https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:25928 −9) more prevalent in genomic regions that are likely to have undergone recent positive selection in humans (i.e., with a low NSS score). Variants in brain-related genes with a low NSS score confer significantly higher susceptibility than variants in other brain-related genes. The enrichment is strongest for schizophrenia, but we cannot rule out enrichment for other phenotypes. The false discovery rate conditional on the evolutionary proxy points to 27 candidate schizophrenia susceptibility loci, 12 of which are associated with schizophrenia and other psychiatric disorders or linked to brain development. Conclusions: Our results suggest that there is a polygenic overlap between schizophrenia and NSS score, a marker of human evolution, which is in line with the hypothesis that the persistence of schizophrenia is related to the evolutionary process of becoming human.]]> Wed 12 Aug 2020 09:42:59 AEST ]]> https://nova.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://nova.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://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46890 Tue 06 Dec 2022 12:02:52 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54811 Thu 14 Mar 2024 14:24:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:29641 Sat 24 Mar 2018 07:41:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30050 Sat 24 Mar 2018 07:31:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28311 Sat 24 Mar 2018 07:27:06 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23379 2 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.]]> Sat 24 Mar 2018 07:16:29 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23306 Sat 24 Mar 2018 07:16:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23305 Sat 24 Mar 2018 07:16:19 AEDT ]]>