Stephanie Boas, Ph.D.

University of Michigan

Stephanie Boas is a postdoctoral researcher in the lab of Catherine Kaczorowski at the University of Michigan. Her research interests focus on understanding cell-type-specific pathogenic mechanisms across neurodegenerative diseases, and how genetic risk factors differentially impact diverse cell types and regions of the brain. Boas has a strong background in molecular techniques and neurodegenerative disease processes. In her graduate work at the University of Alabama at Birmingham (UAB), she studied how heterogeneous neuronal subtypes are differentially affected in rodent models of Parkinson’s disease in the lab of Rita Cowell. She also took advantage of several informal and formal mentorship opportunities, such as training several Cowell Lab undergraduates in molecular techniques and science communication. She also mentored several summer students through UAB’s Summer Program in Neuroscience (SPIN) program. Additionally, she served as a teaching assistant for two semesters of biostatistics. Baos finds mentorship opportunities to be energizing, both to her individually, and to the lab as a whole. While she has had incredible opportunities throughout her education, she’s originally from a rural town in Illinois, so he understands what it’s like to have limited exposure to academic opportunities, and how much this exposure can influence young scientists. Boas is excited to be a part of programs like these that create such opportunities.

Principal Investigator: Catherine Kaczorowski

Fellow: Lauren Benovich

Undergraduate Fellow Project: Genetic mechanisms controlling resilience to Huntington’s disease
This project will focus on identifying drivers of resilience to Huntington’s disease (HD). We have generated a novel mouse panel by crossing an HD mouse line to the genetically-diverse BXD panel for a systems genetic approach to identify modifiers that contribute to HD resilience in a ‘humanized’ mouse population. To quantify resilience across this panel, we are evaluating BXD substrains carrying the HD transgene on various cognitive and motor tasks. The BXD panel allows for quantitative trait loci mapping to correlate genetic variants to a given phenotypic outcome. We will investigate targets identified through trait mapping to inform follow-up genetic knockout/CRISPR editing strategies, using both in vitro and in vivo models. The Kaczorowski lab, and this project in particular, are ideal for a student in this program because there is an opportunity for exposure to diverse techniques, depending on the proclivities of the student. The SURFiN fellow could focus on any of the following: 1) behavioral phenotyping, learning to run mice on behavioral tasks; 2) cell culture assays on BXD cell lines; and/or 3) computational analyses (trait mapping, pathway modeling).

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