R. Lee Mosley, MS, PhD, received his BS and MS in microbiology from the University of Oklahoma. In 1992, he graduated as the first PhD candidate from the University of Tulsa's Department of Biology. Dr. Mosley began his postdoctoral career in the Department of Pathology at the University of Michigan Medical Center and Department of Pathology and Experimental Toxicology at Parke-Davis Pharmaceutical Research Division. In 1994, he joined Dr. Richard A. Millerâ's laboratory as an Assistant Research Professor, where he addressed mechanisms of diminished T cell immunity in the aged. In 1998, Dr. Mosley joined the University of Nebraska Medical Center as Assistant Professor. In 2002, he joined the Center for Neurovirology and Neurodegenerative Disorders (CNND) as Chief of the Immunology Program to focus on vaccine and immunoregulatory therapies for HIV-1 associated neuropathology and neurodegenerative disorders such as Parkinson's disease and amyotrophic lateral sclerosis (ALS, Lou Gerhig's disease). He currently holds appointments in the CNND, Department of Pharmacology and Experimental Neuroscience, Department of Pathology and Microbiology, and Eppley Cancer Center. His recent research with Dr. Howard Gendelman and graduate student Eric Benner showed in a mouse model of Parkinson's disease (PD) that immune cells induced after immunization with glatiramer acetate (GA), a peptide polymer used to treat multiple sclerosis (MS) patients, significantly protect those neurons that are primarily affected by neurodegenerative processes in PD. This has led to recent investigations addressing the potential of natural regulatory T cells (Treg) in the PD model. Because GA has been shown safe and efficacious in MS patients, Dr. Mosley and the CNND in conjunction with Columbia University implemented clinical trials demonstrating the safety of GA treatments in ALS patients, and have recently initiated studies to evaluate the efficacy of GA and Treg therapeutic regimens in transgenic mice that carry the human SOD1 gene, thus rendering them susceptible to ALS-like neurodegeneration.