alcohol Review, 21(4) 409 (2002) [C3] |
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2001 |
Ward PB, Schall U, Lagopoulos J, Bender S, Little C, 'Functional brain imaging of increasing task difficulty, in the Tower of London, in patients with schizophrenia and healthy volunteers', INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY, 41 223-223 (2001) |
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2001 |
Oades RD, Schall U, Bender S, Wolstein J, 'Automatic and controlled attentional processes in schizophrenia: Topographic event-related potentials', JOURNAL OF PSYCHOPHYSIOLOGY, 15 56-56 (2001) |
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2001 |
Muller BW, Achenbach C, Oades RD, Schall U, 'Retest stability of mismatch negativity (MMN) and negative difference (Nd) in a four condition novelty oddball task', JOURNAL OF PSYCHOPHYSIOLOGY, 15 140-140 (2001) |
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2001 |
Muller BW, Grzella I, Oades RD, Bender S, Wolstein J, Schall U, et al., 'Novelty-elicited mismatch negativity (MMN) on admission and discharge in schizophrenia: MMN decreases with treatment', JOURNAL OF PSYCHOPHYSIOLOGY, 15 140-140 (2001) |
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2001 |
Dittmann-Balcar A, Juptner M, Jentzen W, Schall UA, 'Dorsolateral prefrontal cortex activation during automatic auditory duration-mismatch processing in humans: a positron emission tomography study', Neuroscience Letters, 308 119-122 (2001) [C1]
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2001 |
Dittmann-Balcar A, Juptner M, Muller S, Schall UA, 'Functional neuroimaging of automatic and active auditory discrimination processing', SCHIZOPHRENIA RESEARCH, 49 176-176 (2001) |
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2001 |
Ward PB, Schall UA, Juptner M, Muller S, Lagopoulos J, Bender S, Little CL, 'Functional neuroimaging of increasing task difficulty in the Tower of London: A comparison of bold fMRI and rCBF PET data', SCHIZOPHRENIA RESEARCH, 49 188-189 (2001) |
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2001 |
Thienel R, Bender S, Oades RD, Dittmann-Balcar A, Rao M, Schall UA, 'Auditory gating, neuropsychology and D2-receptor occupancy in an one-year follow-up treatment study on schizophrenia', SCHIZOPHRENIA RESEARCH, 49 210-210 (2001)
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2001 |
Ward PB, Schall U, Lagopoulos J, Bender S, Little C, 'Functional brain imaging of increasing task difficulty in the Tower of London in patients with schizophrenia and healthy volunteers: An fMRI study', NEUROIMAGE, 13 S1114-S1114 (2001)
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2001 |
Grzella I, Muller B, Oades R, Bender S, Schall UA, Zerbin D, et al., 'Novelty-elicited mismatch negativity in patients with schizophrenia on admission and discharge', Journal of Psychiatry & Neuroscience, 26(3) 235-246 (2001) [C1]
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2000 |
Von Fersen L, Schall UA, Gunturkun O, 'Visual lateralization of pattern discrimination in the bottlenose dolphin (Tursiops truncatus)', Behavioural Brain Reserch, 107 177-181 (2000) [C1]
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2000 |
Ward PB, Schall U, Juptner M, Jentzen W, Muller S, Boden N, et al., 'fMRI and pet activation during performance of the 'Tower of London' task', SCHIZOPHRENIA RESEARCH, 41 132-132 (2000)
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2000 |
Schall U, Bender S, Oades RD, ''Prepulse-induced non-target positivity' (PINTP): A new ERP measure of selective attention deficits in schizophrenia', SCHIZOPHRENIA RESEARCH, 41 149-149 (2000)
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2000 |
Thienel R, Butorac M, Schall U, Bender S, Wolstein J, Dittmann-Balcar A, Oades RD, 'Tower of London performance in first to third episode patients with schizophrenia: A follow up study on executive function', SCHIZOPHRENIA RESEARCH, 41 284-284 (2000)
