https://ogma.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:45103 Wed 26 Oct 2022 13:14:01 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:14264 −11) was with rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development. Four other schizophrenia loci achieving genome-wide significance contain predicted targets of MIR137, suggesting MIR137-mediated dysregulation as a previously unknown etiologic mechanism in schizophrenia. In a joint analysis with a bipolar disorder sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C (rs4765905, P = 7.0 × 10⁻⁹), ANK3 (rs10994359, P = 2.5 × 10⁻⁸) and the ITIH3-ITIH4 region (rs2239547, P = 7.8 × 10⁻⁹).]]> Wed 11 Apr 2018 18:45:05 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:27630 Froh and schizophrenia (β = 4.86,CI(β) = [0.90,8.83],Z = 2.40,p = 0.02). Since Keller et al. (2012), several studies reported inconsistent association of ROH burden with complex traits, particularly in case-control data. These conflicting results might suggest that the effects of autozygosity are confounded by various factors, such as socioeconomic status, education, urbanicity, and religiosity, which may be associated with both real inbreeding and the outcome measures of interest.]]> Wed 11 Apr 2018 14:15:34 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:20577 Wed 11 Apr 2018 12:29:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:16820 Wed 11 Apr 2018 12:28:20 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:34119 -4) with schizophrenia polygenic risk scores explaining up to 0.12% of the variance in ALS (P=8.4 × 10^-7). A modest increase in comorbidity of ALS and schizophrenia is expected given these findings (odds ratio 1.08-1.26) but this would require very large studies to observe epidemiologically. We identify five potential novel ALS-associated loci using conditional false discovery rate analysis. It is likely that shared neurobiological mechanisms between these two disorders will engender novel hypotheses in future preclinical and clinical studies.]]> Wed 04 Sep 2019 09:40:14 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:44630 Tue 18 Oct 2022 12:11:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:33797 Tue 15 Jan 2019 15:29:29 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:34283 −15), which persisted after excluding loci implicated in previous studies (OR = 1.07, P = 1.7 × 10⁻⁶). CNV burden was enriched for genes associated with synaptic function (OR = 1.68, P = 2.8 × 10⁻¹¹) and neurobehavioral phenotypes in mouse (OR = 1.18, P = 7.3 × 10⁻⁵). Genome-wide significant evidence was obtained for eight loci, including 1q21.1, 2p16.3 (NRXN1), 3q29, 7q11.2, 15q13.3, distal 16p11.2, proximal 16p11.2 and 22q11.2. Suggestive support was found for eight additional candidate susceptibility and protective loci, which consisted predominantly of CNVs mediated by nonallelic homologous recombination.]]> Tue 03 Sep 2019 18:30:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:24086 Thu 24 Mar 2022 08:57:28 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:36040 Thu 22 Jun 2023 10:07:54 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:47202 Thu 15 Dec 2022 11:18:18 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:17582 Sat 24 Mar 2018 08:03:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:21465 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.]]> Sat 24 Mar 2018 07:52:31 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:29641 Sat 24 Mar 2018 07:41:54 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:29335 Sat 24 Mar 2018 07:34:19 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:42338 N = 29,125 cases and 34,836 controls), a robust polygenic signal was observed from gene sets based on TCF4, FMR1, upregulation from MIR137 and downregulation from CHD8. Additional analyses revealed a constant floor effect in the amount of variance explained, consistent with the omnigenic model. Thus, we report that putative core gene sets showed a significant effect above and beyond the floor effect that might be linked with the underlying omnigenic background. In addition, we demonstrate a method to quantify the contribution of specific gene sets within the omnigenic context.]]> Mon 22 Aug 2022 14:00:20 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:38229 Mon 16 Aug 2021 17:39:39 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:43035 Mon 12 Sep 2022 11:49:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/manager/Repository/uon:42814 Mon 05 Sep 2022 14:06:54 AEST ]]>