https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 Analyzing the role of microRNAs in schizophrenia in the context of common genetic risk variants https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29013 P < 2 × 10−16). Further, the gene set analyses revealed several miRNAs regulating schizophrenia risk genes, with the strongest enrichment for targets of miR-9-5p (P = .0056 for enrichment among the top 1% most-associated single-nucleotide polymorphisms, corrected for multiple testing). It is further of note that MIR9-2 is located in a genomic region showing strong evidence for association with schizophrenia (P = 7.1 × 10−8). The second and third strongest gene set signals were seen for the targets of miR-485-5p and miR-137, respectively. Conclusions and Relevance: This study provides evidence for a role of miR-9-5p in the etiology of schizophrenia. Its implication is of particular interest as the functions of this neurodevelopmental miRNA tie in with established disease biology: it has a regulatory loop with the fragile X mental retardation homologue FXR1 and regulates dopamine D2 receptor density.]]> Wed 11 Apr 2018 15:28:50 AEST ]]> Investigating the causal relationship of C-reactive protein with 32 complex somatic and psychiatric outcomes: a large-scale cross-consortium mendelian randomization study https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29040 Wed 07 Jul 2021 12:14:25 AEST ]]> Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49007 Wed 03 May 2023 12:17:36 AEST ]]> Transcriptomic abnormalities in peripheral blood in bipolar disorder, and discrimination of the major psychoses https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41878 Tue 16 Aug 2022 10:04:26 AEST ]]> Australian schizophrenia research bank: a database of comprehensive clinical, endophenotypic and genetic data for aetiological studies of schizophrenia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10415 Sat 24 Mar 2018 08:12:38 AEDT ]]> Evidence for genetic overlap between schizophrenia and age at first birth in women. https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29862 2 = 1.1E-03, P = 4.1E-04), reflecting the published relationship between maternal age and SCZ risk in offspring by McGrath et al in 2014. Conclusions and Relevance: This study provides evidence for a significant overlap between genetic factors associated with risk of SCZ and genetic factors associated with AFB. It has been reported that SCZ risk associated with increased maternal age is explained by the age of the father and that de novo mutations that occur more frequently in the germline of older men are the underlying causal mechanism. This explanation may need to be revised if, as suggested herein and if replicated in future studies, there is also increased genetic risk of SCZ in older mothers.]]> Sat 24 Mar 2018 07:40:47 AEDT ]]> Transcriptome-wide mega-analyses reveal joint dysregulation of immunologic genes and transcription regulators in brain and blood in schizophrenia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25812 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.]]> Sat 24 Mar 2018 07:34:35 AEDT ]]> A polygenic resilience score moderates the genetic risk for schizophrenia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:38229 Mon 16 Aug 2021 17:39:39 AEST ]]> Large-Scale Evidence for an Association between Peripheral Inflammation and White Matter Free Water in Schizophrenia and Healthy Individuals https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46105 Fri 11 Nov 2022 11:44:05 AEDT ]]> Interaction Testing and Polygenic Risk Scoring to Estimate the Association of Common Genetic Variants with Treatment Resistance in Schizophrenia https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49142 Fri 05 May 2023 12:07:01 AEST ]]> BrainGENIE: The Brain Gene Expression and Network Imputation Engine https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51344 Fri 01 Sep 2023 13:34:14 AEST ]]>