- Advancing Knowledge Through Team-Based Research -
Dr. James W. Lewis, received his PhD in Neurobiology from California Institute of Technology. His lab group investigates the general principles of how the human brain processes auditory and multisensory information, advancing models of cognition and of autism research. They primarily use functional magnetic resonance imaging (fMRI), with the 3T scanner at the Center for Advanced Imaging, but also use neurophysiological techniques such as collecting evoked response potentials (ERPs). One of their main research goals is to understand how the brains of people with autism are organized to represent knowledge of sensory events, and be able to gain a sense of meaning behind what they see and hear.
A West Virginia native, I graduated from WVU with a Bachelor of Science in Biology, summa cum laude and with honors. I am currently a post-doctoral fellow in the Simpkins lab, continuing my research project on the effects of the immune system on stroke.
Stroke is the 4th leading cause of death and leading cause of disability in the United States. During stroke and infection, cytokines, a component of your immune system, are increased. One cytokine that is increased is TNF-alpha. My research focuses on the effects of this cytokine on mitochondrial function. Mitochondria are the powerhouses of the cell and provide cells with energy. A decrease in mitochondrial function can result in profound cell death. I found that TNF-alpha rapidly and profoundly decreases mitochondrial function in neurons. This is an important observation because the increase in TNF-alpha after stroke can result in the death of neurons, which contributes to more brain damage after stroke. Understanding how TNF-alpha affects mitochondria and contributes to neuronal cell death provides us with a possible therapeutic target to decrease the amount of brain damage after stroke.
Currently, there is only one FDA approved therapeutic for stroke, tissue plasminogen activator (tPA). With stroke being such a burden not only in the United States but worldwide, new therapeutic targets are critical. Moreover, infection is now recognized as a risk factor for stroke, but clinically it is not well understood how an infection prior to stroke can affect outcome. I studied the effects of administering a bacterial infection mimic, lipopolysaccharide (LPS) prior to stroke on infarct size and post-stroke behavioral outcome. I hypothesized that the bacterial infection mimic would increase infarct size and that, post-stroke, the bacterial infection would exacerbate stroke-induced functional deficits due to the increase in cytokines, such as TNF-alpha, that negatively affect neuronal mitochondrial function and cell viability. I found that in fact a bacterial infection mimic (LPS) increases infarct size, exacerbates sickness behavior, and worsens neurological deficits. A possible mechanism may be decreased mitochondrial function, which highlights mitochondria as a possible therapeutic target for stroke.
As a post-doctoral fellow in Dr. Simpkins’s lab, I'm continuing my project on the effects of the immune system on stroke and learning molecular techniques to increase my current skill set. I want to pursue a career in industry. Ideally, I would like to work in a lab at a pharmaceutical company, and then eventually progress my career at the company to work closely with the FDA.