Tim Schallert (E-mail)

Tim’s CV (Word document, 164kb)

Tim’s publications

Lab phone: (512) 471-6141

Fax: (512) 232-4335

Tim Schallert received his Ph.D. in Behavioral Neuroscience from Arizona State University in 1976. He was a Postdoctoral Fellow at the University of Illinois at Urbana-Champaign and the University of Lethbridge in Alberta, Canada. In 1979 he moved to The University of Texas at Austin, where he is currently a Professor in the Institute for Neuroscience and Departments of Psychology and Neurobiology. He was elected to the Academy of Distinguished Teachers and has received several other teaching awards, including the President’s Associates Teaching Excellence Award and the Amoco Foundation Teaching Award. He has served on the Executive Committee of the Institute for Neuroscience and as the Graduate Advisor for the Neuroscience Ph.D. program. He was Associate Chairman of the Dept of Psychology from 1985-1994. He is currently an Adjunct Professor in the Department of Neurosurgery at the University of Michigan in Ann Arbor and The Center for Human Growth and Development. He is a Fellow of the American Psychological Association, the American Psychological Society and the International Behavioral Neuroscience Society.

Research Interests

The brain and spinal cord are vulnerable to traumatic injury, stroke, tumors and degenerative diseases, often with devastating functional impairments, but at no time in the history of medicine have scientists been as optimistic as they are now about treatment strategies. Understanding how the central nervous system responds to the loss of nerve cells, and how behavior can influence the mechanisms of brain repair, is a major focus of our research.

We develop rat and mouse models of neurological disorders and strive to improve upon existing models. We have a multidisciplinary approach, with extensive collaborative arrangements with experts in other labs on campus, nationally and internationally. Collaborative research projects include searching for novel treatment interventions.

In Parkinson’s disease dopamine cells degenerate, eventually leading to severe impairments of movement. Using a new model of slow degeneration, we have investigated gene therapy, drugs and motor enrichment techniques that increase growth factors in the brain. These growth factors appear to keep the dopamine cells from dying, thereby preventing the behavioral dysfunction.

Whereas skilled motor activity protects neurons, behavioral inactivity is detrimental. In cerebral stroke, Parkinson’s disease, and other models of brain injury, physical activity and inactivity hasve only recently been recognized as highly influential. Behavior is often essential for cellular changes, synapse formation and neurogenesis. We look for sensitive periods after brain damage that provide unique opportunities to intervene beneficially.

We have helped to develop a new model of brain cancer. Unlike other models used to examine anti-cancer treatments, our model includes a highly sensitive behavioral analysis of brain function and neural plasticity, which are often adversely affected by traditional anti-cancer interventions. The hope is to use this model to find treatments that can shrink brain tumors without disturbing mechanisms important to optimal brain function. We also want to understand the stealth nature of brain tumors. Tumor cells slowly activate key mechanisms of plasticity which hide their presence despite ever more extensive encroachment on critical brain tissue. In collaboration with investigators at the University of Michigan and Henry Ford Neuroscience Center, we have developed promising chemical interventions that, unlike traditional treatments, appear to stop mitotic activity in tumor cells implanted in the striatum of the brain, without interfering with mechanisms of recovery of function and with a beneficial impact on behavioral outcome due to a positive effect on remaining tissue.