- Lopinavir plus nucleoside reverse-transcriptase inhibitors, lopinavir plus raltegravir, or lopinavir monotherapy for second-line treatment of HIV (EARNEST): 144-week follow-up results from a randomised controlled trial June 15, 2018
- Stem cell modeling of mitochondrial parkinsonism reveals key functions of OPA1 June 10, 2018
- LRRK2 is a negative regulator of Mycobacterium tuberculosis phagosome maturation in macrophages June 5, 2018
- The nature and nurture of cell heterogeneity: Accounting for macrophage gene-environment interactions with single-cell RNA-Seq May 30, 2018
- Human Induced Pluripotent Stem Cell-Derived Macrophages Share Ontogeny with MYB-Independent Tissue-Resident Macrophages April 29, 2018
DPhil Student | Lincoln College | email@example.com
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.