Magdy Mekdad
Academic and Work Experience Prior to Sept 2024 Programme Start
I completed my undergraduate degree at Imperial College London, where I studied biochemistry and became interested in disease mechanisms and translational science. To further explore these, I completed a 12-monthindustry placement at LifeArc, Stevenage, where I joined the Protein Science team and developed strong skills across protein purification and assay development. I then continued my studies at the University of Cambridge, obtaining an MPhil in Biomolecular Science after working on a project to develop an in vitro model of multiple sclerosis. These experiences showed me that research is very exciting and I decided to pursue a PhD as a setting stone for my academic career.
PhD Programme- Year 1- MRes and Project Rotations
My first rotation project was in the Berninger lab, where I learned how to grow cortical organoids and I studied the formation of astrocytes at different time points. For the second rotation period, I had a joint project between the Spagnoli and Vigilante labs, and I learnt how to analyse single-cell RNA-sequencing data, and how it can be leveraged to understand cell-cell interactions in the developing mouse pancreas. Finally, I did my third rotation project in the Marzi lab, where I further developed my computational skills and I worked with a CUT&Tag dataset from postmortem human striatal tissue to study the cell-type specific H3K27 acetylation patterns in Parkinson's disease.
PhD Programme- Years 2 to 4- Doctoral Studies
For my PhD project, I will be supervised by Dr. Sarah Marzi, Prof. Marc-David Ruepp and Dr. Niamh O'Brien. My project will be investigating cellular senescence as a potential driver of motor neuron vulnerability in amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disorder with an average survival rate of 2-5 years post diagnosis. Most of the work will be done in vitro, and I will use hiPSCs with different mutations that are known to increase the risk of developing ALS (in genes such as TDP-43 and SOD1) to derive motor and cortical neurons. I will then trigger cellular senescence with different stressors, and I will study the interaction between the triggers, senescence, and ALS phenotype developed in each neuronal type at transcriptomic and epigenomic levels using RNA-sequencing, ATAC-sequencing and CUT&Tag (for H3K27 acetylation). A different part of this project will be done in collaboration with Dr. Jackie Mitchell, and I will be looking at the transcriptomic and epigenetic impacts of oxidative stress, as induced through chronic unpredictable mild stress, in a mouse model of ALS. Through this work, I am hoping to uncover some convergent mechanisms that link environmental factors to ALS genetics and identify potential therapeutic targets.
