Project Title: The role of genetic risk variants in regulatory elements in Parkinson’s Disease
Supervisor: Dr Alexi Nott, Professor Steve Gentleman, Dr Sarah Marzi
Location: Level 7, Sir Michael Uren Hub, White City Campus, 86 Wood Lane, W12 0BZ
I am a PhD student in the Nott lab within the Department of Brain Sciences at Imperial College London, investigating the role of genetic risk variants in Parkinson’s Disease. Before I joined the lab, I received both my BSc in Applied Biology and MSc in Biomedical Sciences from the University of Applied Sciences Bonn-Rhein-Sieg, Germany. As part of this, I performed the research project of my bachelor in the Institute of Molecular Psychiatry at the University of Bonn on the characterization of a glia-specific knock-out mouse line, which inspired my interest in the field of neuroscience.
During my MSc, I became fascinated by stem cells and their application in regenerative medicine and as disease models. Hence, to complete my MSc, I investigated molecular processes occurring during osteogenesis using induced pluripotent stem cells (iPSCs) at the University of Applied Sciences Bonn-Rhein-Sieg. In the Nott lab I plan to integrate my experience on working with iPSCs to elucidate functional relevance of neurodegenerative disease-associated risk variants.
2018-2021: MSc Biomedical Sciences, University of Applied Sciences Bonn-Rhein-Sieg, Germany
2015-2018: BSc Applied Biology, University of Applied Sciences Bonn-Rhein-Sieg, Germany
Most cases of Parkinson’s Disease (PD) are idiopathic, only a relatively small fraction can be attributed to monogenic causes. Genome wide association studies have identified many risk variants for PD, however, most reside outside of protein coding genes, often in gene regulatory regions such as enhancers. I am interested in identifying putative gene targets related to PD-associated risk variants. My project will use induced pluripotent stem cells, as well as post-mortem brain tissue, to obtain epigenetic and chromatin conformation data to link noncoding risk variants to target genes.
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