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Parkinson's disease (PD) is characterized by multiple symptoms including olfactory dysfunction, whose underlying mechanisms remain unclear. Here, we explored pathologic changes in the olfactory pathway of transgenic (Tg) mice of both sexes expressing the human A30P mutant α-synuclein (α-syn; α-syn-Tg mice) at 6–7 and 12–14 months of age, representing early and late-stages of motor progression, respectively. α-Syn-Tg mice at late stages exhibited olfactory behavioral deficits, which correlated with severe α-syn pathology in projection neurons (PNs) of the olfactory pathway. In parallel, olfactory bulb (OB) neurogenesis in α-syn-Tg mice was reduced in the OB granule cells at six to seven months and OB periglomerular cells at 12–14 months, respectively, both of which could contribute to olfactory dysfunction. Proteomic analyses showed a disruption in endocytic and exocytic pathways in the OB during the early stages which appeared exacerbated at the synaptic terminals when the mice developed olfactory deficits at 12–14 months. Our data suggest that (1) the α-syn-Tg mice recapitulate the olfactory functional deficits seen in PD; (2) olfactory structures exhibit spatiotemporal disparities for vulnerability to α-syn pathology; (3) α-syn pathology is restricted to projection neurons in the olfactory pathway; (4) neurogenesis in adult α-syn-Tg mice is reduced in the OB; and (5) synaptic endocytosis and exocytosis defects in the OB may further explain olfactory deficits.SIGNIFICANCE STATEMENTOlfactory dysfunction is a characteristic symptom of Parkinson's disease (PD). Using the human A30P mutant α-synuclein (α-syn)-expressing mouse model, we demonstrated the appearance of olfactory deficits at late stages of the disease, which was accompanied by the accumulation of α-syn pathology in projection neurons (PNs) of the olfactory system. This dysfunction included a reduction in olfactory bulb (OB) neurogenesis as well as changes in synaptic vesicular transport affecting synaptic function, both of which are likely contributing to olfactory behavioral deficits.

Objective: We outline the framework of a collaborative process to redesign an existing 5-year health education program, which may prove useful to other similar institutions. The aim was to strengthen evidence-based practice and curriculum alignment. Methods: A whole-of-program approach was used to restructure the existing courses into 3 “streams”: professional practice, clinical research, and clinical science. The process incorporated a series of facilitated workshops organized by the department director of learning and teaching and the faculty facilitation team, and it was inclusive of all available members of the department, a clinic supervisor, a sessional (casual teaching) staff member, and a recent graduate of the program. Results: Unit content and assessments were restructured to progress the program learning outcomes from year to year. The undergraduate program was redesigned to create a more logical learning pathway for students. Consolidation of subject topics in the postgraduate program allowed for the development of stand-alone research-only units. Conclusion: The mechanism of curriculum mapping allowed for discussion about the flow of information from year to year and how evidenced knowledge and understanding can be developed. It is necessary that everyone participates and understands the importance of program goals as developed by the process. Because drift in curriculum can occur incrementally over the years, to be effective, the program requires ongoing monitoring and regular collaboration to continue improvements.