Patricia H Doyle, B.S.

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Patricia Doyle has nurtured an interest in the brain since high school. Before her senior year, she was accepted into a highly competitive Brain Camp program at Muhlenberg College, where she completed a small project on the effect of musical conditioning on performance in a targeted word search. During her undergraduate years at West Virginia University, she majored in Biology with a minor in Music Performance and a concentration in Neuroscience. She worked with Dr. Candice Brown in the Department of Neuroscience from 2016-2018 studying various biochemical aspects of neurodegenerative disease and stroke. In 2016, she completed a summer internship under the SURI program with Dr. Werner Geldenhuys in the West Virginia University Department of Pharmacy examining cellular models of Parkinson's Disease and changes in mitochondrial properties and bioenergetics. In 2017, she completed an REU internship at the University of North Dakota with Dr. Kumi Combs studying the effect of food allergies on cognitive function and gut permeability. She graduated from West Virginia University and was hired by Dr. Catherine Kaczorowski at The Jackson Laboratory as a Research Intern. Here, she utilized a genetically diverse panel of Alzheimer's Disease mice to answer questions related to anxiogenic susceptibility, changes in gene expression related to cognitive decline, and changes in metabolic function. She was accepted into the University of Kentucky Ph.D. program in Integrated Biomedical Sciences in 2020 and started in August of that year. She completed rotations with Dr. Maj-Linda Selenica, Dr. Ramon Sun, Dr. Josh Morganti, and Dr. Mark Ebbert during her first year and focused on different perspectives of studying neurodegenerative disease including biochemical approaches, genomics, metabolic changes, and single-cell changes in inflammation. In May 2021, she joined Josh Morganti's lab in the Department of Neuroscience and Sanders-Brown Center on Aging and began studying how the aging-specific inflammatory profile can increase susceptibility for dementia-like symptoms after traumatic brain injury.
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