My research interests lie in better understanding the molecular mechanisms underlying neurodegenerative diseases, like Parkinson's Disease, using human iPSC-derived lines to study relevant cell types.
My DPhil project aims to elucidate how GBA, a risk factor gene for Parkinson's, interacts with autophagic and mitochondrial pathways to result in neurodegeneration.
As 10% or less of Parkinson's cases are monogenic, risk factor genes play key roles in the disease's pathology. One such risk factor that has come to light in recent years is GBA. Mutant homozygotes develop Gaucher's Disease - a lysosomal storage disorder - while heterozygotes are correlated with earlier-onset Parkinson's; however, how GBA interacts with other cellular processes to give rise to Parkinson's is still poorly understood. To better understand these interactions, I am using human iPSC-derived dopaminergic neurons to examine mitochondrial and autophagic phenotypes. iPSCs provide a number of advantages, namely that they exactly recapitulate the genetic background of patients and allow for studies in the relevant cell types. Through various fluorescent and optogenetic constructs, the basal phenotypes of GBA heterozygotes will be assayed and their respective pathways dissected. Such a characterisation will provide greater understanding into the mechanisms of sporadic Parkinson's as well as novel targets for small-molecule intervention.
Mouse L4V1 Pyramidal Neuron
I obtained two B.S. degrees with Honors in Neuroscience and Molecular & Cellular Biology with a Minor in Spanish for the Professions from Johns Hopkins University, Baltimore, MD, in May 2015. During my time at Johns Hopkins University, I worked in the lab of Dr. Hey-Kyoung Lee where I researched cross-modal plasticity in mouse primary visual and auditory cortices and was named a Goldwater Scholar.
I started my DPhil in Biomedical Science under Drs. Richard Wade-Martins (Oxford/DPAG) and Craig Blackstone (NIH/NINDS) in September 2015 working on human iPSC-derived dopaminergic neurons carrying mutations in the GBA gene. As a National Institutes of Health Oxford-Cambridge Scholar, I am sponsored by the NIH and will divide my DPhil studies equally between the two locations, with my first two years spent in the Wade-Martins Group at Oxford University.