Search

Shared decision making (SDM) has been acknowledged in the last decade. Literature has shown that when physicians are engaged in SDM and form a relationship with their patients, there is higher patient satisfaction of care. Moreover, SDM has been reported to improve patient outcomes and clinical measures. Despite this clear benefit of implementing SDM into clinical practice, there is little evidence for including SDM learning into preclinical medical education. We integrated an exercise for second year medical students to practice the steps of shared decision making. In this paper, the quantitative and qualitative results from a survey of medical students following the SDM learning exercise will be discussed. Students were more educated regarding SDM after this exercise and were motivated to use it in their future clinical careers. They also expressed overall positive attitudes towards SDM tools such as decision aids. Feedback to improve this SDM learning experience included the use of standardized patients, and to expand such education to the clinical environment training. This research provides a model of SDM practice integration into medical education. Similar programs can be beneficial for the development of SDM and other interpersonal skills.

Emerging studies suggest a role for tau in regulating the biology of RNA binding proteins (RBPs). We now show that reducing the RBP T-cell intracellular antigen 1 (TIA1) in vivo protects against neurodegeneration and prolongs survival in transgenic P301S Tau mice. Biochemical fractionation shows co-enrichment and co-localization of tau oligomers and RBPs in transgenic P301S Tau mice. Reducing TIA1 decreased the number and size of granules co-localizing with stress granule markers. Decreasing TIA1 also inhibited the accumulation of tau oligomers at the expense of increasing neurofibrillary tangles. Despite the increase in neurofibrillary tangles, TIA1 reduction increased neuronal survival and rescued behavioral deficits and lifespan. These data provide in vivo evidence that TIA1 plays a key role in mediating toxicity and further suggest that RBPs direct the pathway of tau aggregation and the resulting neurodegeneration. We propose a model in which dysfunction of the translational stress response leads to tau-mediated pathology.