Amelia Smith

I completed my undergraduate degree in Biochemistry at Loughborough University with a first class honours. During this I undertook a year placement with AstraZeneca in their R&D site in Gothenburg, Sweden, where I worked on developing novel genome engineering strategies and became fascinated with the cellular mechanisms of neurodegeneration. To further pursue neurodegeneration from a biochemical approach, I completed an MSc in Neuroscience at the University of Oxford during which, I completed both of my research projects in the field of molecular neurodegeneration. Following on from this I worked in the Carlyle Lab for a year as a research assistant where I utilising iPSC-derived cortical neurons to conduct peptide and CRISPRi screens to explore potential protective effects of targets identified from Dr Becky Carlyles proteomic studies, following Amyloid beta treatment. Additionally, conducted long-read RNA sequencing of post-mortem tissue to create isoform-level region specific references for future proteomic experiments. Currently, I am a DPhil student in the Ryan Lab and Lady Margaret Hall College.

The multifactorial aetiology of Parkinson's Disease results from an interplay between genetic and environmental factors. Pesticides/toxicants continuously emerge as conferring increased risk of developing Parkinson's Disease. Overwhelming evidence implicates mitochondrial dysfunction and mitophagy deficits in Parkinson's Disease with familial PD-genes such as PINK1 and PRKN, as well as pesticides targeting mitochondria. Consequently toxico-genomic interactions have the potential to explain a large proportion of cases. Additionally, these toxicogenomic interactions may be potentiated or contribute to dopaminergic neuronal senescence. My DPhil project will investigate the interplay between patient PINK1 mutations and pesticides by characterising the effects on mitophagy, senescence and the subcellular proteome in patient, iPSC-derived dopaminergic neurons.