https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:24759 -11). The results were replicated in an independent cohort, the Hunter Community Study (p < 0.002) (n = 313). Conditional and joint analysis (COJO) confirmed the association of the chromosomal 17 region with ApoH levels. The set of independent SNPs identified by COJO explained 23% of the variance. The relationships between the top SNPs and cardiovascular/lipid/cognition measures and diabetes were assessed in Sydney MAS, with suggestive results observed for diabetes and cognitive performance. However, replication of these results in the smaller OATS cohort was not found. This work provides impetus for future research to better understand the contribution of genetics to ApoH levels and its possible impacts on health.]]> Wed 15 Dec 2021 16:09:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:34724 Thu 17 Feb 2022 09:27:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10285 Sat 24 Mar 2018 08:09:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17996 Sat 24 Mar 2018 07:56:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:21021 N = 2088) and the Sydney Memory and Ageing Study (Sydney MAS, N = 541). Genotyping was undertaken using Affymetrix microarrays with imputation to HapMap2. Analyses were performed using linear regression. No genome-wide significant results were observed in HCS nor were any of the top signals replicated in Sydney MAS. Gene-based analyses in HCS identified two significant genes (ZNF295, C2CD2), but these results were not replicated in Sydney MAS. One out of eight SNPs previously associated with GS, rs550942, located near the CNTF gene, was significantly associated with GS (p = 0.005) in the HCS cohort only. Study differences may explain the lack of consistent results between the studies, including the smaller sample size of the Sydney MAS cohort. Our modest sample size also had limited power to identify variants of small effect. Our results suggest that similar to various other complex traits, many genetic variants of small effect size may influence GS. Future GWAS using larger samples and consistent measures may prove more fruitful at identifying genetic contributors for GS in middle-aged to older adults.]]> Sat 24 Mar 2018 07:50:32 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:22195 Sat 24 Mar 2018 07:16:25 AEDT ]]>