Shoshanah Longmuir
Florey Neurosciences Instititute, Victoria
Rotary Club of Parkes
Parkinson's Disease 2010
I undertook my undergraduate studies at Monash University, majoring in Molecular Biology, Microbiology and Genetics, before continuing to postgraduate studies in Microbiology at Monash University and Molecular and Cell Biology at La Trobe University.
My studies at Monash University involved host pathogen interactions of H. pylori, the causative organism of stomach ulcers and stomach cancer.
My studies at La Trobe University involved the Parkinson’s Disease (PD) proteins DJ-1 and HtrA2, both implicated in genetic forms of PD.
I am currently a PhD candidate at the Florey Neurosciences Institute, enrolled through the Centre for Neurosciences at Melbourne University.
My PhD project is investigating the mechanism of action of the secretion of the biomarker α-synuclein in Parkinson’s Disease.
SUMMARY OF PROJECT:
Secretion of the biomarker α-synuclein in Parkinson’s Disease
Parkinson’s Disease was first described in 1817. Despite this, molecular mechanisms of action in PD are still unclear.
Lewy Bodies are abnormal aggregates of protein that occur in the brain of patients with PD. They have long been considered the ‘gold standard’ pathological hallmark.
Although the majority of PD cases are not genetic, there are a small proportion that are hereditary. Disruption in the gene encoding α-synuclein (α-syn) was the first of these identified, with mutation and multiplication of the gene both resulting in PD.
Many of the proteins involved in genetic forms of PD have been implicated in the pathology of non-hereditary PD. α-syn is one such, as this protein is the main proteinaceous inclusion in Lewy Bodies, indicating a central involvement in the cause and progression of the disease.
The activity of α-syn has not been fully characterised. Recent studies have indicated that α-syn is secreted from cells, including blood cells and cultured cell lines. Evidence pointing to the central role of lysosome and other vesicle mishandling in PD has been described.
PD research has been hindered for lack of good models of the pathophysiology of PD. Preliminary data generated in the Horne lab provide evidence that a sub-population of blood cells (most likely B cells) may model the way a-syn secretion is changed in PD. This evidence provides support for our view that understanding the disturbance of a-syn secretion is likely to be associated with the central pathophysiology of PD.