https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42660 Wed 31 Aug 2022 13:09:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43709 Wed 28 Sep 2022 10:15:57 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46325 Tue 15 Nov 2022 12:07:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54222 Tue 13 Feb 2024 12:11:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43277 Thu 15 Sep 2022 12:09:32 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55046 Thu 04 Apr 2024 13:58:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:36726 ɛ4/ɛ3> ɛ3/ɛ3> ɛ2/ɛ3> ɛ2/ɛ2). The greatest variation in lipids was related to the ɛ2 isoform, where various lysophosphatidylcholines and all phosphatidylethanolamine (PE) subclasses were elevated relative to ɛ3/ɛ3 and ɛ4 carriers. APOE ɛ4 carriers had reduced phosphatidylinositol relative to ɛ3/ɛ3 and ɛ2 carriers. Logistic regression revealed that ɛ2 carriers were at least 4 times higher odds of being in the highest tertile of PE lipid level relative to ɛ3/ɛ3. The elevation in PE and other phospholipids in ɛ2 carriers may indicate the protective effect of ɛ2 is linked to these phospholipids. Additionally, high baseline PE in cognitively normal participants predicted protection against cognitive decline six years later. Our data suggest substantial modulation of plasma lipids by APOE genotype and therefore indicates possible lipid targets and pathomechanisms involved in AD risk.]]> Thu 02 Jul 2020 09:10:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:10312 0.05). In participants without dementia (n=749), neither serum ferritin in 1994/5 or 2003/4 nor change in serum ferritin between these times was related to total CAMCOG or executive function scores, with or without adjustment for gender, age, National Adult reading test, or stroke history (all p> 0.05). No relationships were observed between ferritin and cognition for participants with possible or probable dementia (n=51). All participants identified as HFE C282Y homozygous or with serum ferritin >1,000 ng/ml had normal CAMCOG scores. We conclude abnormal body iron stores (low or high) are unlikely to have clinically significant effects on cognition or dementia risk in community-dwelling older people.]]> Sat 24 Mar 2018 08:12:22 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19672 Sat 24 Mar 2018 08:01:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:20882 -/- mice, a model of hemochromatosis, relative to age- and gender-matched wildtype controls. Classification by functional pathway analysis revealed transcript changes for various genes important in AD. There were decreases of up to 9-fold in transcripts for amyloid-β protein precursor, tau, apolipoprotein E, presenilin 1, and various other γ-secretase components, as well as Notch signaling pathway molecules. This included decreased transcripts for 'hairy and enhancer of split' Hes1 and Hes5, downstream targets of Notch canonical signaling. The reductions in Hes1 and Hes5 transcripts provide evidence that the changes in levels of transcripts for γ-secretase components and Notch signaling genes have functional consequences. The effects appeared relatively specific for AD in that few genes pertaining to other important neurodegenerative diseases, notably Parkinson's disease and Huntington's disease, or to inflammation, oxidative stress, or apoptosis, showed altered transcript levels. The observed effects on AD-related gene transcripts do not appear to be consistent with increased AD risk in HFE hemochromatosis and might, if anything, be predicted to protect against AD to some extent. As Hfe^-/- mice did not have higher brain iron levels than wildtype controls, these studies highlight the need for further research in models of more severe hemochromatosis with brain iron loading.]]> Sat 24 Mar 2018 07:57:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:17878 Sat 24 Mar 2018 07:56:13 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:26280 Sat 24 Mar 2018 07:40:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:28945 Sat 24 Mar 2018 07:31:25 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52824 Mon 30 Oct 2023 09:18:14 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41897 2, test for interaction p < 0.0001), and among men (test for interaction p < 0.0001). When the underreporting of Indigenous status on the death certificate was taken into account the relative rate increased to 2.17, 95% CI (2.07, 2.29). Indigenous Australians were also more likely to have their dementia coded as 'unspecified' on their death certificate (Odds Ratio 1.92, 95% CI (1.66, 2.21), p<0.0001), compared to the non-Indigenous group. Conclusion: This epidemiological analysis based on population level mortality data demonstrates the higher dementia-related mortality rate for Indigenous Australians especially at younger ages.]]> Mon 15 Aug 2022 12:23:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39219 HFE p.C282Y variant can cause iron overload and hemochromatosis, mostly in homozygous males. Objective: To estimate p.C282Y associations with brain MRI features plus incident dementia diagnoses during follow-up in a large community cohort. Methods: UK Biobank participants with follow-up hospitalization records (mean 10.5 years). MRI in 206 p.C282Y homozygotes versus 23,349 without variants, including T2* measures (lower values indicating more iron). Results: European ancestry participants included 2,890 p.C282Y homozygotes. Male p.C282Y homozygotes had lower T2* measures in areas including the putamen, thalamus, and hippocampus, compared to no HFE mutations. Incident dementia was more common in p.C282Y homozygous men (Hazard Ratio HR = 1.83; 95% CI 1.23 to 2.72, p = 0.003), as was delirium. There were no associations in homozygote women or in heterozygotes. Conclusion: Studies are needed of whether early iron reduction prevents or slows related brain pathologies in male HFE p.C282Y homozygotes.]]> Fri 27 May 2022 11:37:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46149 40 and Aβ₄₂ concentrations were measured using the ultrasensitive Single Molecule Array (Simoa) assay in 95 cognitively normal elderly individuals, who have all undergone PET to assess brain Aβ deposition. Based on the standard uptake value ratios (SUVR) obtained from PET imaging, using the tracer ¹⁸F-Florbetaben, plasma Aβ was compared between 32 participants assessed to have low brain Aβ load (Aβ–, SUVR <1.35) and 63 assessed to have high brain Aβ load (Aβ+, SUVR ≥1.35). Results: Plasma Aβ₄₂/Aβ₄₀ ratios were lower in the Aβ+ group compared to the Aβ–group. Plasma Aβ₄₀ and Aβ₄₂ levels were not significantly different between Aβ–and Aβ+ groups, although a trend of higher plasma Aβ₄₀ was observed in the Aβ+ group. Additionally, plasma Aβ₄₂/Aβ₄₀ ratios along with the known AD risk factors, age and APOE ɛ4 status, resulted in Aβ+ participants being distinguished from Aβ–participants based on an area under the receiver operating characteristic curve shown to be 78%. Conclusion: Plasma Aβ ratios in this study are a potential biomarker for brain Aβ deposition and therefore, for preclinical AD. However, this method to measure plasma Aβ needs further development to increase the accuracy of this promising AD blood biomarker.]]> Fri 11 Nov 2022 18:51:47 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33774 Fri 11 Jan 2019 14:26:39 AEDT ]]>