https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30287 Wed 11 Apr 2018 12:31:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30094 Wed 09 Mar 2022 16:00:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49081 Wed 03 May 2023 16:22:13 AEST ]]> 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: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 ]]>