Todd Christian Peterson, PhD

Professional Education and Training:

University of Wisconsin-Milwaukee, B.A., 2006
University of Wisconsin-Milwaukee, M.S., 2010
Southern Illinois University – Carbondale, Ph.D., 2013
Stanford University, Post-doctoral scholar, present


Email:
tcpeters@stanford.edu


Research Interests:

Relatively permanent changes to the nervous system occur in response to environmental conditions imposed upon an organism, including stimulus characteristics, behavioral processes, or neural insult. I am interested in the response of the central nervous system to insult specifically traumatic brain injury or stroke. These types of injury are two of the leading causes of death and disability in the United States, for which there are few effective treatments.

One of the major consequences of neural insult is neuroinflammation. This cascade can be both beneficial and detrimental, and there is much to be learned about the dynamics of this complicated response. It is characterized by increases in pro and anti-inflammatory cytokines, leukocyte invasion, blood-brain barrier permeability, and glial activation. Astrocytes are one glial cell type that is activated following injury and have been shown to regulate the immune response. I am interested in elucidating astrocyte specific aspects of neuroinflammation in hopes of developing therapeutic treatments for central nervous system damage. In particular I am focusing on a master regulatory cytokine called transforming growth factor-beta1 that is increased following neural insult and is anti-inflammatory.

In the future, I also want to study a phenomenon called experience-dependent plasticity; neural changes that occur throughout the organism’s life in response to the environment. More specifically, I am interested in how stimuli in the environment, whether detrimental or facilitative, directly affect brain morphology and behavior. Developing a better understanding of these brain-behavior relationships can be utilized to promote functional recovery following injury. The ultimate goal of this line of research will inform rehabilitative strategies for human traumatic brain injury and stroke.


About me:

I grew up in the Midwest, but I have quickly been adapting to the west coast lifestyle. When I am not working vigorously in the laboratory, I enjoy many sports including long distance running, volleyball, snowboarding, and most water sports (wakeboarding, kiteboarding, and surfing).

My graduate work began with Dr. Rodney Swain at the University of Wisconsin – Milwaukee where I explored the manner in which the cerebellum contributes to complex behaviors. More specifically I was interested in the behavioral deficits that emerge following ablation of the deep cerebellar nuclei and modifications of both behavior and brain morphology with the potential to reverse these deficits by modulating reinforcement characteristics.

After receiving my M.S. degree, I began working in Dr. Michael R. Hoane’s Restorative Neuroscience Laboratory at Southern Illinois University-Carbondale. I focused on examining recovery of function following traumatic brain injury (TBI) and other neurodegenerative diseases. I conducted several preliminary experiments on different neuroprotective compounds (including nicotinamide and progesterone) demonstrating the dosing and administration techniques at which each individual compound is neuroprotective. I also characterized two TBI experimental models; by comparing behavioral and histological deficits of a more diffuse type of injury (fluid percussion injury) with a more focal type of injury (controlled cortical impact) over the sensorimotor cortex. Either type of damage to this area resulted in abundant, long lasting deficits, which are ideal for multiple group comparisons.

My dissertation research used this model to concentrate on the beneficial effects of a combination therapy of nicotinamide and progesterone following TBI. The majority of TBI researchers agree that the future clinical treatment of TBI will include polytreatments to combat the deficits induced by damage to the central nervous system. I combined two relevant compounds known to be neuroprotective following TBI; progesterone, a steroid hormone that is in phase II human clinical trials and nicotinamide, a B-vitamin with over a decade of research demonstrating its neuroprotective properties. I demonstrated the behavioral and histological benefits of this polytreatment following injury.