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Background Dental practitioners can have low confidence when addressing patient mental health as part of wider patient management. This is increasingly relevant due to the rising prevalence of mental health conditions and the relationship that can exist between mental and oral health. Interactive workshop teaching on patient mental health may enhance the confidence of dental students when addressing mental health conditions in patients. This study trialled workshop teaching as an educational intervention in five UK and Irish dental schools. Methods A quantitative, scenario-based confidence survey to further establish the need for intervention, followed by delivery of a workshop intervention to volunteer participants. Pre- and post-workshop surveys were used to assess the effectiveness of the workshop. Results Survey data showed low confidence among dental students when addressing patient mental health. Workshop intervention improved dental student confidence on average from 2.3-3.7 on a five-point scale, with less than 0.5% likelihood that reported changes in confidence were due to chance. Discussion Low confidence of dental students addressing patient mental health scenarios echoed wider literature findings surrounding dental clinicians' ability to address patient mental health. This further demonstrated the need for educational intervention, with workshop effectiveness demonstrated within this paper. Conclusion Workshop teaching is an effective way to enhance dental student confidence when addressing patient mental health and should be considered for implementation in the Bachelor of Dental Surgery curriculum., Key points Dental students across the UK and Ireland self-report low confidence when addressing patient mental health in the dental clinic, especially when addressing undiagnosed psychiatric conditions.Interactive workshop teaching is an effective method to significantly improve the confidence of dental students when addressing patient mental health.This study recommends the implementation of interactive workshop teaching within BDS curricula to ensure graduates can 'identify, explain and manage the impact of medical and psychological conditions', as recommended by the GDC.

© 2014 Elsevier Inc. Zinc transporter-3 (ZnT3) protein is responsible for loading zinc into presynaptic vesicles and consequently controls the availability of zinc at the glutamatergic synapse. ZnT3 has been shown to decline with age and in Alzheimer's disease (AD) and is crucially involved in learning and memory. In this study, we utilised whole animal behavioural analyses in the ZnT3 KO mouse line, together with electrophysiological analysis of long-term potentiation in brain slices from ZnT3 KO mice, to show that metal chaperones (clioquinol, 30 mg/kg/day for 6 weeks) can prevent the age-dependent cognitive phenotype that characterises these animals. This likely occurs as a result of a homeostatic restoration of synaptic protein expression, as clioquinol significantly restored levels of various pre- and postsynaptic proteins that are critical for normal cognition, including PSD-95; AMPAR and NMDAR2b. We hypothesised that this clioquinol-mediated restoration of synaptic health resulted from a selective increase in synaptic zinc content within the hippocampus. While we demonstrated a small regional increase in hippocampal zinc content using synchrotron x-ray fluorescence microscopy, further sub-region analyses are required to determine whether this effect is seen in other regions of the hippocampal formation that are more closely linked to the synaptic plasticity effects observed in this study. These data support our recent report on the use of a different metal chaperone (PBT2) to prevent normal age-related cognitive decline and demonstrate that metal chaperones are efficacious in preventing the zinc-mediated cognitive decline that characterises ageing and disease.

Cognitive decline in Alzheimer's disease (AD) involves pathological accumulation of synaptotoxic amyloid-β (Aβ) oligomers and hyperphosphorylated tau. Because recent evidence indicates that glycogen synthase kinase 3β (GSK3β) activity regulates these neurotoxic pathways, we developed an AD therapeutic strategy to target GSK3β. The strategy involves the use of copper- bis (thiosemicarbazonoto) complexes to increase intracellular copper bioavailability and inhibit GSK3β through activation of an Akt signaling pathway. Our lead compound Cu II (gtsm) significantly inhibited GSK3β in the brains of APP/PS1 transgenic AD model mice. Cu II (gtsm) also decreased the abundance of Aβ trimers and phosphorylated tau, and restored performance of AD mice in the Y-maze test to levels expected for cognitively normal animals. Improvement in the Y-maze correlated directly with decreased Aβ trimer levels. This study demonstrates that increasing intracellular copper bioavailability can restore cognitive function by inhibiting the accumulation of neurotoxic Aβ trimers and phosphorylated tau.