This summer, I worked in the Lithgow Lab on a project aiming to improve our understanding of some of the processes involved in aging and age-related diseases, such as Parkinson’s disease. Dysfunction in mitochondria, a part of the cell involved in energy production, is commonly seen in aging, but how organisms respond to this dysfunction, and which responses are beneficial, is not fully understood. I investigated the relationships between some of these responses to mitochondrial dysfunction. More specifically, I was looking at how the mitochondrial unfolded protein response (UPR^mt), one of the ways cells attempt to restore malfunctioning mitochondria, is related to apoptosis and necrosis, processes that eliminate mitochondrial dysfunction by killing the entire cell. To complete my project, I used C. elegans, a microscopic nematode worm that has proven to be an excellent model for aging and age-related diseases. Overall, my project sheds light on the relationships between cellular mechanisms for addressing mitochondrial dysfunction. This work provides a foundation for future therapies that might promote mitochondrial rehabilitation and mitigate mitochondrial dysfunction and cell death, improving management of aging and treatment of age-related diseases

My name is Marta Williams, I am a graduate of Luther College, and this summer I interned in the Lithgow Lab at the Buck Institute for Research on Aging in Novato, CA, working under the mentorship of Dr. Suzanne Angeli and Dr. Gordon Lithgow. Broadly speaking, the Lithgow Lab is interesting in studying aging and age-related diseases, especially identifying genes and/or drug-like molecules that may prolong lifespan and mitigate aging’s deleterious effects. I also conducted research related to aging at both my home institution of Luther College in the lab of Dr. Stephanie Fretham and during an internship in the Rice Lab at NYU last summer, specifically focusing on neurodegenerative diseases, such as Alzheimer’s disease.