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2000 |
Muller BW, Achenbach C, Oades RD, Schall UC, 'Retest stability of attentional modulation in duration- and novelty-elicited mismatch negativity', EUROPEAN JOURNAL OF NEUROSCIENCE, 12 167-167 (2000)
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1999 |
Kroner S, Schall UA, Ward PB, Sticht G, Banger M, Haffner T, Catts SV, 'Effects of prepulses and d-amphetamine on performance and event-related potential measures on an auditory discrimination task', Psychopharmacology, 145 123-132 (1999) [C1]
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1999 |
Schall UA, Keysers C, Kast B, 'Pharmacology of sensory gating in the ascending auditory system of the pigeon (Columba livia)', Psychopharmacology, 145 273-282 (1999) [C1]
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1999 |
Muller BW, Grzella I, Oades RD, Bender S, Wolstein J, Schall U, et al., 'Novelty-elicited mismatch negativity (MMN) on admission and discharge in schizophrenia', PSYCHOPHYSIOLOGY, 36 S83-S83 (1999) |
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1999 |
Muller BW, Oades RD, Schall U, 'Duration - But not novelty-elicited mismatch negativity increases with attention: A test/restest study', PSYCHOPHYSIOLOGY, 36 S83-S83 (1999) |
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1999 |
Dittmann-Balcar A, Thienel R, Schall UA, 'Attention-dependent allocation of auditory processing resources as measured by mismatch negativity', Neurophysiology, 10 1-5 (1999) [C1] |
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1999 |
Bender S, Schall U, Wolstein J, Grzella I, Zerbin D, Oades RD, 'A topographic event-related potential follow-up study on 'prepulse inhibition' in first and second episode patients with schizophrenia', PSYCHIATRY RESEARCH-NEUROIMAGING, 90 41-53 (1999)
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1999 |
Dittmann-Balcar A, Thienel R, Schall U, 'Attention-dependent allocation of auditory processing resources as measured by mismatch negativity', NEUROREPORT, 10 3749-3753 (1999)
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1999 |
Schall U, Catts S, Karayanidis F, Ward P, 'Auditory event-related potential indices of frontotemporal information processing in schizophrenia syndromes: Valid outcome prediction of clozapine therapy in a three years follow-up', International Journal of Neuropsychopharmocology, 2 83-93 (1999) [C1]
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1998 |
Schall U, Bender S, Wolstein J, Grzella I, Butorac M, Muller B, et al., 'Prepulse inhibition of ERPs in an auditory discrimination: Effects of neuroleptic treatment in schizophrenia', JOURNAL OF PSYCHOPHYSIOLOGY, 12 320-320 (1998) |
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1998 |
Bender S, Schall U, Oades RD, Olbrich HM, Falkai P, Hornstein C, Schone W, 'Schizophrenic sub-syndromes remain stable while pharmacological treatment improves symptoms', SCHIZOPHRENIA RESEARCH, 29 31-31 (1998)
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1998 |
Wolstein J, Schall U, Bender S, Butorac M, Muller B, Hagen S, et al., 'Abnormal lateralization of certain event-related potential (ERP) indices is present after but not during an acute exacerbation of schizophrenia', SCHIZOPHRENIA RESEARCH, 29 74-74 (1998)
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1998 |
Kroner S, Schall U, Catts SV, Ward PB, 'Prepulse inhibition (PPI) of event-related potentials (ERPs) in an auditory discrimination is impaired in normal subjects after amphetamine: Support for a model of schizophrenia', SCHIZOPHRENIA RESEARCH, 29 120-121 (1998)
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1998 |
