Dr. Jeff Johnson received a BS in Biology (1984) and MS in Pharmacology (1986) from the University of Minnesota-Duluth, and a PhD in Environmental Toxicology (1992) from the University of Wisconsin. He did postdoctoral training in the Department of Pharmacology at the University of Washington and spent four years as an assistant professor at the University of Kansas Medical Center before joining the University of Wisconsin School of Pharmacy faculty in 1999. Dr. Johnson is the Director of the Pharmacology and Toxicology BS program. He is also a member of the Waisman Center, Center for Neuroscience, Neuroscience Training Program, Cellular and Molecular Biology Training Program, MD/PhD Training Program, Molecular and Environmental Toxicology Training Program, and Molecular and Cellular Pharmacology Training Program.
The focus of his laboratory is Molecular Neuropharmacology/Neurotoxicology. Oxidative stress is believed to be a principal factor in the development of many chronic neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's and Amyotrophic Lateral Sclerosis. In general, oxidative stress can be defined as an imbalance in which free radicals and their products exceed the capacity cellular antioxidant defense mechanisms. A gain in product formation or loss in protective mechanisms can disturb this equilibrium leading to programmed cell death (PCD). PCD occurs normally with the aging process but appears to be accelerated in chronic neurodegenerative diseases due in part to increased oxidative stress. My laboratory's goal is to discover ways to increase the defense mechanisms in brain by activating multiple antioxidant defense genes simultaneously through activation of the antioxidant response element (ARE)—a process we refer to as programmed cell life (PCL). Any increase in the forces that drive PCD therefore must be balanced by increasing the forces driving PCL or the cell will die. Present work in the laboratory is designed to: 1) Identification of novel small molecules that activate the Nrf2-ARE pathway; 2) Characterize the expression pattern and regulation of the ARE in vivo and in primary neuronal and glial cultures derived from ARE transgenic reporter mice; 3) determine the neuroprotective efficacy of transplanted astrocytes and/or neural progenitor cells overexpressing Nrf2; 4) characterize the how changes in glutathione levels effect neurodegeneration; and 5) determine the effect of soluble amyloid precursor protein cleavage products on gene expression and neuronal survival. The laboratory is actively using chemical and genetic models of Parkinson's disease, Alzheimer's disease, Huntington's disease, Amyotrophic Lateral Sclerosis (Lou Gehrig's disease), and Epilepsy.