My name is Emily Parlan. I’m a recent graduate of the University of Puget Sound, where I received a degree in Molecular and Cellular Biology and a minor in Business. Through my placement with the SENS Research Foundation Postbaccalaureate Fellowship Program, I have been working in the lab of Dr. Lisa Ellerby at the Buck Institute for Research on Aging, which focuses on understanding the molecular mechanisms underlying Huntington’s disease and other neurodegenerative disorders. Prior to my work in the Ellerby lab, I participated in the University of Washington Neurological Surgery Summer Student Program, where I investigated the effects of chronic intermittent hypoxia on adult neurogenesis in Dr. Nino Ramirez’s lab at Seattle Children’s Research Institute. I also completed a senior thesis project with Dr. Bryan Thines at the University of Puget Sound, characterizing a novel protein family involved in cellular stress responses of the model plant Arabidopsis thaliana.
My project in the Ellerby lab focuses on understanding the effects of apolipoprotein E on longevity pathways. Apolipoprotein E (ApoE) is a protein that helps transport cholesterol and other lipids throughout the body to provide energy to cells. Three versions, or isoforms, of the ApoE protein exist based on an individual’s genetic background – ApoE2, ApoE3, and ApoE4 – and each of these versions has unique roles in health and disease. Specifically, ApoE4 is a major risk factor for Alzheimer’s disease, while ApoE2 is associated with enhanced lifespan and reduced risk of neurodegeneration.
My project aims to understand the differences between these isoforms, particularly how they contribute to aging and neurodegeneration. To do this, I am using a systems biology approach to characterize stem cell lines with ApoE2, ApoE3 and ApoE4 backgrounds. This systems biology approach involves the high-throughput analysis of all genes, proteins, and lipids found within a cell, thus providing a broad overview of cellular status. By applying this systems biology approach to different cell types with different genetic backgrounds, I will be able to identify specific factors that are altered between ApoE isoforms, gaining insight to specific molecular pathways that might be responsible for the observed effects on aging and disease. In doing so, I hope to better understand the role of ApoE in disease and to potentially identify novel therapeutic targets for the treatment of Alzheimer’s and aging.