Schall U, Bender S, Wolstein J, Grzella I, Martens R, Zerbin D, Oades RD, 'Prepulse inhibition (PPI) of event-related potentials (ERPs) in an auditory discrimination in schizophrenic patients on admission and at discharge', SCHIZOPHRENIA RESEARCH, 29 122-122 (1998)
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1998 |
Schall U, Catts S, Chaturvedi S, Liebert B, Redenbach J, Karayanidis F, Ward P, 'The effect of clozapine therapy on frontal lobe dysfunction in schizophrenia: Neuropsychological and event-related potential measures', International Journal Of Neuropsychopharmacology, 1 19-29 (1998) [C1]
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1997 |
Schall U, Schon A, Zerbin D, Bender S, Eggers C, Oades RD, 'A left temporal lobe impairment of auditory information processing in schizophrenia: An event-related potential study', NEUROSCIENCE LETTERS, 229 25-28 (1997)
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1996 |
Schall U, Schon A, Zerbin D, Eggers C, Oades RD, 'Event-related potentials during an auditory discrimination with prepulse inhibition in patients with schizophrenia, obsessive-compulsive disorder and healthy subjects', INTERNATIONAL JOURNAL OF NEUROSCIENCE, 84 15-33 (1996)
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1996 |
Schall U, Katta T, Pries E, Kloppel A, Gastpar M, 'Pain perception of intravenous heroin users on maintenance therapy with levomethadone', PHARMACOPSYCHIATRY, 29 176-179 (1996)
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1996 |
Bender S, Wolstein J, Butorac M, Grzella I, Ortmann K, Zerbin D, et al., 'Therapy monitoring with prepulse inhibition in an active auditory discrimination in patients with schizophrenia', SCHIZOPHRENIA RESEARCH, 18 XIII4-XIII4 (1996) |
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1996 |
Keysers C, Kast B, Schall U, 'Pharmacology of sensory gating in the ascending auditory system of the pigeon (Columba livia)', SCHIZOPHRENIA RESEARCH, 18 XII13-XII13 (1996) |
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1996 |
Schall U, Ward PB, ''Prepulse inhibition' facilitates a liberal response bias in an auditory discrimination task', NEUROREPORT, 7 652-656 (1996)
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1996 |
Schall U, Pries E, Katta T, Kloppel A, Gastpar M, 'Pharmacokinetic and pharmacodynamic interactions in an outpatient maintenance therapy of intravenous heroin users with levomethadone', ADDICTION BIOLOGY, 1 105-113 (1996)
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1996 |
Schall U, Katta T, Pries E, Klöppel A, Gastpar M, 'Pain perception of intravenous heroin users on maintenance therapy with levomethadone', Pharmacopsychiatry, 29 176-179 (1996)
Methadone is a very potent analgesic drug. Accordingly, maintenance therapy of heroin addicts with methadone may conceal pain producing processes. Here we report on the pain perce... [more]
Methadone is a very potent analgesic drug. Accordingly, maintenance therapy of heroin addicts with methadone may conceal pain producing processes. Here we report on the pain perception of 42 patients on a levomethadone maintenance treatment for intravenous heroin users. Pain perception was measured by single-blind, non-invasive pressure stimulation of the nociceptors located in the dorsal extension aponeurosis and the underlying periosteum of the middle phalanx of a digit before and respectively 1, 2, and 4 hours after oral routine drug administration. Measures were related to the individual levomethadone plasma levels. Under steady-state conditions, the pain perception of the patients did not differ from a drug-free placebo control group and was not related to individual levomethadone plasma levels, although an analgesic effect in the reabsorption phase was observed. It is concluded that the individual pain perception of maintained patients is adapted to a normal response range and that even prolonged opioid consumption does not diminish dynamic analgesic responsiveness to levomethadone.
