Manny and Rosalyn Rosenthal – Dr. John Trotter MS Center Chair in Neuroimmunology; Professor of Neurology; Division of Adult Neurology; Section Head, Neuroimmunology
My main interest involves lymphocyte migration to the central nervous system (CNS) and cell-mediated factors underlying demyelination and axon injury, including cytokines, chemokines and free radicals. I employ a mouse model of relapsing/remitting inflammatory CNS demyelination (experimental allergic encephalomyelitis) in these studies. Using information gained through all of these studies, my goal is to modulate the pathogenic lymphocytes in the mouse model, and eventually in humans with MS, to prevent CNS injury. My laboratory is also interested in the role of B lymphocytes in MS, and is near completion of a clinical trial using B cell depletion in MS patients who have not responded optimally to standard therapies alone.
- BSc: 1976 Chemistry, University of South Alabama, Mobile, Alabama
- PhD: 1987 Department of Virology/Molecular Biology, St. Jude Children’s Research Hospital, Memphis, TN
- PhD: 1990 Neuropathology, National Multiple Sclerosis Society, Albert Einstein College of Medicine, Bronx, New York
- Postdoc: 1984 Neurology, George Washington University, Washington, District of Columbia
- Adult Neurology
The goal of our research is to understand the mechanisms involved in pathogenesis of inflammation and demyelination in the central nervous system (brain and spinal cord). Our research is primarily focused on the human disease multiple sclerosis (MS), which is very common (1/1000 in the US population). We study human tissues (blood, DNA, RNA, spinal fluid) and perform cutting-edge imaging of the human nervous system. We sometimes employ an animal model for MS known as experimental autoimmune encephalomyelitis (EAE). We are currently performing longitudinal imaging studies to help devise methods to differentiate the various types of pathologies in the human disease, such as demyelination, inflammation with cells and or edema due to blood-brain barrier breakdown, and axon damage and loss. We are funded to devise better methods to measure progression of MS over time, which might be used in clinical trials. We also study the effects of diet and calorie restriction upon neuro-inflammation, having shown previously that calorie restriction ameliorates EAE, the prime animal model for MS, at least partly through the upregulation of adiponectin and downregulation of leptin.
PI: Anne Cross, MD