Ashley Frakes, Ph.D., Stadtman Tenure-Track Investigator
Professional Experience
- NIH NRSA post-doctoral fellow, University of California Berkeley, 2015-2021
- Ph.D., The Ohio State University, 2014
- B.S., John Carroll University, 2009
Current Research
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.
Select Publications
- Measurements of Physiological Stress Responses in C. Elegans.
- Bar-Ziv R, Frakes AE, Higuchi-Sanabria R, Bolas T, Frankino PA, Gildea HK, Metcalf MG, Dillin A.
- J Vis Exp (2020 May 21) Abstract/Full Text
- Four glial cells regulate ER stress resistance and longevity via neuropeptide signaling in C. elegans.
- Frakes AE, Metcalf MG, Tronnes SU, Bar-Ziv R, Durieux J, Gildea HK, Kandahari N, Monshietehadi S, Dillin A.
- Science (2020 Jan 24) 367:436-440. Abstract/Full Text
Research in Plain Language
One central hallmark of aging and many age-onset diseases such as Alzheimer’s and type 2 diabetes, is the loss of the cell’s ability to maintain healthy, functional proteins. We found that glial cells, non-neuronal cells in the brain, can coordinate an organism-wide protective response to maintain healthy proteins, thereby increasing whole organism health and lifespan. We propose to identify the required components of this response which may produce novel therapeutic targets to promote healthy aging and to prevent or delay age-onset disease.