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1995 |
SCHALL U, SCHON A, ZERBIN D, EGGERS C, OADES R, 'ERP MEASURES OF PREPULSE INHIBITION IN AN AUDITORY ODDBALL DISCRIMINATION TASK - SPECIFICITY ACCORDING TO MEASURE AND DIAGNOSIS OF SCHIZOPHRENIA AND OBSESSIVE-COMPULSIVE DISORDER', BIOLOGICAL PSYCHOLOGY, 39 199-199 (1995) |
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1994 |
Schall U, Bender S, Lodemann E, Lutz KH, Rosinger C, Gastpar M, 'Drug abuse in the course of an outpatient substitution-supported therapy with L-methadone', Sucht, 40 315-324 (1994)
Drug abuse during methadone-supported out-patient therapy of opiate addicts is crucial to the outcome of this therapy. Here we report on the probable role of state and trait marke... [more]
Drug abuse during methadone-supported out-patient therapy of opiate addicts is crucial to the outcome of this therapy. Here we report on the probable role of state and trait markers as predictors of the patients' drug abuse in an out-patient methadone program with 247 participants over a five year period. Actual self-reported state of health and/or quality of life is more closely related to the individual drug consumption than trait-markers such as the psychiatric diagnosis. Depressive mood and psychosomatic complaints in general increase the probability of drug abuse during the methadone substitution supported therapy. Relapses seem to represent an activation of a 'drug seeking' behavioural pattern as an instrumental modification of the patient's state. Later on in the course of the therapy drug abuse becomes less frequent and alternative cognitive and behavioural strategies which are more adapted to social norms and requirements take place.
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1992 |
JAGER R, ARENDS JJA, SCHALL U, ZEIGLER HP, 'THE VISUAL FOREBRAIN AND EATING IN PIGEONS (COLUMBA-LIVIA)', BRAIN BEHAVIOR AND EVOLUTION, 39 153-168 (1992)
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1992 |
SCHALL U, ZERBIN D, OADES RD, 'EARLY SIGNAL-PROCESSING DEFICITS IN YOUNG SCHIZOPHRENICS', EUROPEAN JOURNAL OF NEUROSCIENCE, 226-226 (1992) |
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1991 |
SCHALL U, DELIUS JD, 'GRASPING IN THE PIGEON - CONTROL THROUGH SOUND AND VIBRATION FEEDBACK MEDIATED BY THE NUCLEUS BASALIS', PHYSIOLOGY & BEHAVIOR, 50 983-988 (1991)
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1991 |
BUNK D, SCHALL U, 'THE EFFICIENCY OF THE BACKGROUND INTERFERENCE PROCEDURE IN DISCRIMINATING BRAIN DAMAGES IN CHILDREN', PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE, 40 134-137 (1991) |
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1987 |
SCHALL U, 'VESTIBULAR, OLFACTORY, AND VIBRATORY RESPONSES OF NUCLEUS BASALIS PROSENCEPHALI NEURONS IN PIGEONS', NEUROSCIENCE RESEARCH, 4 376-384 (1987)
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1986 |
SCHALL U, GUNTURKUN O, DELIUS JD, 'SENSORY PROJECTIONS TO THE NUCLEUS BASALIS PROSENCEPHALI OF THE PIGEON', CELL AND TISSUE RESEARCH, 245 539-546 (1986)
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1986 |
SCHALL U, DELIUS JD, 'SENSORY INPUTS TO THE NUCLEUS BASALIS PROSENCEPHALI, A FEEDING-PECKING CENTER IN THE PIGEON', JOURNAL OF COMPARATIVE PHYSIOLOGY A-SENSORY NEURAL AND BEHAVIORAL PHYSIOLOGY, 159 33-41 (1986)
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1985 |
SCHALL U, GUNTURKUN O, DELIUS JD, 'AFFERENCES OF A FEEDING CENTER IN THE PIGEON', BEHAVIOURAL BRAIN RESEARCH, 16 227-227 (1985)
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Johnson EC, Bjelland DW, Howrigan DP, Abdellaoui A, Breen G, Borglum A, et al., 'No Reliable Association between Runs of Homozygosity and Schizophrenia in a Well-Powered Replication Study', PLOS Genetics, 12 e1006343-e1006343 [C1]
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Wang Y, Thompson WK, Schork AJ, Holland D, Chen C-H, Bettella F, et al., 'Leveraging Genomic Annotations and Pleiotropic Enrichment for Improved Replication Rates in Schizophrenia GWAS', PLOS Genetics, 12 e1005803-e1005803 [C1]
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