Neuroscience Student Pursues Genetic Underpinnings of Alzheimer’s Disease
Neuroscience major Kirsten Bonawitz ’17 received a Bass Connections follow-on grant to build on her research elucidating the role of genetics in the development of late-onset Alzheimer’s disease, mentored by Ornit Chiba-Falek. Follow-on research funds are available to undergraduate and graduate students who have completed (or are completing) a Bass Connections project team and propose to continue some aspect of the team’s work. Proposals are due March 10.

Upon receiving my Bass Connections grant, I began the summer of 2016 with the goal of continuing my research on the genetics of Alzheimer’s disease. My research project is aimed at analyzing the expression profiles of late-onset Alzheimer’s disease (LOAD) risk genes in neurons and glial cells from normal human brain tissue and tissue from three different pathological stages of LOAD (mild cognitive impairment, mild AD and severe AD). This approach will aid in determining at which point in disease progression and within which specific cells gene expression changes occur.
A main objective of this project is to further understanding about the genetic underpinnings of the etiology and pathophysiology of LOAD. I spent much of the summer and the beginning of the fall continuing my collection of neurons and astrocytes from frozen human brain tissue.
Additionally, a large achievement during the summer of 2016 was the publication of a paper detailing the procedures and the measures we used to confirm accuracy and reproducibility of our project methods. The paper was published in Frontiers for Molecular Neuroscience and is titled “Gene Expression Analysis of Neurons and Astrocytes Isolated by Laser Capture Microdissection from Frozen Human Brain Tissues” (Tagliafierro, Bonawitz, Glenn & Chiba-Falek, 2016).
My work has introduced me to an important concept in research: the inevitability of hitting a roadblock and the necessity of having the perseverance and creativity to look for a way around that obstacle.
My work during the past summer and previous semester has also introduced me to an important concept in research: the inevitability of hitting a roadblock and the necessity of having the perseverance and creativity to look for a way around that obstacle. Upon receiving my gene expression data, I discovered that all of the astrocyte samples that I had collected displayed neuronal contamination. Upon reviewing literature on the topic, I found a few studies that claimed that neurons express some amounts of GFAP, the marker that I used to stain for astrocytes, and moreover, that throughout Alzheimer’s disease progression, neurons may express increasing amounts of GFAP. Therefore, it was deemed that GFAP was not an adequate antibody to use for astrocyte selectivity, and we decided upon a new astrocyte marker, S100B.
By the end of the spring semester, I hope to have finished re-collecting neurons from samples that did not work during the first round of gene expression analysis as well as collecting astrocytes and microglia. This will hopefully allow me to better understand how expression of LOAD risk genes changes throughout progression of disease.
Learn More
- Save the date for the Bass Connections Showcase on April 20.
- Explore Bass Connections in Brain & Society.
- Read another grant recipient’s update, Going to the Source to Understand Ocean Energy Issues in Alaska.