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Division of Natural Sciences & MathematicsDepartment of Biological Sciences

Faculty & Staff

Assistant Professor

Alysia Vrailas Mortimer

Alysia Mortimer 

Office: SG Mudd 303

Office Phone: (303) 871-4386

E-mail: alysia.mortimer@du.edu

Degrees

  • 2001 B.S., Biology - Univ of Tennessee at Chattanooga
  • 2005 Ph.D., Genetics and Molecular Biology - Emory University, Atlanta, GA

Research Interests

As we age we have an increased risk of developing a number of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and ALS (Lou Gehrig’s disease), as well as a variety of muscular dystrophies. However, this connection between aging and degenerative disease is not well understood. One common feature of both aging and many degenerative diseases is the presence of oxidative stress, such as superoxide ions, hydroxide ions, and hydrogen peroxide. Oxidative stress can result through exposure to oxidizing agents, such as certain toxins and pesticides, but it is also produced naturally within the body as a byproduct of mitochondrial cellular respiration, a process by which the cell generates energy. One hypothesis as to why we age is the Oxidative Stress Theory of Aging, which states that as an organism ages it accumulates oxidative damage to cellular structures such as DNA and proteins. This accumulated damage is detrimental to the cell potentially leading to cell death and the subsequent aging of the organism. In addition, increased oxidative stress is associated with a number of neurodegenerative diseases and muscular dystrophies. Interestingly, another key feature in common with aging, oxidative stress, degenerative disease is the formation of protein aggregates, such as amyloid-β plaques seen in Alzheimer’s disease and α-synuclein aggregates seen in Parkinson’s disease. Protein aggregation can be caused by disruptions in protein quality control (protein homeostasis), the process by which protein expression, folding, trafficking and degradation is regulated.

We are interested in understanding the molecular mechanisms that play a role in aging, neuronal and muscular degeneration and oxidative stress with ties to protein quality control. We utilize the model system Drosophila melanogaster (fruit fly) to identify genetic factors that are involved in aging, oxidative stress and muscle and neurodegeneration and how manipulating these genes affect the organism at the cellular, tissue, and whole organism level using a variety of genetic, molecular biology, and biochemical tools as well as behavioral analysis. Drosophila has proven to be an exceedingly effective system for studying these questions as the genes involved are highly conserved across species. In addition, fly models of human disease have characteristics that are often reminiscent of the symptoms seen in human patients, thus we can assess how different genes interact to contribute to or possible prevent a disease state. We have developed a new model of aging and oxidative stress in the fly by manipulating levels of the stress activated protein kinase, p38 MAP Kinase (p38K). We have found that increasing the levels of p38K leads to increased lifespan and increased resistance to environmental exposure to oxidizing agents. However, loss of p38K results in a dramatically reduced lifespan, age dependent locomotor dysfunction, increased levels of endogenous oxidative stress and increased sensitivity to oxidizing agents. We are currently exploring how p38K influences muscle and neurodegeneration and using the p38K model to screen for potential therapeutics.

View Mortimer's publications through PubMed