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The Levinson Emerging Scholars Program
Kien-Thiet Nguyen - Neurobiology
It was during his time at a high school internship at Seattle Biomedical Research Institute that Kien-Thiet Nguyen first became exposed to research culture. Since his first ELISA, he has eagerly pursued research opportunities. As an undergraduate intern in the lab of Theodore White, he researched the import and transcriptional effects of certain classes of antifungals. During his sophomore year, he joined Gwenn Garden's lab researching the neurodegenerative disease, spinocerebellar ataxia type 7 (SCA7). His earlier research has shown in SCA7 there are changes in climbing fiber inputs to Purkinje cells, a vulnerable neuronal cell type in the cerebellum. His current research involves analysis of microRNA expression in microdissected Purkinje cells in SCA7 and nontransgenic mice. By utilizing basic bioinformatics techniques, Kien-Thiet hopes to identify and validate microRNA and their mRNA targets that are most differentially affected in SCA7. Kien-Thiet plans on pursuing a Ph.D. in neuroscience, with the goal of a career in translational research focusing on neurodegenerative diseases.
Mentor: Gwenn Garden, Neurology
Project Title: Analysis of Altered miRNA Expression in a Transgenic Mouse Model of SCA7
Abstract: Spinocerebellar ataxia type 7 (SCA7) belongs to a family of neurodegenerative diseases. It is characterized by degeneration of the cerebellum and brainstem. The disease is caused by an expanded polyglutamine tract in ataxin 7. This type of polyglutamine mutation is a common feature in many neurodegenerative diseases. Other neurodegenerative disease including those involving polyglutamine expansions demonstrate altered microRNA (miRNA) expression. Given the supporting evidence that miRNA are differentially expressed in other polyglutamine diseases, I seek to determine the role of miRNAs in SCA7. My proposed research will analyze altered miRNA expression in Purkinje cell neurons, a selectively vulnerable neuronal population that degenerate in SCA7. I will first identify miRNAs that are upregulated or downregulated in Purkinje neurons from SCA7 mice. Next using predictive databases I will identify their potential mRNA targets. I will then test identified miRNAs in cell culture to see if they will inhibit expression of their predicted target. If expression is inhibited, I will then measure the level of mRNA and protein of the predicted target in transgenic mouse tissue. By identifying miRNAs that are differentially expressed in SCA7 mice and confirming their activity, we can build our understanding of the mechanisms of disease progression in SCA7.