- Variant U1 snRNAs are implicated in human pluripotent stem cell maintenance and neuromuscular disease April 4, 2017
- LRRK2 in peripheral and central nervous system innate immunity: Its link to Parkinson’s disease March 20, 2017
- James S Porterfield Prize in International Virology 2017 February 9, 2017
- Differentially expressed, variant U1 snRNAs regulate gene expression in human cells January 31, 2017
- Human Induced Pluripotent Stem Cell-Derived Macrophages Share Ontogeny with MYB-Independent Tissue-Resident Macrophages January 28, 2017
DPhil Student | Lincoln College | firstname.lastname@example.org
I graduated from Emory University receiving a bachelor’s degree in Neuroscience and Behavioral Biology (NBB). As an honours student, my research project focused on delineating topological pattern of dendritic spine loss in animal models of Parkinson’s disease (PD). This study illustrated that in the MPTP-treated monkeys, the loss of dendritic spines was most severely shown in the sensorimotor striatal territory, which may explain motor disturbance seen in PD.
After graduating from Emory, I became a full-time research specialist in Professor Smith’s laboratory where I carried out an independent research project on Leucine Rich Repeat Kinase 2 (LRRK2), a recently discovered protein known to be the most common cause of autosomal dominant PD. My project created a detailed analysis of LRRK2 protein expression pattern in the basal ganglia and related thalamic nuclei of rhesus monkeys and further demonstrated that LRRK2 protein is predominantly expressed in dendrites and axon terminals in neurons.
My current DPhil project involves unravelling roles of LRRK2 in the immune system. Evidences of chronic inflammatory processes are often seen in PD and microglia-mediated neurotoxicity is suggested to play significant role in neurodegeneration. Recent studies have shown that LRRK2, along with other PD-associated genes, is highly present in various immune cells, including macrophages. I am currently using iPSC-derived macrophages as a cellular model to discover various aspect of LRRK2 biology and its possible contribution to PD pathogenesis.