- Senior Research Technologist
Kelly Ross has research expertise in cell biology and molecular genetics, with a focus on neurodegenerative disorders including Alzheimer's disease, related dementias and Parkinson's disease. She performs studies using human brain tissues donated by patients and their families to the Mayo Clinic brain bank. Her goal is to elucidate what goes wrong with specific genes and proteins involved in the disease process and identify clinicopathological subtypes of disease that may improve therapeutic strategies for individuals in a targeted way. Ross extracts DNA and RNA from brain tissues to run on expression arrays, generating large data sets to identify novel genes that may modulate disease progression. These approaches also provide data that can be shared with colleagues and collaborators around the world with the common mission of halting, and even preventing, the progression of these devastating disorders.
Ross received her Bachelor of Science in 2002 from the University of North Florida, Jacksonville, Florida. She joined Mayo Clinic in August 2005. Her research focus was on characterizing the most clinically relevant Parkinson's disease gene-protein leucine-rich repeat kinase 2 (LRRK2) using cell culture model systems and developing novel antibodies. As her research progressed, Kelly performed behavioral studies on various LRRK2 mouse models (developed by Heather L. Melrose, Ph.D., at Mayo Clinic's campus in Florida). In 2011, she received a master's degree in biomedical sciences from the Mayo Clinic Graduate School of Biomedical Sciences. Her thesis is titled "Characterization of Leucine-Rich Repeat Kinase 2-Associated Parkinson's Disease Using In Vivo Models."
Ross joined the Neuropathology and Microscopy Lab, led by Dennis W. Dickson, M.D., to study how neuropathological changes in the microtubule-associated protein tau (MAPT) lead to Alzheimer's disease. In 2017, she began investigating the heterogeneity of Alzheimer's disease with Dr. Murray to understand the molecular mechanisms that cause selective hippocampal vulnerability.