Ashley Elizabeth Frakes, Ph.D.

Life expectancy is increasing globally. The economic and societal impact of a growing elderly population will be immense, because aging is inherently associated with physical frailty, cognitive decline, metabolic deterioration, and increased susceptibility to disease. Understanding the complex mechanisms leading to the gradual accumulation of cellular and tissue damage during aging are essential towards beginning to develop strategies to promote healthy aging and to prevent chronic disease.

Glial cells in the brain are first responders to disruptions in homeostasis, detecting changes in brain health long before patients or neurologists are aware of disease. Therefore, our lab seeks to identify mechanisms by which glia sense and respond to cellular stressors (such as excess/insufficient nutrients or misfolded proteins) as a unique opportunity to identify therapeutic targets and biomarkers for disease. We leverage the versatility of multiple model systems (C. elegans, cell culture, and mice) to reveal the mechanisms glial cells employ to sense and respond to cellular stressors to coordinate homeostasis within the central nervous system and peripheral tissues. We use a combination of tools including genetics, microscopy, animal behavioral assays, viral transduction, and single-cell functional genomics. Our long-term goal is to identify the fundamental cellular mechanisms that drive aging and give rise to age-onset metabolic and neurodegenerative diseases.

• NIH NRSA post-doctoral fellow, University of California Berkeley, 2015-2021
• Ph.D., The Ohio State University, 2014
• B.S., John Carroll University, 2009