Biography
I am a first year PhD student in the Martins Team at the University of Cambridge and I am a member of the Medical Research Council Doctoral Training Programme student committee. Before starting my PhD studies at Cambridge, I completed a Master’s Degree in Pharmacology at the University of Bristol. There, I lead sessions for first year pharmacology undergraduates and was awarded a first-class honours degree. Because of my desire to help discover novel treatments for neurodegenerative disorders throughout my master’s, I participated in summer placements researching the relationship between neurons and astrocytes with Dr Anja Teschemacher and Dr Sergey Kasparov. I also spent a year working in the neuroscience department at AstraZeneca, where I performed target validation research associated with neuroinflammation. Through this, I gained experience in a range of molecular techniques, such as western blotting, immunocytochemistry, and RT-qPCR assays. I learnt how to mature iPSCs into motor neurons. I also learnt how to generate transgenic cell lines and perform live cell image analysis. These experiences further fuelled my desire to research neurodegenerative diseases, and I am thrilled to be conducting research with the Martins team.
Research Interests
Mitochondrial dysfunction is a prevalent feature among various neurodegenerative diseases. Notably, analyses of Alzheimer's disease (AD) post-mortem brains showed an increase in contact sites between the mitochondria and endoplasmic reticulum. Our lab has previously shown that an increase in mitochondrial-endoplasmic reticulum contact sites (MERCS) may confer a protective role in models of AD, potentially by improving mitochondrial function and increasing neuronal health. However, findings from different research groups suggest MERCS could exert detrimental effects. My research is directed towards elucidating the differential expression of genes regulating MERCS in Alzheimer's disease and determining whether such variations contribute to protective or harmful outcomes.
In parallel, I am conducting research investigating whether clinically approved compounds which have been identified to increase MERCS have protective or toxic effects in iPSC-derived cortical neurons. This will hopefully complement my ongoing genetic work and enable the identification of specific molecular networks that regulate MERCS and might be manipulated to achieve neuroprotection in neurodegenerative diseases such as AD.
