https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:45031 Wed 26 Oct 2022 10:52:42 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:53636 Tue 12 Dec 2023 16:00:49 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:35750 Thu 30 Jan 2020 17:02:08 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:36990 Thu 28 Oct 2021 12:36:02 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:53925 85 years and those with two or more admissions had greater odds of having CI screening documented. Among patients without CI screening documented, 72% (n = 78) were identified as cognitively impaired. While healthcare providers agreed CI screening was beneficial, they identified lack of time and poor knowledge as barriers to undertaking screening. Conclusions: CI is frequently unrecognised in the hospital setting which is a missed opportunity for the provision of appropriate care. Future research should identify feasible and effective strategies to increase implementation of CI screening in hospitals.]]> Mon 22 Jan 2024 16:41:34 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:42362 Mon 22 Aug 2022 14:08:28 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:15257 Mon 10 Sep 2018 13:48:41 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/ /manager/Repository/uon:34031 Herba cistanche, are known to exert protective effects on cognitive deficits in Alzheimer's disease (AD); however, the underlying mechanisms of this herbal extract on cognitive performance remain unclear. The aim of this study was thus to examine the protective mechanism attributed to PhG on cognitive deficits in an AD senescence accelerated mouse prone 8 (SAMP8) model. Cognitive deficit parameters examined included (1) Morris water maze (MWM) assessing cognitive performance and (2) quantification of dendritic spine density in hippocampal CA1 region by Golgi staining, a molecular biomarker of synaptic function. In addition, levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and gluthathione peroxidase (GSH-Px) were determined to examine the potential role of oxidant processes in cognitive dysfunction. Data showed that PhG significantly decreased escape latency and path length, associated with a rise in the percentage of time spent in the target quadrant and number of platform crossings. In addition, PhG significantly increased dendritic spine density in the hippocampal CA1 region accompanied by elevated expression levels of synaptophysin (SYN) and post synaptic density 95 (PSD-95), reduced MDA content, and elevated the activities of SOD and GSH-Px. Data suggest that the ability of PhG to ameliorate cognitive deficits in SAMP8 mice may be related to promotion in synaptic plasticity involving antioxidant processes.]]> Mon 04 Feb 2019 11:38:53 AEDT ]]>